Page last updated: 2024-10-19

niacinamide and Neoplasms

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.

Research Excerpts

ExcerptRelevanceReference
"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."9.24Phase 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."9.16A 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."8.90Incidence 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)."8.89Risk 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."8.84Incidence 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)."7.78Sorafenib 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."7.76Hypertension 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."6.53Toxic 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."5.35Rapid 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."5.31Rat 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."5.24Phase 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."5.16A 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."4.90Incidence 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)."4.89Risk 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."4.86Biochemical effects of SIRT1 activators. ( Baur, JA, 2010)
" Sunitinib and sorafenib are multitargeted TKIs that have been demonstrated to induce hypothyroidism and thyroid dysfunction."4.85Hypothyroidism 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."4.84Incidence 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."3.80Sorafenib 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)."3.78Sorafenib 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."3.76Hypertension 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."3.75Ambulatory 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."3.30A 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."3.30A 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."3.01Nicotinamide 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."3.01Selective 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."3.01Safety 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."2.90A 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."2.84Phase 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."2.84EVESOR, 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."2.84Phase 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."2.82A 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."2.82Pediatric 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."2.82Phase 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)."2.82Pimasertib, 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."2.80Phase 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."2.80Dual 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."2.80A 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."2.80Multiparameter 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."2.79Phase 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)."2.78The 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."2.78Alternative 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."2.78Phase 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."2.78Phase 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."2.77A 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."2.77Phase 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."2.77Saturable 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."2.77Plasma 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."2.77Phase 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%)."2.77Phase 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."2.77Safety 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."2.76A 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."2.76Pharmacokinetic 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%)."2.76Safety 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."2.76Two 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."2.76Safety 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."2.75Phase 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."2.75A 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."2.75A 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."2.74Phase 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."2.73Effect 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."2.73Combination 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)."2.73Safety 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)."2.73Results 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%)."2.73Safety, 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."2.73Phase 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."2.73Phase 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."2.72Pharmacodynamic 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."2.72Results 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."2.71Phase 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."2.71Phase 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."2.71Safety 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."2.68Human 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."2.58Pharmacology of Pimasertib, A Selective MEK1/2 Inhibitor. ( Srinivas, NR, 2018)
"Sorafenib is a multikinase-tyrosine kinase inhibitor commonly used in a variety of cancers."2.55Risk 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."2.55Kinase 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."2.55Inefficiencies 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."2.53Toxic 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."2.53Design 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."2.53The 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."2.52The 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."2.52Risk 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."2.50Risk 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)."2.50Drug 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."2.50Sorafenib: 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."2.50Clinicopathological 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."2.49Body 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."2.49Assessment 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."2.49Inhibition 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."2.48Molecular 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."2.48Using 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."2.48Evidence 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."2.48Polymorphisms 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."2.47The 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."2.46Compounds 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."2.46Sorafenib. ( 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."2.46Cardiovascular 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."2.46Tumor-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."2.45Cardiac dysfunction induced by novel targeted anticancer therapy: an emerging issue. ( Chen, MH, 2009)
"Future potential uses of bevacizumab in cancer therapy will be discussed."2.45The 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."2.44Selected 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."2.44Safety, 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."2.44Design 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."2.44Sorafenib: 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."2.44Mechanisms 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."2.44New 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."2.44Safety 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."2.44Systematic 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."2.44Mcl-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."2.43Sorafenib (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."2.43Pooled 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."1.91NAD ( 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."1.72Remote 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)."1.56Disturbed 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."1.48Influence 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."1.43The 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."1.43Widespread 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."1.43Pilot 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."1.42Biological 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."1.42Cardiovascular 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."1.42Combinatorial 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."1.42Population 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."1.40ROS-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."1.40Downregulation 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."1.40Coupled 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."1.39NNMT 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."1.38Skin 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."1.38RAIN-Droplet: a novel 3D in vitro angiogenesis model. ( Dong, Z; Nör, JE; Zeitlin, BD, 2012)
"Sorafenib displays major interpatient pharmacokinetic variability."1.38Variability 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."1.37Sorafenib 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."1.37Sorafenib 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."1.36Sensitivity 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."1.36Initial 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."1.35Cutaneous 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."1.35Selecting 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."1.35Therapeutic 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."1.35Multiple 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."1.35Rapid 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."1.32BAY 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."1.31Rat 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."1.29Nicotinamide 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."1.27Synergistic 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)

Research

Studies (374)

TimeframeStudies, this research(%)All Research%
pre-199026 (6.95)18.7374
1990's20 (5.35)18.2507
2000's111 (29.68)29.6817
2010's189 (50.53)24.3611
2020's28 (7.49)2.80

Authors

AuthorsStudies
Abdelghany, L2
Zhang, X2
Kawabata, T1
Goto, S1
El-Mahdy, N1
Jingu, K2
Li, TS2
Gasparrini, M1
Audrito, V1
Wang, W1
Yang, C1
Wang, T1
Deng, H3
ElMokh, O1
Matsumoto, S1
Biniecka, P1
Bellotti, A1
Schaeuble, K1
Piacente, F1
Gallart-Ayala, H1
Ivanisevic, J1
Stamenkovic, I1
Nencioni, A3
Nahimana, A2
Duchosal, MA2
Mizuno, R1
Hojo, H1
Takahashi, M1
Kashio, S1
Enya, S1
Nakao, M1
Konishi, R1
Yoda, M1
Harata, A1
Hamanishi, J1
Kawamoto, H1
Mandai, M1
Suzuki, Y1
Miura, M1
Bamba, T1
Izumi, Y1
Kawaoka, S1
Hofer, SJ1
Kroemer, G2
Kepp, O1
Sun, D1
Dong, G2
Wu, Y1
Du, L1
Li, M1
Sheng, C1
Almeida, KH1
Avalos-Irving, L1
Berardinelli, S1
Chauvin, K1
Yanez, S1
Puszkiel, A1
You, B3
Payen, L1
Lopez, J1
Guitton, J3
Rousset, P1
Fontaine, J1
Péron, J2
Maillet, D2
Tartas, S1
Bonnin, N1
Trillet-Lenoir, V1
Colomban, O2
Augu-Denechere, D1
Freyer, G3
Tod, M8
Beltrà, M1
Pöllänen, N1
Fornelli, C1
Tonttila, K1
Hsu, MY1
Zampieri, S1
Moletta, L1
Corrà, S1
Porporato, PE1
Kivelä, R1
Viscomi, C1
Sandri, M1
Hulmi, JJ1
Sartori, R1
Pirinen, E1
Penna, F1
Spencer, KR1
Portal, DE1
Aisner, J1
Stein, MN1
Malhotra, J1
Shih, W1
Chan, N1
Silk, AW1
Ganesan, S1
Goodin, S1
Gounder, M1
Lin, H2
Li, J2
Cerchio, R1
Marinaro, C1
Chen, S1
Mehnert, JM1
Jabbari, P1
Ardakany, MR1
Ebrahimi, S1
Rezaei, N1
Xu, Y1
Sekiya, R1
Yan, C1
Megarity, CF1
Timson, DJ1
Yamazaki, K1
Doi, T1
Ikeda, M1
Okusaka, T1
Schueler, A1
Watanabe, M1
Ohtsu, A1
Song, SB1
Park, JS1
Chung, GJ1
Lee, IH1
Hwang, ES1
Witkowska-Patena, E1
Budzyńska, A1
Giżewska, A1
Dziuk, M1
Walęcka-Mazur, A1
Nikas, IP1
Paschou, SA1
Ryu, HS1
Buqué, A1
Bloy, N1
Galluzzi, L1
Hamity, MV1
White, SR1
Blum, C1
Gibson-Corley, KN1
Hammond, DL1
Jones, JK1
Thompson, EM1
Yu, YR1
Imrichova, H1
Wang, H2
Chao, T1
Xiao, Z1
Gao, M1
Rincon-Restrepo, M1
Franco, F1
Genolet, R1
Cheng, WC1
Jandus, C1
Coukos, G1
Jiang, YF1
Locasale, JW1
Zippelius, A1
Liu, PS1
Tang, L2
Bock, C1
Vannini, N1
Ho, PC1
Delord, JP1
Italiano, A2
Awada, A9
Aftimos, P1
Houédé, N1
Lebbé, C1
Pages, C1
Lesimple, T1
Dinulescu, M1
Schellens, JHM2
Leijen, S1
Rottey, S1
Kruse, V1
Kefford, R1
Faivre, S3
Gomez-Roca, C1
Scheuler, A1
Massimini, G2
Raymond, E3
Patnaik, A4
Yap, TA1
Chung, HC1
de Miguel, MJ1
Bang, YJ1
Lin, CC1
Su, WC1
Chow, KH1
Szpurka, AM1
Yu, D2
Zhao, Y2
Carlsen, M1
Schmidt, S1
Vangerow, B1
Gandhi, L2
Xu, X1
Bendell, J1
Roberti, A1
Fernández, AF1
Fraga, MF1
Zhong, Y1
Yang, S1
Cui, J2
Wang, J1
Li, L4
Chen, Y2
Chen, J3
Feng, P1
Huang, S1
Li, H1
Han, Y1
Tang, G1
Hu, K1
Hayat, F1
Sonavane, M1
Makarov, MV1
Trammell, SAJ1
McPherson, P1
Gassman, NR1
Migaud, ME1
Mattiello, L1
Pucci, G1
Marchetti, F1
Diederich, M1
Gonfloni, S1
Gao, Y1
Martin, NI1
van Haren, MJ1
Ghanem, MS1
Monacelli, F1
Novak Kujundžić, R1
Prpić, M1
Đaković, N1
Dabelić, N1
Tomljanović, M1
Mojzeš, A1
Fröbe, A1
Trošelj, KG1
Chu, YY2
Cheng, HJ1
Tian, ZH1
Zhao, JC1
Li, G2
Sun, CJ1
Li, WB1
Gong, L1
Giacomini, MM1
Giacomini, C1
Maitland, ML7
Altman, RB1
Klein, TE1
Murray, L1
Longo, J1
Wan, J2
Chung, C1
Wang, L3
Dawson, L1
Milosevic, M1
Oza, A2
Brade, A1
Garrido, A1
Djouder, N1
Covell, DG1
Bruner, JK1
Ma, HS1
Qin, ACR1
Rudek, MA3
Jones, RJ1
Levis, MJ1
Pratz, KW2
Pratilas, CA1
Small, D1
Schloss, J1
Colosimo, M1
Hori, Y1
Ito, K1
Hamamichi, S1
Ozawa, Y1
Matsui, J1
Umeda, IO1
Fujii, H1
Srinivas, NR1
Zhang, C1
Chi, H1
Meng, Z1
Tharmalingham, H1
Hoskin, P1
Fuss, H1
Lademann, J1
Jung, S1
Schram, AM1
Mita, MM2
Damstrup, L1
Campana, F1
Hidalgo, M1
Grande, E1
Hyman, DM1
Heist, RS1
de Weger, VA1
de Jonge, M2
Langenberg, MHG1
Lolkema, M1
Varga, A1
Demers, B1
Thomas, K1
Hsu, K1
Tuffal, G1
Goodstal, S1
Macé, S1
Deutsch, E1
Ulanovskaya, OA1
Zuhl, AM1
Cravatt, BF1
Poot, AJ1
van der Wildt, B1
Stigter-van Walsum, M1
Rongen, M1
Schuit, RC1
Hendrikse, NH1
Eriksson, J1
van Dongen, GA1
Windhorst, AD1
Montecucco, F1
Cea, M1
Bauer, I1
Soncini, D1
Caffa, I1
Lasigliè, D1
Uccelli, A1
Bruzzone, S1
Funakoshi, T1
Latif, A1
Galsky, MD1
Rosen, LS4
Lipton, L2
Price, TJ2
Belman, ND1
Boccia, RV1
Hurwitz, HI1
Stephenson, JJ2
Wirth, LJ1
McCoy, S3
Hei, YJ1
Hsu, CP2
Tebbutt, NC1
Ganesan, P1
Piha-Paul, S1
Naing, A4
Falchook, G1
Wheler, J1
Fu, S3
Hong, DS4
Kurzrock, R6
Janku, F3
Laday, S1
Bedikian, AY1
Kies, M1
Wolff, RA1
Tsimberidou, AM2
Navid, F2
Christensen, R1
Inaba, H1
Chen, Z1
Cai, X1
Regel, J1
Baker, SD3
Prado, CM2
Kumar, SK1
Jett, J1
Marks, R1
Richardson, R1
Quevedo, F1
Moynihan, T1
Croghan, G1
Markovic, SN1
Bible, KC1
Qin, R1
Tan, A1
Molina, J1
Kaufmann, SH1
Erlichman, C1
Adjei, AA4
Bhatta, SS1
Wroblewski, KE1
Agarwal, KL1
Sit, L2
Cohen, EE3
Seiwert, TY1
Karrison, T2
Bakris, GL2
Ratain, MJ5
Vokes, EE1
Maia, YL1
Ormsbee, M1
Sawyer, MB1
Baracos, VE1
Hatzivassiliou, G1
Haling, JR1
Chen, H1
Song, K1
Price, S1
Heald, R1
Hewitt, JF1
Zak, M1
Peck, A1
Orr, C1
Merchant, M1
Hoeflich, KP1
Chan, J1
Luoh, SM1
Anderson, DJ1
Ludlam, MJ1
Wiesmann, C1
Ultsch, M1
Friedman, LS1
Malek, S1
Belvin, M1
Mieszawska, AJ1
Kim, Y1
Gianella, A1
van Rooy, I1
Priem, B1
Labarre, MP1
Ozcan, C1
Cormode, DP1
Petrov, A1
Langer, R1
Farokhzad, OC1
Fayad, ZA1
Mulder, WJ1
Lazar, V1
Lassau, N1
Meurice, G1
Loriot, Y1
Peña, C1
Massard, C1
Robert, C6
Robert, T1
Le Berre, MA1
de Baere, T1
Dessen, P1
Soria, JC5
Armand, JP4
Abdulghani, J1
Allen, JE1
Dicker, DT1
Liu, YY1
Goldenberg, D1
Smith, CD1
Humphreys, R1
El-Deiry, WS2
Santoni, M1
Conti, A1
De Giorgi, U1
Iacovelli, R1
Pantano, F1
Burattini, L1
Muzzonigro, G1
Berardi, R2
Santini, D1
Cascinu, S2
Wang, CF2
Mäkilä, EM2
Kaasalainen, MH1
Liu, D1
Sarparanta, MP2
Airaksinen, AJ2
Salonen, JJ2
Hirvonen, JT2
Santos, HA2
Escudero-Ortiz, V1
Pérez-Ruixo, JJ1
Valenzuela, B1
Thomeas, V2
Chow, S2
Gutierrez, JO1
Karovic, S2
Wroblewski, K1
Kistner-Griffin, E1
Karrison, TG2
Zhang, XJ1
Zhang, TY1
Yu, FF1
Wei, X1
Li, YS1
Xu, F1
Wei, LX1
He, J1
Park, GB1
Choi, Y1
Kim, YS1
Lee, HK1
Kim, D1
Hur, DY1
Liu, Y1
Feng, L1
Liu, T1
Zhang, L2
Yao, Y1
Zhang, N1
Liu, X1
Yu, C1
Li, W2
Li, Y2
Li, S1
Zhu, Y1
Liang, X1
Meng, H1
Zhang, D1
Guo, H1
Shi, B1
Wen, Y1
Levine, MR1
House, LK2
Wu, K2
Wright, JJ8
Fleming, GF2
Abdel-Rahman, O2
Fouad, M2
Toffalorio, F1
Spitaleri, G1
Catania, C1
Dal Zotto, L1
Noberasco, C1
Delmonte, A1
Santarpia, M1
Vecchio, F1
Brunelli, V1
Rampinelli, C1
Barberis, M1
Fumagalli, C1
Zucchetti, M1
Zangarini, M1
Diena, T1
Danesi, R2
de Braud, F1
De Pas, T1
Koldenhof, JJ1
Witteveen, PO1
de Vos, R1
Walraven, M1
Tillier, CN1
Verheul, HM1
Teunissen, SC1
Huillard, O2
Boissier, E1
Blanchet, B9
Thomas-Schoemann, A4
Cessot, A2
Boudou-Rouquette, P5
Durand, JP4
Coriat, R7
Giroux, J3
Alexandre, J2
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Goldwasser, F10
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Clinical Trials (31)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
A Multicenter, Open Label, Phase I Trial of the MEK Inhibitor MSC1936369B Given Orally to Subjects With Solid Tumours[NCT00982865]Phase 1182 participants (Actual)Interventional2007-12-31Completed
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 1215 participants (Anticipated)Interventional2016-06-29Active, not recruiting
A Phase 1 Study of Combination Therapy With SAR405838 and Pimasertib in Patients With Advanced Cancer[NCT01985191]Phase 126 participants (Actual)Interventional2013-11-30Completed
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 149 participants (Actual)Interventional2007-02-28Completed
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 1180 participants (Actual)Interventional2010-08-31Completed
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 150 participants (Actual)Interventional2005-12-31Completed
A Phase 1/2 Study of the Combination of RDEA119 and Sorafenib in Patients With Advanced Cancer[NCT00785226]Phase 1/Phase 262 participants (Actual)Interventional2008-11-30Completed
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 16 participants (Actual)Interventional2012-11-30Completed
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 160 participants (Anticipated)Interventional2013-04-30Recruiting
Phase I Dose Escalation Trial of MEK1/2 Inhibitor MSC1936369B Combined With Temsirolimus in Subjects With Advanced Solid Tumors[NCT01378377]Phase 133 participants (Actual)Interventional2011-05-27Terminated (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 136 participants (Anticipated)Interventional2010-07-31Completed
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 2106 participants (Anticipated)Interventional2014-12-31Recruiting
An Open Label, Pilot Study Evaluating the Effect of Topical Sildenafil as Pre-Treatment for Hand-Foot Skin Reaction[NCT03229512]Early Phase 12 participants (Actual)Interventional2017-04-11Completed
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 4288 participants (Actual)Interventional2016-01-28Completed
A Phase I Study of BAY 43-9006 (Sorafenib) in Combination With OSI-774 (Erlotinib; Tarceva) in Advanced Solid Tumors[NCT00126620]Phase 117 participants (Actual)Interventional2005-09-30Completed
Effect of BAY 43-9006 (Sorafenib) on Cardiovascular Safety Parameters in Cancer Patients[NCT00259129]Phase 153 participants (Actual)Interventional2005-08-31Completed
A Phase II Study of BAY 43-9006 (Sorafenib) in Metastatic, Androgen-Independent Prostate Cancer[NCT00090545]Phase 246 participants (Actual)Interventional2004-09-01Completed
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 157 participants (Actual)Interventional2005-09-30Completed
Single Agent Sorafenib in Advanced Solid Tumors: Phase II Evaluation of Dose Re-Escalation Following a Dose Reduction (IST000375)[NCT00810394]Phase 250 participants (Actual)Interventional2008-12-31Completed
Phase I and Pharmacokinetics Study of Lapatinib in Combination With Sorafenib in Patients With Advanced Refractory Solid Tumors[NCT00984425]Phase 130 participants (Actual)Interventional2009-09-30Completed
Mechanism of Sorafenib Resistance in Patients With Advanced Hepatocellular Carcinoma[NCT02733809]Phase 440 participants (Anticipated)Interventional2014-01-31Recruiting
Accelerated Growth of Synchronous Colorectal Liver Metastases: Effects of Neo-adjuvant Therapy[NCT00659022]Phase 260 participants (Anticipated)Interventional2008-07-31Recruiting
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 212 participants (Actual)Interventional2016-08-31Completed
Histological Characterization and Differentiation of Rash From Other EGFR Inhibitors[NCT00709878]32 participants (Actual)Observational2008-04-30Completed
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 136 participants (Actual)Interventional2009-07-31Completed
Angiogenesis Inhibitors and Hypertension: Clinical Aspects[NCT00511511]80 participants (Anticipated)Observational2007-08-31Completed
A Study of the Pharmacodynamic Effects of Anti-Vascular Endothelial Growth[NCT00698659]0 participants Observational2007-08-31Terminated
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 155 participants (Actual)Interventional2013-03-15Completed
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 257 participants (Actual)Interventional2013-07-08Active, not recruiting
Personalized Cancer Therapy for Patients With Metastatic Medullary Thyroid or Metastatic Colon Cancer[NCT02363647]10 participants (Actual)Interventional2015-01-31Terminated (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 171 participants (Actual)Interventional2003-07-31Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Number of Subjects Experienced Any Dose-Limiting Toxicity (DLT) Over the First Cycle - Day 1 to 21

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

InterventionSubjects (Number)
MSC1936369B Regimen 12
MSC1936369B Regimen 2 (Without Food Effect + With Food Effect)6
MSC1936369B Regimen 3 Once Daily (QD)0
MSC1936369B Regimen 3 Twice Daily6

Number of Subjects With Treatment-Emergent Adverse Events (TEAEs) Leading to Death

(NCT00982865)
Timeframe: Baseline up to 253 weeks

InterventionSubjects (Number)
MSC1936369B Regimen 110
MSC1936369B Regimen 2 (Without Food Effect + With Food Effect)14
MSC1936369B Regimen 3 Once Daily (QD)2
MSC1936369B Regimen 3 Twice Daily2

Apparent Terminal Half-life (t1/2) of MSC1936369B: Regimen 1

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

,,
InterventionHours (h) (Geometric Mean)
C1D1C1D12
MSC1936369B 28 mg4.7816.750
MSC1936369B 3.5 mg3.3464.985
MSC1936369B 68 mg5.3356.926

Apparent Terminal Half-life (t1/2) of MSC1936369B: Regimen 1

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

,,,,
InterventionHours (h) (Geometric Mean)
C1D1C1D12C3D1
MSC1936369B 120 mg5.2473.9643.038
MSC1936369B 14 mg4.5993.2362.811
MSC1936369B 45 mg5.3894.6882.931
MSC1936369B 7 mg3.4059.2492.959
MSC1936369B 94 mg5.3515.6722.842

Apparent Terminal Half-life (t1/2) of MSC1936369B: Regimen 2 (With Food Effect)

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

,
InterventionHour (h) (Geometric Mean)
FastedFed
MSC1936369B 150 mg4.4526.123
MSC1936369B 90 mg4.8984.534

Apparent Terminal Half-life (t1/2) of MSC1936369B: Regimen 2 (Without Food Effect)

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

,,,
InterventionHours (h) (Geometric Mean)
C1D1C1D15
MSC1936369B 7 mg2.5942.335
MSC1936369B 14 mg5.1194.443
MSC1936369B 28 mg5.1156.646
MSC1936369B 45 mg4.1875.277

Apparent Terminal Half-life (t1/2) of MSC1936369B: Regimen 2 (Without Food Effect)

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

InterventionHours (h) (Geometric Mean)
C1D15C3D1
MSC1936369B 5 mg2.9412.732

Apparent Terminal Half-life (t1/2) of MSC1936369B: Regimen 2 (Without Food Effect)

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

,,,,,
InterventionHours (h) (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 120 mg5.0574.8512.863
MSC1936369B 150 mg4.9045.4792.418
MSC1936369B 195 mg5.6416.0162.628
MSC1936369B 68 mg3.3056.4413.477
MSC1936369B 255 mg4.3134.8472.260
MSC1936369B 94 mg4.8265.1932.853

Apparent Terminal Half-life (t1/2) of MSC1936369B: Regimen 3 Once Daily

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

,
InterventionHour (h) (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 60 mg4.2365.2591.780
MSC1936369B 90 mg4.0975.5992.680

Apparent Terminal Half-life (t1/2) of MSC1936369B: Regimen 3 Twice Daily

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

,,
InterventionHour (h) (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 45 mg2.0502.8903.144
MSC1936369B 60 mg2.5093.2652.636
MSC1936369B 75 mg2.8143.2103.260

Apparent Volume of Distribution During the Terminal Phase Following Extravascular Administration (Vz/F) of MSC1936369B: Regimen 2 (With Food Effect)

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

,
InterventionLiter (Geometric Mean)
FastedFed
MSC1936369B 150 mg288.1235.2
MSC1936369B 90 mg402.4393.6

Apparent Volume of Distribution During the Terminal Phase Following Extravascular Administration (Vz/F) of MSC1936369B: Regimen 2 (Without Food Effect)

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

,,,
InterventionLiter (Geometric Mean)
C1D1C1D15
MSC1936369B 14 mg473.32555.9
MSC1936369B 28 mg319.40432.5
MSC1936369B 45 mg331.36378.0
MSC1936369B 7 mg339.58454.6

Apparent Volume of Distribution During the Terminal Phase Following Extravascular Administration (Vz/F) of MSC1936369B: Regimen 2 (Without Food Effect)

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

InterventionLiter (Geometric Mean)
C1D15C3D1
MSC1936369B 5 mg252.7352.10

Apparent Volume of Distribution During the Terminal Phase Following Extravascular Administration (Vz/F) of MSC1936369B: Regimen 2 (Without Food Effect)

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

,,,,,
InterventionLiter (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 120 mg361.12646.9201.39
MSC1936369B 150 mg463.92642.1212.92
MSC1936369B 195 mg440.55464.2274.24
MSC1936369B 255 mg377.28295.1144.24
MSC1936369B 68 mg366.00406.6206.07
MSC1936369B 94 mg428.99385.6244.16

Apparent Volume of Distribution During the Terminal Phase Following Extravascular Administration (Vz/F) of MSC1936369B: Regimen 3 Once Daily

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

,
InterventionLiter (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 60 mg292.61366.5137.0
MSC1936369B 90 mg336.38507.7292.5

Apparent Volume of Distribution During the Terminal Phase Following Extravascular Administration (Vz/F) of MSC1936369B: Regimen 3 Twice Daily

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

,,
InterventionLiter (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 45 mg339.51297.9571.8
MSC1936369B 60 mg292.59315.0392.9
MSC1936369B 75 mg340.43437.6362.6

Apparent Volume of Distribution Following Extravascular Administration (Vz/F) of MSC1936369B: Regimen 1

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

,,
InterventionLiter (Geometric Mean)
C1D1C1D12
MSC1936369B 28 mg336.32365.1
MSC1936369B 3.5 mg640.60507.8
MSC1936369B 68 mg307.90357.8

Apparent Volume of Distribution Following Extravascular Administration (Vz/F) of MSC1936369B: Regimen 1

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

,,,,
InterventionLiter (Geometric Mean)
C1D1C1D12C3D1
MSC1936369B 120 mg361.99351.4316.63
MSC1936369B 14 mg396.76291.9422.04
MSC1936369B 45 mg378.56333.9348.19
MSC1936369B 7 mg561.27594.5928.91
MSC1936369B 94 mg389.49416.3438.91

Area Under the Concentration Time Curve Extrapolated From Last Observation to Infinity Given as Percentage of AUC 0-∞ (AUC Extra): Regimen 1

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

,
InterventionPercentage of AUC 0-∞ (Geometric Mean)
C1D1C1D12
MSC1936369B 1.5 mg42.2333.84
MSC1936369B 68 mg4.086.56

Area Under the Concentration Time Curve Extrapolated From Last Observation to Infinity Given as Percentage of AUC 0-∞ (AUC Extra): Regimen 1

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

,,,,,,,,
InterventionPercentage of AUC 0-∞ (Geometric Mean)
C1D1C1D12C3D1
MSC1936369B 1 mg81.3350.6055.15
MSC1936369B 120 mg5.282.9726.05
MSC1936369B 14 mg5.317.8315.84
MSC1936369B 2.5 mg43.4540.6055.79
MSC1936369B 28 mg5.396.5728.06
MSC1936369B 3.5 mg26.8021.2732.85
MSC1936369B 45 mg3.528.1727.67
MSC1936369B 7 mg13.0819.8221.27
MSC1936369B 94 mg4.097.9416.54

Area Under the Concentration Time Curve Extrapolated From Last Observation to Infinity Given as Percentage of AUC 0-∞ (AUC Extra): Regimen 2 (With Food Effect)

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

,
InterventionPercentage of AUC 0-∞ (Geometric Mean)
FastedFed
MSC1936369B 150 mg1.749.96
MSC1936369B 90 mg2.542.21

Area Under the Concentration Time Curve Extrapolated From Last Observation to Infinity Given as Percentage of AUC 0-∞ (AUC Extra): Regimen 2 (Without Food Effect)

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

InterventionPercentage of AUC 0-∞ (Geometric Mean)
C1D15
MSC1936369B 1 mg40.86

Area Under the Concentration Time Curve Extrapolated From Last Observation to Infinity Given as Percentage of AUC 0-∞ (AUC Extra): Regimen 2 (Without Food Effect)

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

,
InterventionPercentage of AUC 0-∞ (Geometric Mean)
C1D1C1D15
MSC1936369B 45 mg1.462.96
MSC1936369B 14 mg12.1712.45

Area Under the Concentration Time Curve Extrapolated From Last Observation to Infinity Given as Percentage of AUC 0-∞ (AUC Extra): Regimen 2 (Without Food Effect)

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

,,,,,,,,,,
InterventionPercentage of AUC 0-∞ (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 120 mg2.945.8216.22
MSC1936369B 150 mg2.644.8217.54
MSC1936369B 195 mg4.365.7723.45
MSC1936369B 2 mg55.7833.3433.93
MSC1936369B 255 mg3.575.2211.15
MSC1936369B 28 mg3.296.8926.32
MSC1936369B 3.5 mg31.6335.2933.77
MSC1936369B 5 mg27.2521.9317.27
MSC1936369B 68 mg2.665.0015.35
MSC1936369B 7 mg15.1019.4520.68
MSC1936369B 94 mg2.603.4018.02

Area Under the Concentration Time Curve Extrapolated From Last Observation to Infinity Given as Percentage of AUC 0-∞ (AUC Extra): Regimen 3 Once Daily

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

,
Interventionpercentage of AUC 0-∞ (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 60 mg1.887.959.11
MSC1936369B 90 mg2.114.2817.56

Area Under the Concentration Time Curve Extrapolated From Last Observation to Infinity Given as Percentage of AUC 0-∞ (AUC Extra): Regimen 3 Twice Daily

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

,,
InterventionPercentage of AUC 0-∞ (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 45 mg16.8211.7830.63
MSC1936369B 60 mg7.7014.1416.43
MSC1936369B 75 mg10.9019.1921.34

Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of MSC1936369B : Regimen 1

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

,
Interventionhour*ng/mL (Geometric Mean)
C1D1C1D12
MSC1936369B 1.5 mg6.29.4
MSC1936369B 68 mg1699.72108.2

Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of MSC1936369B : Regimen 1

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

,,,,,,,,
Interventionhour*ng/mL (Geometric Mean)
C1D1C1D12C3D1
MSC1936369B 1 mg136.238.315.4
MSC1936369B 120 mg2773.52022.83477.6
MSC1936369B 14 mg234.1206.3134.5
MSC1936369B 2.5 mg55.543.847.6
MSC1936369B 28 mg574.2805.6489.8
MSC1936369B 3.5 mg31.447.534.4
MSC1936369B 45 mg924.2960.71072.1
MSC1936369B 7 mg61.3105.655.5
MSC1936369B 94 mg1836.42257.61056.0

Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of MSC1936369B: Regimen 2 (With Food Effect)

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

,
Interventionhour*ng/mL (Geometric Mean)
FastedFed
MSC1936369B 150 mg3344.35633.8
MSC1936369B 90 mg1580.61495.7

Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of MSC1936369B: Regimen 2 (Without Food Effect)

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

Interventionhour*ng/mL (Geometric Mean)
C1D15
MSC1936369B 1 mg15.7

Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of MSC1936369B: Regimen 2 (Without Food Effect)

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

,
Interventionhour*ng/mL (Geometric Mean)
C1D1C1D15
MSC1936369B 45 mg820.4933.9
MSC1936369B 14 mg218.4172.2

Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of MSC1936369B: Regimen 2 (Without Food Effect)

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

,,,,,,,,,,
Interventionhour*ng/mL (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 120 mg2424.22129.02461.3
MSC1936369B 195 mg3602.23900.83452.9
MSC1936369B 2 mg23.433.315.4
MSC1936369B 255 mg4300.36232.15651.1
MSC1936369B 28 mg646.9669.1415.6
MSC1936369B 3.5 mg23.621.941.2
MSC1936369B 150 mg2287.82029.92796.2
MSC1936369B 5 mg59.1102.049.5
MSC1936369B 68 mg885.81665.21655.1
MSC1936369B 7 mg90.389.758.1
MSC1936369B 94 mg1525.61893.21584.8

Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of MSC1936369B: Regimen 3 Once Daily

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

,
Interventionhour*ng/mL (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 60 mg1253.11753.91597.0
MSC1936369B 90 mg1581.41517.11400.3

Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of MSC1936369B: Regimen 3 Twice Daily

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

,,
Interventionhour*ng/mL (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 45 mg527.6674.1696.0
MSC1936369B 60 mg742.31004.2700.8
MSC1936369B 75 mg939.9978.41285.7

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 (AUC0-t) of MSC1936369B: : Regimen 2 (Without Food Effect)

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

,
Interventionhour*ng/mL (Geometric Mean)
C1D1C1D15
MSC1936369B 14 mg188.4161.5
MSC1936369B 45 mg808.0906.3

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 (AUC0-t) of MSC1936369B: : Regimen 2 (Without Food Effect)

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

,,,,,,,,,,,
Interventionhour*ng/mL (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 1 mg1.94.30.5
MSC1936369B 120 mg2287.01862.32053.6
MSC1936369B 150 mg2216.52086.62171.2
MSC1936369B 195 mg3415.63436.82484.5
MSC1936369B 2 mg8.222.210.2
MSC1936369B 255 mg4041.35765.94906.3
MSC1936369B 28 mg625.7621.2306.2
MSC1936369B 3.5 mg6.713.826.2
MSC1936369B 5 mg67.979.340.5
MSC1936369B 68 mg861.11553.91394.7
MSC1936369B 7 mg74.467.846.1
MSC1936369B 94 mg1484.61826.21299.3

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 (AUC0-t) of MSC1936369B: Regimen 1

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

Interventionhour*nanogram per milliliter (h*ng/mL) (Geometric Mean)
C1D1C1D12
MSC1936369B 68 mg1624.81900.3

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 (AUC0-t) of MSC1936369B: Regimen 1

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

,,,,,,,,,
Interventionhour*nanogram per milliliter (h*ng/mL) (Geometric Mean)
C1D1C1D12C3D1
MSC1936369B 1.5 mg5.26.02.7
MSC1936369B 120 mg2292.41682.42064.1
MSC1936369B 14 mg213.9182.0113.2
MSC1936369B 2.5 mg18.526.021.0
MSC1936369B 28 mg531.3691.9334.9
MSC1936369B 3.5 mg22.735.923.0
MSC1936369B 45 mg889.0880.0666.3
MSC1936369B 1 mg4.67.06.9
MSC1936369B 7 mg52.783.645.2
MSC1936369B 94 mg1748.11991.4876.7

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 (AUC0-t) of MSC1936369B: Regimen 2 (With Food Effect)

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

,
Interventionhour*ng/mL (Geometric Mean)
FastedFed
MSC1936369B 150 mg32865072.9
MSC1936369B 90 mg1509.61458.3

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 (AUC0-t) of MSC1936369B: Regimen 3 Once Daily

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

,
Interventionhour*ng/mL (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 60 mg1229.31532.41392.3
MSC1936369B 90 mg1544.91428.81122.5

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 (AUC0-t) of MSC1936369B: Regimen 3 Twice Daily

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

,,
Interventionhour*ng/mL (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 45 mg407.2589.3450.0
MSC1936369B 60 mg681.4838.8577.0
MSC1936369B 75 mg791.1710.31005.0

Maximum Observed Plasma Concentration (Cmax) of MSC1936369B: Regimen 1

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

Interventionnanogram per milliliter (ng/mL) (Geometric Mean)
C1D1C1D12
MSC1936369B 68 mg357.39413.58

Maximum Observed Plasma Concentration (Cmax) of MSC1936369B: Regimen 1

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

,,,,,,,,,
Interventionnanogram per milliliter (ng/mL) (Geometric Mean)
C1D1C1D12C3D1
MSC1936369B 1 mg2.022.922.00
MSC1936369B 1.5 mg3.202.692.90
MSC1936369B 120 mg428.85425.26652.70
MSC1936369B 14 mg62.3254.4751.30
MSC1936369B 2.5 mg4.216.295.60
MSC1936369B 28 mg126.21150.6784.70
MSC1936369B 3.5 mg6.699.758.06
MSC1936369B 45 mg212.96175.94167.75
MSC1936369B 7 mg12.6021.9310.90
MSC1936369B 94 mg325.99602.12282.44

Maximum Observed Plasma Concentration (Cmax) of MSC1936369B: Regimen 2 (With Food Effect)

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

,
Interventionng/mL (Geometric Mean)
FastedFed
MSC1936369B 150 mg1158.00370.70
MSC1936369B 90 mg321.14305.94

Maximum Observed Plasma Concentration (Cmax) of MSC1936369B: Regimen 2 (Without Food Effect)

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

,
Interventionng/mL (Geometric Mean)
C1D1C1D15
MSC1936369B 14 mg39.1934.87
MSC1936369B 45 mg321.85286.88

Maximum Observed Plasma Concentration (Cmax) of MSC1936369B: Regimen 2 (Without Food Effect)

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

,,,,,,,,,,,
Interventionng/mL (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 120 mg605.11492.81568.49
MSC1936369B 150 mg539.02450.29795.86
MSC1936369B 195 mg680.87629.85773.14
MSC1936369B 2 mg2.877.774.30
MSC1936369B 255 mg990.921535.602344.91
MSC1936369B 28 mg187.98131.7196.60
MSC1936369B 3.5 mg4.554.216.56
MSC1936369B 1 mg1.652.281.25
MSC1936369B 5 mg17.2618.7814.81
MSC1936369B 68 mg306.63539.17710.94
MSC1936369B 7 mg30.9018.4716.10
MSC1936369B 94 mg373.59432.46532.80

Maximum Observed Plasma Concentration (Cmax) of MSC1936369B: Regimen 3 Once Daily

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

,
Interventionng/mL (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 60 mg241.27316.08473.27
MSC1936369B 90 mg402.77324.80376.62

Maximum Observed Plasma Concentration (Cmax) of MSC1936369B: Regimen 3 Twice Daily

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

,,
Interventionng/mL (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 45 mg132.57178.09139.60
MSC1936369B 60 mg206.46231.12157.46
MSC1936369B 75 mg263.08190.42329.28

Number of Subjects With Clinical Benefit (Complete Response [CR], Partial Response [PR] or Stable Disease [SD}) and Progressive Disease (PD) Based on the Best Overall Response (BOR)

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])

,,,
InterventionSubjects (Number)
CRPRSDPD
MSC1936369B Regimen 1001920
MSC1936369B Regimen 2 and Regimen 2 Food Effect043433
MSC1936369B Regimen 3 Once Daily (QD)0294
MSC1936369B Regimen 3 Twice Daily161412

Number of Subjects With Clinical Significant Laboratory Abnormalities and Vital Signs Reported as Treatment Emergent Adverse Events

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

,,,
InterventionSubjects (Number)
Haemoglobin decreasedAnaemiaLymphopeniaThrombocytopeniaPlatelet count decreasedNeutropeniaLeukopeniaPancytopeniaHyponatraemiaHypokalaemiaHyperkalaemiaHypocalcaemiaHypercalcaemiaHypomagnesaemiaHypophosphataemiaHepatic enzyme increasedHepatic function abnormalAlanine aminotransferase increasedAspartate aminotransferase increasedBlood alkaline phosphatase increasedHyperbilirubinaemiaBlood lactate dehydrogenase increasedBlood creatine phosphokinase increasedBlood creatinine increasedBlood 25-hydroxycholecalciferol decreasedVitamin D decreasedBlood parathyroid hormone increasedHyperglycaemiaC-reactive protein increasedProteinuriaHyperthyroidismHypoalbuminaemiaWeight increasedWeight decreasedHyperthermiaHypertensionHypotensionHeart rate increasedTachycardiaBlood potassium increased
MSC1936369B Regimen 111033000004120200001111101010000306173131
MSC1936369B Regimen 2 (Without Food Effect + With Food Effect)223761400110073321111010211111100438551000
MSC1936369B Regimen 3 Once Daily (QD)0302001002000200000000100000010004012020
MSC1936369B Regimen 3 Twice Daily0301010112010000022101500000011232140000

Number of Subjects With Treatment-Emergent Adverse Events (TEAE), Serious TEAEs, TEAEs Leading to Discontinuation

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

,,,
InterventionSubjects (Number)
TEAEsSerious TEAEsTEAEs leading to discontinuation
MSC1936369B Regimen 1472313
MSC1936369B Regimen 2 (Without Food Effect + With Food Effect)824522
MSC1936369B Regimen 3 Once Daily (QD)1582
MSC1936369B Regimen 3 Twice Daily34216

Phosphorylated Extra-Cellular Signal-Regulated Kinase (pERK) Fold Change in Peripheral Blood Monocyte Cells (PBMC) and Tot ERK Fold Change in Peripheral Blood Monocyte Cells (PBMC)

(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

,
Interventionfold 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 Daily4.1211.1781.8783.0812.5413.2411.4711.9022.5981.021.0781.0781.0130.9441.3331.3351.0441.048
MSC1936369B Regimen 3 Twice Daily3.6291.2491.8212.0692.2352.161.3151.982.0431.0861.0791.0981.1081.0491.0471.0591.0261.068

Phosphorylated Extra-Cellular Signal-Regulated Kinase (pERK) Fold Change in Peripheral Blood Monocyte Cells (PBMC) and Tot ERK Fold Change in Peripheral Blood Monocyte Cells (PBMC)

(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

Interventionfold 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)3.9371.3053.4221.4542.4112.8683.2651.2931.6532.4763.7161.2882.6881.0751.0691.0121.0951.131.1081.1181.1251.0411.0451.1381.2511.052

Phosphorylated Extra-Cellular Signal-Regulated Kinase (pERK) Fold Change in Peripheral Blood Monocyte Cells (PBMC) and Tot ERK Fold Change in Peripheral Blood Monocyte Cells (PBMC)

(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

Interventionfold 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 14.5241.2353.8281.4542.8532.7224.483.2571.2521.5142.7685.1791.7953.1061.11.0631.0591.0581.0751.1631.2331.2231.040.9941.0471.0741.0870.674

Time to Reach Maximum Plasma Concentration (Tmax) of MSC1936369B: Regimen 1

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

InterventionHours (h) (Median)
C1D1C1D12
MSC1936369B 68 mg1.0001.000

Time to Reach Maximum Plasma Concentration (Tmax) of MSC1936369B: Regimen 1

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

,,,,,,,,,
InterventionHours (h) (Median)
C1D1C1D12C3D1
MSC1936369B 1 mg1.5001.6331.52
MSC1936369B 1.5 mg0.7500.5330.500
MSC1936369B 120 mg1.0171.0832.000
MSC1936369B 14 mg1.0001.5001.500
MSC1936369B 2.5 mg1.5001.0001.52
MSC1936369B 28 mg1.5001.0001.000
MSC1936369B 3.5 mg1.5001.0001.000
MSC1936369B 45 mg1.0172.0001.508
MSC1936369B 7 mg1.5001.0171.517
MSC1936369B 94 mg1.4831.5001.767

Time to Reach Maximum Plasma Concentration (Tmax) of MSC1936369B: Regimen 2 (With Food Effect)

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

,
InterventionHours (h) (Median)
FastedFed
MSC1936369B 150 mg1.0006.000
MSC1936369B 90 mg1.6002.033

Time to Reach Maximum Plasma Concentration (Tmax) of MSC1936369B: Regimen 2 (Without Food Effect)

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

,
InterventionHours (h) (Median)
C1D1C1D15
MSC1936369B 14 mg1.5001.500
MSC1936369B 45 mg0.5001.500

Time to Reach Maximum Plasma Concentration (Tmax) of MSC1936369B: Regimen 2 (Without Food Effect)

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

,,,,,,,,,,,
InterventionHours (h) (Median)
C1D1C1D15C3D1
MSC1936369B 1 mg1.5001.5001.250
MSC1936369B 120 mg1.2502.0001.042
MSC1936369B 150 mg1.5001.5171.333
MSC1936369B 195 mg1.2501.2501.000
MSC1936369B 2 mg1.0170.9672.000
MSC1936369B 255 mg2.0001.4581.000
MSC1936369B 28 mg1.0001.0171.50
MSC1936369B 3.5 mg1.5002.0001.258
MSC1936369B 5 mg1.0000.6671.000
MSC1936369B 68 mg1.0001.2500.500
MSC1936369B 7 mg0.5331.0082.500
MSC1936369B 94 mg1.5001.5002.000

Time to Reach Maximum Plasma Concentration (Tmax) of MSC1936369B: Regimen 3 Once Daily

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

,
InterventionHours (h) (Median)
C1D1C1D15C3D1
MSC1936369B 60 mg1.0332.5002.000
MSC1936369B 90 mg1.5001.4921.000

Time to Reach Maximum Plasma Concentration (Tmax) of MSC1936369B: Regimen 3 Twice Daily

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

,,
InterventionHours (h) (Median)
C1D1C1D15C3D1
MSC1936369B 45 mg1.5001.5001.467
MSC1936369B 60 mg1.0001.5001.183
MSC1936369B 75 mg0.6671.5001.467

Total Body Clearance From Plasma Following Extravascular Administration (CL/f) of MSC1936369B: Regimen 1

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

,,
InterventionLiter per hour (Geometric Mean)
C1D1C1D12
MSC1936369B 28 mg48.7637.49
MSC1936369B 3.5 mg132.6970.60
MSC1936369B 68 mg40.0135.80

Total Body Clearance From Plasma Following Extravascular Administration (CL/f) of MSC1936369B: Regimen 1

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

,,,,
InterventionLiter per hour (Geometric Mean)
C1D1C1D12C3D1
MSC1936369B 120 mg47.8261.4472.25
MSC1936369B 14 mg59.8062.53104.07
MSC1936369B 45 mg48.6949.3782.35
MSC1936369B 7 mg114.2644.55217.56
MSC1936369B 94 mg50.4550.88107.06

Total Body Clearance From Plasma Following Extravascular Administration (CL/f) of MSC1936369B: Regimen 2 (With Food Effect)

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

,
InterventionLiter per hour (Geometric Mean)
FastedFed
MSC1936369B 150 mg44.8526.62
MSC1936369B 90 mg56.9460.17

Total Body Clearance From Plasma Following Extravascular Administration (CL/f) of MSC1936369B: Regimen 2 (Without Food Effect)

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

,,,
InterventionLiter per hour (Geometric Mean)
C1D1C1D15
MSC1936369B 14 mg64.0986.72
MSC1936369B 28 mg43.2845.10
MSC1936369B 45 mg54.8549.65
MSC1936369B 7 mg90.76134.9

Total Body Clearance From Plasma Following Extravascular Administration (CL/f) of MSC1936369B: Regimen 2 (Without Food Effect)

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

InterventionLiter per hour (Geometric Mean)
C1D15C3D1
MSC1936369B 5 mg59.5589.34

Total Body Clearance From Plasma Following Extravascular Administration (CL/f) of MSC1936369B: Regimen 2 (Without Food Effect)

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

,,,,,
InterventionLiter per hour (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 120 mg49.5092.4248.76
MSC1936369B 150 mg65.5781.2261.04
MSC1936369B 195 mg54.1353.4972.33
MSC1936369B 255 mg60.6342.2044.23
MSC1936369B 68 mg76.7743.7641.08
MSC1936369B 94 mg61.6151.4759.31

Total Body Clearance From Plasma Following Extravascular Administration (CL/f) of MSC1936369B: Regimen 3 Once Daily

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

,
InterventionLiter per hour (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 60 mg47.8848.3153.36
MSC1936369B 90 mg56.9162.8575.63

Total Body Clearance From Plasma Following Extravascular Administration (CL/f) of MSC1936369B: Regimen 3 Twice Daily

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

,,
InterventionLiter per hour (Geometric Mean)
C1D1C1D15C3D1
MSC1936369B 45 mg114.8271.44126.1
MSC1936369B 60 mg80.8366.89103.3
MSC1936369B 75 mg83.8694.4877.09

Apparent Terminal Elimination Rate Constant (λz) of Total [14C] Radioactivity

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

Interventionper hour (Geometric Mean)
Pimasertib0.04084

Apparent Terminal Half-life (t1/2) of Total [14C] Radioactivity

(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

Interventionhour (Median)
Pimasertib14.41

Apparent Volume of Distribution of Total [14C] Radioactivity During the Terminal Phase Following Oral Administration (Vz/f)

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

InterventionLiter (Geometric Mean)
Pimasertib253.5

Area Under the Plasma Concentration Time Curve From Time Zero to Infinity (AUC0-inf) of [14C]-Pimasertib Following IV Administration on Day 1

(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

Interventionhour*picogram equivalent/milliliter (Geometric Mean)
Pimasertib37.4

Area Under the Plasma Concentration Time Curve From Time Zero to Infinity (AUC0-inf) of Pimasertib Following Oral Administration on Day 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

Interventionhour*nanogram/milliliter (Geometric Mean)
Pimasertib957.4

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 (AUC0-t) of Total [14C] Radioactivity

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

Interventionhr*ng eq/mL (Geometric Mean)
Pimasertib5318

Area Under the Plasma Concentration Time Curve From Time Zero to the Last Sampling Time Point (AUC0-t) of [14C]-Pimasertib Following Intravenous (IV) Administration on Day 1

(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

Interventionhour*picogram equivalent/milliliter (Geometric Mean)
Pimasertib36.0

Area Under the Plasma Concentration Time Curve From Time Zero to the Last Sampling Time Point (AUC0-t) of Pimasertib Following Oral Administration on Day 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

Interventionhour*nanogram/milliliter (Geometric Mean)
Pimasertib937.2

Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of Total [14C] Radioactivity

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

Interventionhr*ng eq/mL (Geometric Mean)
Pimasertib5711

Blood/ Plasma Concentration Ratios of Total [14C] Radioactivity

(NCT01713036)
Timeframe: 1.5 hour post [14C]-labeled pimasertib dose on Day 8

InterventionRatio (Mean)
Pimasertib0.687

Fraction Unbound of [14C] Pimasertib

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

Interventionpercentage of unbound drug (Mean)
Pimasertib6.702

Maximum Observed Plasma Concentration (Cmax) of Intravenous [14C] Pimasertib

(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

Interventionpicogram equivalent per milliliter (Geometric Mean)
Pimasertib12.67

Maximum Observed Plasma Concentration (Cmax) of Total [14C] Radioactivity

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

Interventionng eq/mL (Geometric Mean)
Pimasertib774.1

Maximum Observed Plasma Concentration (Cmax) of Unlabeled Pimasertib

(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

Interventionng/mL (Geometric Mean)
Pimasertib265

Oral Bioavailability of Pimasertib After Single Oral Dose of Unlabeled Pimasertib and Intravenous (IV) Single Tracer Dose of [14C] Pimasertib

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

Interventionpercentage bioavailability (Number)
Pimasertib73

The Volume of Distribution of the Central or Plasma Compartment (Vc) of Intravenous [14C] Pimasertib

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

InterventionLiter (Geometric Mean)
Pimasertib83.668

Time to Reach Maximum Plasma Concentration (Tmax) of Total [14C] Radioactivity

(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

Interventionhour (Median)
Pimasertib1.5

Total Body Clearance of Total [14C] Radioactivity From Plasma Following Oral Administration (CL/f)

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

Interventionliter per hour (Geometric Mean)
Pimasertib10.35

Apparent Terminal Elimination Rate Constant (λz) of M445 and M554

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

Interventionper hour (Geometric Mean)
M445M554
Pimasertib0.25420.07021

Apparent Terminal Elimination Rate Constant (λz) of Unlabeled Pimasertib and Intravenous [14C] Pimasertib

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

Interventionper hour (Geometric Mean)
Unlabeled pimasertibIntravenous [14C] pimasertib
Pimasertib0.10960.1994

Apparent Terminal Half-life (t1/2) of M445 and M554

(NCT01713036)
Timeframe: Predose, 1.0, 2.0, 4.0, 10 and 24 hour post [14C]-labeled pimasertib dose on Day 8

Interventionhour (Median)
M445M554
Pimasertib2.65310.81

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 (Vz) of [14C] Pimasertib

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

InterventionLiter (Geometric Mean)
Unlabeled pimasertibIntravenous [14C] pimasertib
Pimasertib571.77229.35

Area Under the Plasma Concentration-time Curve From Time Zero to Infinity (AUC0-inf) of M445 and M554

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

Interventionhr*ng eq/mL (Geometric Mean)
M445M554
Pimasertib1134.723135.61

Area Under the Plasma Concentration-time Curve From Time Zero to the Last Sampling Time (AUC0-t) of M445 and M554

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

Interventionhr*ng eq/mL (Geometric Mean)
M445M554
Pimasertib976.391410.30

Mass Balance: Amount of Total Radioactivity Recovered Into the Urine and Feces From Time Zero to the Last Sampling Time Point (Ae0-t)

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

Interventionpercentage of dose recovered (Geometric Mean)
UrineFecesTotal
Pimasertib52.830.785.1

Maximum Observed Plasma Concentration (Cmax) of M445 and M554

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

InterventionNanogram equivalent per milliliter (Geometric Mean)
M445M554
Pimasertib300.93174.64

Number of Metabolites Identified Overall and as Major

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

Interventionmetabolites (Number)
OverallMajor
Pimasertib142

Number of Subjects With Treatment Emergent Adverse Events (TEAEs), Serious TEAEs, TEAEs Leading to Death, and TEAEs Leading to Discontinuation

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

Interventionsubjects (Number)
TEAEsSerious TEAEsTEAEs leading to deathTEAEs leading to discontinuation
Pimasertib6213

Part B: Number of Subjects Who Experienced Complete Response (CR), Partial Response (PR), Stable Disease (SD) and Progressive Disease (PD)

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

Interventionsubjects (Number)
Stable diseaseProgressive diseaseConfirmed ResponsePartial ResponseNon evaluable
Pimasertib31001

Plasma Concentrations of [14C] Pimasertib

(NCT01713036)
Timeframe: Pre-dose 1.0, 2.0, 4.0, 10 and 24 hours post [14C]-labeled Pimasertib dose on Day 8

Interventionnanogram equivalent per milliliter (Mean)
PredoseHour 1Hour 2.0Hour 4.0Hour 10.0Hour 24.0
Pimasertib0.0695.2691.2379.3165.646.62

Plasma Concentrations of Pimasertib Metabolites

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

InterventionNanogram 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)
Pimasertib0.0285.2262.285.0528.580.00.087.53167.6169.1108.851.33

Time to Reach Maximum Plasma Concentration (Tmax) of M445 and M554

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

Interventionhour (Median)
M445M554
Pimasertib1.54

Time to Reach Maximum Plasma Concentration (Tmax) of Unlabeled Pimasertib and Intravenous [14C] Pimasertib

(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

Interventionhours (Median)
Unlabeled pimasertib[14C] intravenous pimasertib
Pimasertib0.750.5

Total Body Clearance of Unlabeled Pimasertib (CL/f) and Intravenous [14C] Pimasertib (CL)

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

Interventionliter per hour (Geometric Mean)
Unlabeled pimasertibIntravenous [14C] pimasertib
Pimasertib62.6745.73

Number of Subjects With Dose Limiting Toxicities (DLTs)

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)

Interventionsubjects (Number)
Pimasertib 45 mg+Temsirolimus 12.5 mg0
Pimasertib 45 mg+Temsirolimus 25 mg7
Pimasertib 75 mg+Temsirolimus 25 mg2

Number of Subjects With Treatment-emergent Adverse Events (TEAEs)

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)

Interventionsubjects (Number)
Pimasertib 45 mg+Temsirolimus 12.5 mg4
Pimasertib 45 mg+Temsirolimus 25 mg23
Pimasertib 75 mg+Temsirolimus 25 mg6

Apparent Clearance From Plasma Following Oral Administration (CL/f) of Pimasertib

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

,
Interventionliter/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

Apparent Clearance From Plasma Following Oral Administration (CL/f) of Pimasertib

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

,
Interventionliter/hour (Median)
DDI: Day 1DDI: Day 9
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI)81.2571.99
Pimasertib 45 mg+Temsirolimus 25 mg (DDI)54.3655.9

Apparent Terminal Half-life (t1/2) of Pimasertib

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

,
Interventionhour (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

Apparent Terminal Half-life (t1/2) of Pimasertib

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

,
Interventionhour (Median)
DDI: Day 1DDI: Day 9
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI)5.9156.08
Pimasertib 45 mg+Temsirolimus 25 mg (DDI)5.8865.896

Apparent Terminal Half-life (t1/2) of Temsirolimus

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

,
Interventionhour (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

Apparent Terminal Half-life (t1/2) of Temsirolimus

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

,
Interventionhour (Median)
DDI: Day 9DDI: Day 16
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI)25.5720.62
Pimasertib 45 mg+Temsirolimus 25 mg (DDI)13.219.14

Apparent Volume of Distribution (Vz/F) of Pimasertib

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

,
Interventionliter (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

Apparent Volume of Distribution (Vz/F) of Pimasertib

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

,
Interventionliter (Median)
DDI: Day 1DDI: Day 9
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI)691.3517.6
Pimasertib 45 mg+Temsirolimus 25 mg (DDI)536.5519.5

Area Under Plasma Concentration Time Curve From Time Zero to Infinity (AUC0-inf) of Temsirolimus

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

,
Interventionhour*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

Area Under Plasma Concentration Time Curve From Time Zero to Infinity (AUC0-inf) of Temsirolimus

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

,
Interventionhour*nanogram/milliliter (Median)
DDI: Day 9DDI: Day 16
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI)24522006
Pimasertib 45 mg+Temsirolimus 25 mg (DDI)21302743

Area Under the Concentration Time Curve During a Dosing Interval (AUCtau) and Area Under the Concentration Time Curve From Time Zero to Infinity (AUC0-inf) of Pimasertib

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

,
Interventionhour*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

Area Under the Concentration Time Curve During a Dosing Interval (AUCtau) and Area Under the Concentration Time Curve From Time Zero to Infinity (AUC0-inf) of Pimasertib

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

,
Interventionhour*nanogram/milliliter (Median)
DDI: AUCtau: Day 9DDI: AUC0-inf: Day 1
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI)628573.2
Pimasertib 45 mg+Temsirolimus 25 mg (DDI)805828.6

Maximum Plasma Concentration (Cmax) of Pimasertib

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

,
Interventionnanogram/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

Maximum Plasma Concentration (Cmax) of Pimasertib

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

,
Interventionnanogram/milliliter (Median)
DDI: Day 1DDI: Day 9
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI)185.2131
Pimasertib 45 mg+Temsirolimus 25 mg (DDI)193.5192.1

Maximum Plasma Concentration (Cmax) of Temsirolimus

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

,
Interventionnanogram/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

Maximum Plasma Concentration (Cmax) of Temsirolimus

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

,
Interventionnanogram/milliliter (Median)
DDI: Day 9DDI: Day 16
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI)457.5281.1
Pimasertib 45 mg+Temsirolimus 25 mg (DDI)505.3511.8

Time to Reach Maximum Plasma Concentration (Tmax) of Pimasertib

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

,
Interventionhour (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

Time to Reach Maximum Plasma Concentration (Tmax) of Pimasertib

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

,
Interventionhour (Median)
DDI: Day 1DDI: Day 9
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI)12.3
Pimasertib 45 mg+Temsirolimus 25 mg (DDI)1.51.133

Time to Reach Maximum Plasma Concentration (Tmax) of Temsirolimus

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

,
Interventionhour (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

Time to Reach Maximum Plasma Concentration (Tmax) of Temsirolimus

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

,
Interventionhour (Median)
DDI: Day 9DDI: Day 16
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI)0.74170.9333
Pimasertib 45 mg+Temsirolimus 25 mg (DDI)0.56670.5

Total Body Clearance From Plasma Following Intravenous Administration (CL) of Temsirolimus

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

,
Interventionliter/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

Total Body Clearance From Plasma Following Intravenous Administration (CL) of Temsirolimus

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

,
Interventionliter/hour (Median)
DDI: Day 9DDI: Day 16
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI)5.3787.528
Pimasertib 45 mg+Temsirolimus 25 mg (DDI)11.739.292

Volume of Distribution (Vz) of Temsirolimus

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

,
Interventionliter (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

Volume of Distribution (Vz) of Temsirolimus

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

,
Interventionliter (Median)
DDI: Day 9DDI: Day 16
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI)152189.5
Pimasertib 45 mg+Temsirolimus 25 mg (DDI)244.5233

Geometric Mean for Exposure Area Under the Curve (AUC) 0-12

Geometric mean exposure for sorafenib. (NCT00090545)
Timeframe: 0, 0.25, 0.50, 1, 2, 4, 6, 8, 12, and 24 hours post-dose

Interventionmg/L.h (Geometric Mean)
First Stage - Disease Progression9.76
Second Stage - Increased Accrual18.63

Maximum Observed Plasma Concentration (Cmax) of BAY 43-9006 (Sorafenib)

Plasma concentration-time profile for sorafenib. (NCT00090545)
Timeframe: 0, 0.25, 0.50, 1, 2, 4, 6, 8, 12, AND 24 hours post dose

Interventionmg/L (Mean)
First Stage - Disease Progression1.28
Second Stage - Increased Accrual2.57

Median Overall Survival

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.

InterventionMonths (Median)
First Stage - Disease Progression18
Second Stage - Increased Accrual18.3

Number of Participants With Adverse Events

Here is the number of participants with adverse events. For the detailed list of adverse events, see the adverse event module. (NCT00090545)
Timeframe: Date treatment consent signed to date off study, approximately 49 months.

InterventionParticipants (Count of Participants)
First Stage - Disease Progression22
Second Stage - Increased Accrual23

Progression Free Survival

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

Interventionmonths (Median)
First Stage - Disease Progression1.83
Second Stage - Increased Accrual3.7

Time to Maximum Observed Plasma Concentration (Tmax) of BAY 43-9006 (Sorafenib)

Time to maximum concentration for sorafenib. (NCT00090545)
Timeframe: 0, 0.25, 0.50, 1, 2, 4, 6, 8, 12, and 24 hours post-dose

Interventionhours (Median)
First Stage - Disease Progression0.68
Second Stage - Increased Accrual8

Overall Response Evaluated by the Response Evaluation Criteria in Solid Tumors (RECIST)

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)

,
InterventionParticipants (Count of Participants)
Complete ResponsePartial ResponseProgressive DiseaseStable Disease
First Stage - Disease Progression0080
Second Stage - Increased Accrual011310

Overall Response Rate

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

InterventionParticipants (Count of Participants)
Sorafenib0

Percentage of Patients Tolerating Re-escalated Dose of Sorafenib for 28 Days Without Dose Interruption or De-escalation for Toxicity

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

InterventionParticipants (Count of Participants)
Sorafenib11

Time to Disease Progression

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

Interventionmonths (Median)
Sorafenib4.7

Median Time Course to Development of Worst Grade (Grade 3) HFSR as Assessed by CTCAE v4.03 Criteria When Treated With a Combination of Regorafenib and Perindopril

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)

Interventiondays (Median)
Single Arm Trial12

Median Time to Progression Free Survival (PFS)

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.

InterventionMonths (Median)
Single Arm Trial2.60

Number of Participants That Have Any Grade HFSR Toxicity

"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)

InterventionParticipants (Count of Participants)
Single Arm Trial7

Number of Participants With Maximal Severity of HFSR as Assessed by CTCAE v4.03 Criteria When Treated With a Combination of Regorafenib and Perindopril

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)

InterventionParticipants (Count of Participants)
Single Arm Trial5

The Number of Participants That Experienced All Grade Toxicities as Assessed by CTCAE v4.03 Criteria When Treated With a Combination of Regorafenib and Perindopril

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

Interventionparticipants (Number)
Single Arm Trial10

The Number of Participants That Experienced Any Grade of Hypertension as Assessed by CTCAE v4.03 Criteria When Treated With a Combination of Regorafenib and Perindopril

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

InterventionParticipants (Count of Participants)
Single Arm Trial6

Differences in Histologic Alterations in Rash Caused by Lapatinib, a Dual HER1/2 Inhibitor (HER1/2i), and the Single HER1 Inhibitors (HER1i) Cetuximab, Erlotinib,and Panitumumab.

(NCT00709878)
Timeframe: 6 months

,,,
InterventionTotal number of cases (Number)
UlcerationParakeratosisAcanthosisEpidermal atrophyEpidermal dysmaturationEpidermal dyskeratosisEpidermal neutrophilc infiltrateEpidermal monocytic infiltrateEpidermal eosinophilic infiltrateDermal neutrophilic infiltrateDermal monocytic infiltrateDermal eosinophilic infiltrateFollicular concretionsFollicular neutrophilic pustuleDysmorphic follicleFollicular dyskeratosisFollicular neurtrophilic infiltrateFollicular monocytic infiltrateFollicular eosinophilic infiltrateEccrine dyskeratosisEccrine necrosisEccrine infiltrateSebaceous infiltrate
Patients Treated With Cetuximab (C)12153310004254235211201
Patients Treated With Erlotinib (E)20040010144036417210103
Patients Treated With Lapatinib (L)11172310021233445220000
Patients Treated With Panitumumab (P)01021002024023213210001

Reviews

141 reviews available for niacinamide and Neoplasms

ArticleYear
NAMPT: A critical driver and therapeutic target for cancer.
    The international journal of biochemistry & cell biology, 2022, Volume: 145

    Topics: Animals; Cytokines; Mammals; NAD; Neoplasms; Niacinamide; Nicotinamide Phosphoribosyltransferase

2022
Complex roles of nicotinamide N-methyltransferase in cancer progression.
    Cell death & disease, 2022, 03-25, Volume: 13, Issue:3

    Topics: Humans; Neoplasms; Niacinamide; Nicotinamide N-Methyltransferase

2022
Nicotinamide N-methyl transferase and cancer-associated thrombosis: insights to prevention and management.
    Epigenomics, 2023, Volume: 15, Issue:6

    Topics: Antineoplastic Agents; Carcinogenesis; Humans; Neoplasms; Niacinamide; Nicotinamide N-Methyltransfer

2023
Diverse therapeutic efficacies and more diverse mechanisms of nicotinamide.
    Metabolomics : Official journal of the Metabolomic Society, 2019, 10-05, Volume: 15, Issue:10

    Topics: Animals; Cell Survival; Fibrosis; Humans; Inflammation; Mitochondria; Neoplasms; Niacinamide; Skin D

2019
The Role of Nicotinamide in Cancer Chemoprevention and Therapy.
    Biomolecules, 2020, 03-20, Volume: 10, Issue:3

    Topics: Clinical Trials, Phase III as Topic; Humans; NAD; Neoplasm Proteins; Neoplasms; Niacinamide; Poly (A

2020
Possible mechanisms of cancer prevention by nicotinamide.
    British journal of pharmacology, 2021, Volume: 178, Issue:10

    Topics: Dietary Supplements; Humans; Neoplasms; Niacinamide; Randomized Controlled Trials as Topic

2021
Allosteric Inhibition of ABL Kinases: Therapeutic Potential in Cancer.
    Molecular cancer therapeutics, 2020, Volume: 19, Issue:9

    Topics: Allosteric Regulation; Animals; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Clinical

2020
Nicotinamide N-methyltransferase: At the crossroads between cellular metabolism and epigenetic regulation.
    Molecular metabolism, 2021, Volume: 45

    Topics: Adipose Tissue; Animals; Epigenesis, Genetic; Humans; Insulin Resistance; Liver; NAD; Neoplasms; Nia

2021
Nicotinamide N-methyl transferase (NNMT): An emerging therapeutic target.
    Drug discovery today, 2021, Volume: 26, Issue:11

    Topics: Enzyme Inhibitors; Humans; Metabolic Diseases; Neoplasms; Neurodegenerative Diseases; Niacinamide; N

2021
Advances in NAD-Lowering Agents for Cancer Treatment.
    Nutrients, 2021, May-14, Volume: 13, Issue:5

    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.
    International journal of molecular sciences, 2021, May-26, Volume: 22, Issue:11

    Topics: Humans; Methylation; NAD; Neoplasm Proteins; Neoplasms; Neoplastic Stem Cells; Niacinamide; Nicotina

2021
PharmGKB summary: sorafenib pathways.
    Pharmacogenetics and genomics, 2017, Volume: 27, Issue:6

    Topics: Animals; Antineoplastic Agents; Clinical Trials as Topic; Gene Regulatory Networks; Humans; Neoplasm

2017
NAD
    Trends in cancer, 2017, Volume: 3, Issue:8

    Topics: Aging; Humans; Incidence; Life Expectancy; Longevity; NAD; Neoplasms; Niacinamide; Nicotinamide Mono

2017
B Vitamin Complex and Chemotherapy-Induced Peripheral Neuropathy.
    Current oncology reports, 2017, Oct-05, Volume: 19, Issue:12

    Topics: Animals; Humans; Neoplasms; Niacinamide; Organoplatinum Compounds; Oxaliplatin; Peripheral Nervous S

2017
Pharmacology of Pimasertib, A Selective MEK1/2 Inhibitor.
    European journal of drug metabolism and pharmacokinetics, 2018, Volume: 43, Issue:4

    Topics: Humans; MAP Kinase Kinase 1; MAP Kinase Kinase 2; Neoplasms; Niacinamide; Protein Kinase Inhibitors

2018
Clinical trials targeting hypoxia.
    The British journal of radiology, 2019, Volume: 92, Issue:1093

    Topics: Animals; Cell Hypoxia; Female; Humans; Male; Misonidazole; Neoplasms; Niacinamide; Oxygen Consumptio

2019
Nicotinamide phosphoribosyltransferase (NAMPT) inhibitors as therapeutics: rationales, controversies, clinical experience.
    Current drug targets, 2013, Jun-01, Volume: 14, Issue:6

    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.
    Journal of human hypertension, 2013, Volume: 27, Issue:10

    Topics: Antineoplastic Agents; Blood Pressure; Chi-Square Distribution; Drug Administration Schedule; Humans

2013
Body composition in chemotherapy: the promising role of CT scans.
    Current opinion in clinical nutrition and metabolic care, 2013, Volume: 16, Issue:5

    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.
    Anti-cancer agents in medicinal chemistry, 2013, Volume: 13, Issue:8

    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.
    International journal of cancer, 2014, Aug-15, Volume: 135, Issue:4

    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.
    Asian Pacific journal of cancer prevention : APJCP, 2014, Volume: 14, Issue:11

    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.
    Journal of clinical hypertension (Greenwich, Conn.), 2014, Volume: 16, Issue:3

    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.
    Expert review of anticancer therapy, 2014, Volume: 14, Issue:6

    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.
    Expert opinion on drug safety, 2014, Volume: 13, Issue:5

    Topics: Antineoplastic Agents; Case Management; Drug Interactions; Humans; Neoplasms; Niacinamide; Phenylure

2014
Sorafenib: targeting multiple tyrosine kinases in cancer.
    Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer, 2014, Volume: 201

    Topics: Animals; Antineoplastic Agents; Humans; Neoplasms; Niacinamide; Phenylurea Compounds; Protein Kinase

2014
Sirtuin inhibitors as anticancer agents.
    Future medicinal chemistry, 2014, Volume: 6, Issue:8

    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.
    Human pathology, 2014, Volume: 45, Issue:9

    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.
    Future oncology (London, England), 2014, Volume: 10, Issue:12

    Topics: Antineoplastic Agents; Cardiotoxicity; Cardiovascular Diseases; Clinical Trials, Phase II as Topic;

2014
The adverse effects of sorafenib in patients with advanced cancers.
    Basic & clinical pharmacology & toxicology, 2015, Volume: 116, Issue:3

    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.
    Expert opinion on drug metabolism & toxicology, 2015, Volume: 11, Issue:5

    Topics: Animals; Antineoplastic Agents; Biological Transport; Glucuronides; Glucuronosyltransferase; Humans;

2015
CDK8 kinase--An emerging target in targeted cancer therapy.
    Biochimica et biophysica acta, 2015, Volume: 1854, Issue:10 Pt B

    Topics: Cyclin-Dependent Kinase 8; Gene Expression Regulation, Neoplastic; Humans; Molecular Structure; Neop

2015
Gastrointestinal Toxicities With Combined Antiangiogenic and Stereotactic Body Radiation Therapy.
    International journal of radiation oncology, biology, physics, 2015, Jul-01, Volume: 92, Issue:3

    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.
    International journal of clinical pharmacy, 2015, Volume: 37, Issue:6

    Topics: Antineoplastic Agents; Humans; Neoplasms; Niacinamide; Phenylurea Compounds; Protein Kinase Inhibito

2015
[Kinase inhibitors and their resistance].
    Nihon rinsho. Japanese journal of clinical medicine, 2015, Volume: 73, Issue:8

    Topics: Antibodies, Monoclonal, Humanized; Benzamides; Biomarkers, Tumor; Crizotinib; Drug Discovery; Drug R

2015
[Anti-angiogenesis and molecular targeted therapies].
    Nihon rinsho. Japanese journal of clinical medicine, 2015, Volume: 73, Issue:8

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Pro

2015
Targeting the RAS pathway by mitogen-activated protein kinase inhibitors.
    Swiss medical weekly, 2015, Volume: 145

    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.
    JAMA oncology, 2016, Volume: 2, Issue:4

    Topics: Antineoplastic Agents; Carcinoma; Humans; Neoplasms; Niacinamide; Phenylurea Compounds; Sorafenib; T

2016
Antiangiogenic therapy in oncology: current status and future directions.
    Lancet (London, England), 2016, Jul-30, Volume: 388, Issue:10043

    Topics: Angiogenesis Inhibitors; Angiopoietin-1; Biomarkers, Tumor; Disease-Free Survival; Drug Resistance,

2016
Telomerase inhibitors: a patent review (2010-2015).
    Expert opinion on therapeutic patents, 2016, Volume: 26, Issue:6

    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.
    Cancer research, 2016, 08-15, Volume: 76, Issue:16

    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.
    Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy, 2016, Volume: 27

    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†.
    Annals of oncology : official journal of the European Society for Medical Oncology, 2017, 02-01, Volume: 28, Issue:2

    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.
    Cancer treatment reviews, 2017, Volume: 53

    Topics: Antineoplastic Combined Chemotherapy Protocols; Bevacizumab; Cetuximab; CTLA-4 Antigen; Humans; Immu

2017
Kinase Inhibitors in Multitargeted Cancer Therapy.
    Current medicinal chemistry, 2017, Volume: 24, Issue:16

    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.
    PLoS biology, 2017, Volume: 15, Issue:2

    Topics: Antineoplastic Agents; Clinical Trials as Topic; Confidence Intervals; Humans; Molecular Targeted Th

2017
[Oncology 2008].
    Deutsche medizinische Wochenschrift (1946), 2008, Volume: 133, Issue:25-26

    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?
    Nature clinical practice. Oncology, 2008, Volume: 5, Issue:7

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzenesulfonate

2008
Sorafenib (BAY 43-9006): review of clinical development.
    Current clinical pharmacology, 2006, Volume: 1, Issue:3

    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.
    The oncologist, 2008, Volume: 13, Issue:8

    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.
    The oncologist, 2008, Volume: 13, Issue:9

    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.
    The oncologist, 2008, Volume: 13, Issue:9

    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.
    The oncologist, 2008, Volume: 13, Issue:9

    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.
    The oncologist, 2008, Volume: 13, Issue:9

    Topics: Benzenesulfonates; Foot Dermatoses; Hand Dermatoses; Humans; Indoles; Neoplasms; Niacinamide; Phenyl

2008
Dermatologic symptoms associated with the multikinase inhibitor sorafenib.
    Journal of the American Academy of Dermatology, 2009, Volume: 60, Issue:2

    Topics: Antineoplastic Agents; Benzenesulfonates; Humans; Neoplasms; Niacinamide; Phenylurea Compounds; Prot

2009
[Targeted therapies and their indications in solid neoplasias].
    La Revue de medecine interne, 2009, Volume: 30, Issue:5

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic C

2009
Hypothyroidism related to tyrosine kinase inhibitors: an emerging toxic effect of targeted therapy.
    Nature reviews. Clinical oncology, 2009, Volume: 6, Issue:4

    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.
    Targeted oncology, 2009, Volume: 4, Issue:2

    Topics: Angiogenesis Inhibitors; Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineo

2009
Cardiac dysfunction induced by novel targeted anticancer therapy: an emerging issue.
    Current cardiology reports, 2009, Volume: 11, Issue:3

    Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Benzenesulfonates;

2009
Renal toxicity of targeted therapies.
    Targeted oncology, 2009, Volume: 4, Issue:2

    Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzenesulfonates; Bevacizumab; Clinical

2009
Angiogenesis regulated by VEGF and its receptors and its clinical application.
    [Rinsho ketsueki] The Japanese journal of clinical hematology, 2009, Volume: 50, Issue:5

    Topics: Angiogenesis Inhibitors; Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineo

2009
The role of antiangiogenesis therapy: bevacizumab and beyond.
    Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2009, Volume: 11, Issue:6

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic A

2009
An overview of small-molecule inhibitors of VEGFR signaling.
    Nature reviews. Clinical oncology, 2009, Volume: 6, Issue:10

    Topics: Angiogenesis Inhibitors; Animals; Antineoplastic Agents; Benzenesulfonates; Cadherins; Clinical Tria

2009
NAD(+) -dependent histone deacetylases (sirtuins) as novel therapeutic targets.
    Medicinal research reviews, 2010, Volume: 30, Issue:6

    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.
    Cancer science, 2010, Volume: 101, Issue:1

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic C

2010
Biochemical effects of SIRT1 activators.
    Biochimica et biophysica acta, 2010, Volume: 1804, Issue:8

    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].
    Zhonghua zhong liu za zhi [Chinese journal of oncology], 2009, Volume: 31, Issue:9

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antimetabolites,

2009
Compounds in clinical Phase III and beyond.
    Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer, 2010, Volume: 180

    Topics: Angiogenesis Inhibitors; Axitinib; Benzenesulfonates; Clinical Trials, Phase III as Topic; Endostati

2010
Sorafenib.
    Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer, 2010, Volume: 184

    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.
    The Lancet. Oncology, 2010, Volume: 11, Issue:4

    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.
    Current opinion in molecular therapeutics, 2010, Volume: 12, Issue:2

    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.
    Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG, 2010, Volume: 8, Issue:9

    Topics: Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Dermatolog

2010
[Anti-angiogenic drugs].
    Nihon rinsho. Japanese journal of clinical medicine, 2010, Volume: 68, Issue:6

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzenesulfonate

2010
Cardiovascular safety of VEGF-targeting therapies: current evidence and handling strategies.
    The oncologist, 2010, Volume: 15, Issue:7

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic A

2010
[Cutaneous side effects of the multikinase inhibitors sorafenib and sunitinib].
    Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete, 2010, Volume: 61, Issue:8

    Topics: Antineoplastic Agents; Benzenesulfonates; Drug Delivery Systems; Drug Eruptions; Humans; Indoles; Ne

2010
Tumor-stromal cell interactions and opportunities for therapeutic intervention.
    Current opinion in pharmacology, 2010, Volume: 10, Issue:4

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic A

2010
Inherited hepatocellular carcinoma.
    Best practice & research. Clinical gastroenterology, 2010, Volume: 24, Issue:5

    Topics: Algorithms; Antineoplastic Agents; Benzenesulfonates; Carcinoma, Hepatocellular; Catheter Ablation;

2010
In pursuit of new anti-angiogenic therapies for cancer treatment.
    Frontiers in bioscience (Landmark edition), 2011, 01-01, Volume: 16, Issue:3

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic A

2011
Meta-analysis of dermatological toxicities associated with sorafenib.
    Clinical and experimental dermatology, 2011, Volume: 36, Issue:4

    Topics: Antineoplastic Agents; Benzenesulfonates; Humans; Neoplasms; Niacinamide; Phenylurea Compounds; Prot

2011
[Indications and current development of new targeted therapies in pediatric oncology].
    Bulletin du cancer, 2011, Volume: 98, Issue:5

    Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Benzamides; Benzen

2011
Targeted-therapy and imaging response: a new paradigm for clinical evaluation?
    Reviews on recent clinical trials, 2011, Volume: 6, Issue:3

    Topics: Antineoplastic Agents; Benzamides; Benzenesulfonates; Clinical Trials as Topic; Diagnostic Imaging;

2011
[Targeting the RAS signalling pathway in cancer].
    Bulletin du cancer, 2011, Volume: 98, Issue:9

    Topics: Antineoplastic Agents; Benzenesulfonates; Colorectal Neoplasms; ErbB Receptors; Extracellular Signal

2011
The two faces of FBW7 in cancer drug resistance.
    BioEssays : news and reviews in molecular, cellular and developmental biology, 2011, Volume: 33, Issue:11

    Topics: Amyloid Precursor Protein Secretases; Apoptosis; Benzenesulfonates; Biphenyl Compounds; Cell Cycle P

2011
Anti-angiogenic therapy: concept to clinic.
    Microcirculation (New York, N.Y. : 1994), 2012, Volume: 19, Issue:2

    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.
    Clinical and experimental immunology, 2012, Volume: 167, Issue:2

    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.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2012, Mar-10, Volume: 30, Issue:8

    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).
    Oncology reports, 2012, Volume: 27, Issue:5

    Topics: Animals; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; C

2012
Using NF-κB as a molecular target for theranostics in radiation oncology research.
    Expert review of molecular diagnostics, 2012, Volume: 12, Issue:2

    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].
    Magyar onkologia, 2012, Volume: 56, Issue:1

    Topics: Angiogenesis Inhibitors; Animals; Axitinib; Benzenesulfonates; Humans; Imidazoles; Indazoles; Indole

2012
Combining antiangiogenics to overcome resistance: rationale and clinical experience.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2012, Jul-15, Volume: 18, Issue:14

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Pro

2012
Evidence for therapeutic drug monitoring of targeted anticancer therapies.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2012, Nov-10, Volume: 30, Issue:32

    Topics: Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antibodies, Monoclonal, Murine-D

2012
Hypothyroidism during treatment with tyrosine kinase inhibitors.
    Endokrynologia Polska, 2012, Volume: 63, Issue:4

    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.
    Current pharmaceutical design, 2013, Volume: 19, Issue:5

    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.
    Current topics in medicinal chemistry, 2012, Volume: 12, Issue:15

    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].
    Magyar onkologia, 2012, Volume: 56, Issue:3

    Topics: Animals; Antineoplastic Agents; Axitinib; Benzenesulfonates; Carcinoma, Hepatocellular; Clinical Tri

2012
[Advances in the study of structural modifications of multi-target anticancer drug sorafenib].
    Yao xue xue bao = Acta pharmaceutica Sinica, 2012, Volume: 47, Issue:9

    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.
    Advances in enzyme regulation, 2002, Volume: 42

    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.
    Current pharmaceutical design, 2002, Volume: 8, Issue:25

    Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Clinical Trials, Phase I as Topic; Humans; Neopla

2002
BAY 43-9006: preclinical data.
    Current pharmaceutical design, 2002, Volume: 8, Issue:25

    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.
    Hematology/oncology clinics of North America, 2002, Volume: 16, Issue:5

    Topics: Adult; Animals; Antineoplastic Agents; Benzamides; Benzenesulfonates; Child; Clinical Trials as Topi

2002
BAY-43-9006 Bayer/Onyx.
    Current opinion in investigational drugs (London, England : 2000), 2003, Volume: 4, Issue:6

    Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Clinical Trials as Topic; Drugs, Investigational;

2003
Raf pathway inhibitors in oncology.
    Current opinion in investigational drugs (London, England : 2000), 2003, Volume: 4, Issue:12

    Topics: Animals; Benzenesulfonates; Enzyme Inhibitors; Humans; MAP Kinase Signaling System; Neoplasms; Niaci

2003
High interstitial fluid pressure - an obstacle in cancer therapy.
    Nature reviews. Cancer, 2004, Volume: 4, Issue:10

    Topics: Alprostadil; Animals; Antineoplastic Agents; Biological Transport; Bradykinin; Extracellular Fluid;

2004
Raf kinase inhibitors in oncology.
    Onkologie, 2005, Volume: 28, Issue:2

    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.
    Current opinion in pharmacology, 2005, Volume: 5, Issue:4

    Topics: Animals; Benzamides; Benzenesulfonates; Clinical Trials as Topic; Diphenylamine; Extracellular Signa

2005
Cutaneous side-effects of kinase inhibitors and blocking antibodies.
    The Lancet. Oncology, 2005, Volume: 6, Issue:7

    Topics: Antibodies, Blocking; Antineoplastic Agents; Benzamides; Benzenesulfonates; ErbB Receptors; Hair Dis

2005
Cutaneous side-effects of kinase inhibitors and blocking antibodies.
    The Lancet. Oncology, 2005, Volume: 6, Issue:7

    Topics: Antibodies, Blocking; Antineoplastic Agents; Benzamides; Benzenesulfonates; ErbB Receptors; Hair Dis

2005
Cutaneous side-effects of kinase inhibitors and blocking antibodies.
    The Lancet. Oncology, 2005, Volume: 6, Issue:7

    Topics: Antibodies, Blocking; Antineoplastic Agents; Benzamides; Benzenesulfonates; ErbB Receptors; Hair Dis

2005
Cutaneous side-effects of kinase inhibitors and blocking antibodies.
    The Lancet. Oncology, 2005, Volume: 6, Issue:7

    Topics: Antibodies, Blocking; Antineoplastic Agents; Benzamides; Benzenesulfonates; ErbB Receptors; Hair Dis

2005
Raf: a strategic target for therapeutic development against cancer.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2005, Sep-20, Volume: 23, Issue:27

    Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Down-Regulation; Drug Delivery Systems; Humans; M

2005
Update on angiogenesis inhibitors.
    Current opinion in oncology, 2005, Volume: 17, Issue:6

    Topics: Angiogenesis Inhibitors; Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzene

2005
Regulation of c-Raf-1: therapeutic implications.
    Clinical advances in hematology & oncology : H&O, 2003, Volume: 1, Issue:8

    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?
    European journal of cancer (Oxford, England : 1990), 2006, Volume: 42, Issue:4

    Topics: Administration, Oral; Adolescent; Adult; Aged; Antineoplastic Agents; Benzenesulfonates; Clinical Tr

2006
Targeting Raf-kinase: molecular rationales and translational issues.
    Annals of oncology : official journal of the European Society for Medical Oncology, 2006, Volume: 17 Suppl 7

    Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Humans; Neoplasms; Niacinamide; Phenylurea Compou

2006
Cancer targets in the Ras pathway.
    Cold Spring Harbor symposia on quantitative biology, 2005, Volume: 70

    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.
    Seminars in oncology, 2006, Volume: 33, Issue:4

    Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Carcinoma, Renal Cell; Cell Transformation, Neopl

2006
Raf kinases: oncogenesis and drug discovery.
    International journal of cancer, 2006, Nov-15, Volume: 119, Issue:10

    Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Clinical Trials as Topic; Disease Models, Animal;

2006
Discovery and development of sorafenib: a multikinase inhibitor for treating cancer.
    Nature reviews. Drug discovery, 2006, Volume: 5, Issue:10

    Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Carcinoma, Renal Cell; Clinical Trials as Topic;

2006
Protein kinases as drug targets in cancer.
    Current cancer drug targets, 2006, Volume: 6, Issue:7

    Topics: Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzamides; Benzenesulfonates; G

2006
The hypoxic tumour microenvironment, patient selection and hypoxia-modifying treatments.
    Clinical oncology (Royal College of Radiologists (Great Britain)), 2007, Volume: 19, Issue:6

    Topics: Anemia; Biomarkers, Tumor; Carbon Dioxide; Cell Hypoxia; Humans; Hyperbaric Oxygenation; Neoplasms;

2007
Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition.
    Nature reviews. Cancer, 2007, Volume: 7, Issue:5

    Topics: Adaptor Proteins, Signal Transducing; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Ben

2007
Angiogenesis in cancer: molecular mechanisms, clinical impact.
    Langenbeck's archives of surgery, 2007, Volume: 392, Issue:3

    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.
    The oncologist, 2007, Volume: 12, Issue:4

    Topics: Antineoplastic Agents; Benzenesulfonates; Clinical Trials, Phase I as Topic; Humans; Neoplasm Metast

2007
Design of clinical trials of radiation combined with antiangiogenic therapy.
    The oncologist, 2007, Volume: 12, Issue:4

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzenesulfonate

2007
Sorafenib: delivering a targeted drug to the right targets.
    Expert review of anticancer therapy, 2007, Volume: 7, Issue:5

    Topics: Antineoplastic Agents; Benzenesulfonates; Carcinoma, Hepatocellular; Carcinoma, Renal Cell; Clinical

2007
Mechanisms of adverse effects of anti-VEGF therapy for cancer.
    British journal of cancer, 2007, Jun-18, Volume: 96, Issue:12

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic A

2007
Multitarget tyrosine kinase inhibition: [and the winner is...].
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2007, Jun-10, Volume: 25, Issue:17

    Topics: Antineoplastic Agents; Clinical Trials, Phase I as Topic; Humans; Indoles; Neoplasms; Niacinamide; O

2007
B-Raf kinase inhibitors for cancer treatment.
    Current opinion in investigational drugs (London, England : 2000), 2007, Volume: 8, Issue:6

    Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Enzyme Inhibitors; Humans; Imidazoles; Neoplasms;

2007
[Oral drugs inhibiting the VEGF pathway].
    Bulletin du cancer, 2007, Volume: 94 Spec No

    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.
    BioEssays : news and reviews in molecular, cellular and developmental biology, 2007, Volume: 29, Issue:11

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antineoplastic Agents; Benzenesulfonates; Carcinoma

2007
New developments in multitargeted therapy for patients with solid tumours.
    Cancer treatment reviews, 2008, Volume: 34, Issue:1

    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.
    Cancer chemotherapy and pharmacology, 2008, Volume: 61, Issue:4

    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.
    Medical oncology (Northwood, London, England), 2008, Volume: 25, Issue:3

    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.
    Acta oncologica (Stockholm, Sweden), 2008, Volume: 47, Issue:2

    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.
    The Lancet. Oncology, 2008, Volume: 9, Issue:2

    Topics: Angiogenesis Inhibitors; Antineoplastic Agents; Benzenesulfonates; Humans; Hypertension; Incidence;

2008
From single- to multi-target drugs in cancer therapy: when aspecificity becomes an advantage.
    Current medicinal chemistry, 2008, Volume: 15, Issue:5

    Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Antineoplastic Com

2008
Mcl-1: a gateway to TRAIL sensitization.
    Cancer research, 2008, Apr-01, Volume: 68, Issue:7

    Topics: Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Down-Regulation; Drug Resistance,

2008
Physiology aspects of pyridine nucleotide regulation in mammals.
    Molecular and cellular biochemistry, 1980, Dec-16, Volume: 33, Issue:3

    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.
    Acta oncologica (Stockholm, Sweden), 1995, Volume: 34, Issue:5

    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.
    The British journal of cancer. Supplement, 1996, Volume: 27

    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.
    Acta oncologica (Stockholm, Sweden), 1997, Volume: 36, Issue:5

    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].
    Nihon rinsho. Japanese journal of clinical medicine, 1999, Volume: 57, Issue:10

    Topics: Apoptosis; Caspase Inhibitors; HeLa Cells; HL-60 Cells; Humans; K562 Cells; Neoplasms; Niacinamide;

1999
Improvement of tumor oxygenation by mild hyperthermia.
    Radiation research, 2001, Volume: 155, Issue:4

    Topics: Animals; Carbon Dioxide; Cell Hypoxia; Combined Modality Therapy; Dogs; Humans; Hyperthermia, Induce

2001
Hypoxia as a target for combined modality treatments.
    European journal of cancer (Oxford, England : 1990), 2002, Volume: 38, Issue:2

    Topics: Antineoplastic Combined Chemotherapy Protocols; Carbon Dioxide; Cell Hypoxia; Combined Modality Ther

2002
Nicotinamide and the hypoxia problem.
    Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 1991, Volume: 22, Issue:2

    Topics: Humans; Hypoxia; Neoplasms; Niacinamide; Radiation Injuries; Radiation Tolerance

1991
Today's carcinochemotherapy: some of its achievements, failures and prospects.
    Ergebnisse der Physiologie, biologischen Chemie und experimentellen Pharmakologie, 1970, Volume: 62

    Topics: Alkylating Agents; Antibiotics, Antineoplastic; Antibody-Producing Cells; Antimetabolites; Antineopl

1970
Some developments in the use of radiophosphorus.
    Modern trends in radiotherapy, 1972, Volume: 2

    Topics: Amplifiers, Electronic; Androgens; Animals; Breast Neoplasms; DNA; Electrons; Estrogens; Eye Neoplas

1972

Trials

72 trials available for niacinamide and Neoplasms

ArticleYear
A PK-PD model linking biomarker dynamics to progression-free survival in patients treated with everolimus and sorafenib combination therapy, EVESOR phase I trial.
    Cancer chemotherapy and pharmacology, 2023, Volume: 91, Issue:5

    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.
    Oncotarget, 2023, 04-10, Volume: 14

    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.
    Cancer chemotherapy and pharmacology, 2019, Volume: 84, Issue:5

    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.
    Targeted oncology, 2021, Volume: 16, Issue:1

    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.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2021, 03-01, Volume: 27, Issue:5

    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.
    Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 2017, Volume: 124, Issue:1

    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.
    British journal of cancer, 2018, Volume: 119, Issue:12

    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.
    British journal of cancer, 2019, Volume: 120, Issue:3

    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.
    BMC cancer, 2013, May-16, Volume: 13

    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.
    Investigational new drugs, 2014, Volume: 32, Issue:2

    Topics: Adult; Aged; Angiogenesis Inhibitors; Antineoplastic Combined Chemotherapy Protocols; Disease-Free S

2014
Alternative formulations of sorafenib for use in children.
    Pediatric blood & cancer, 2013, Volume: 60, Issue:10

    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.
    Investigational new drugs, 2013, Volume: 31, Issue:5

    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.
    Investigational new drugs, 2014, Volume: 32, Issue:2

    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.
    Journal of clinical pharmacology, 2014, Volume: 54, Issue:6

    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.
    Clinical pharmacology and therapeutics, 2014, Volume: 96, Issue:1

    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.
    The oncologist, 2014, Volume: 19, Issue:4

    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.
    Investigational new drugs, 2015, Volume: 33, Issue:1

    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.
    Investigational new drugs, 2015, Volume: 33, Issue:1

    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.
    Investigational new drugs, 2015, Volume: 33, Issue:1

    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.
    Oncotarget, 2014, Nov-30, Volume: 5, Issue:22

    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.
    Future oncology (London, England), 2015, Volume: 11, Issue:10

    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.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2016, 05-15, Volume: 22, Issue:10

    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.
    Cancer medicine, 2016, Volume: 5, Issue:2

    Topics: Administration, Oral; Adolescent; Antineoplastic Agents; Child; Drug Administration Schedule; Drug M

2016
Phase I study of pemetrexed with sorafenib in advanced solid tumors.
    Oncotarget, 2016, 07-05, Volume: 7, Issue:27

    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.
    British journal of clinical pharmacology, 2016, Volume: 82, Issue:6

    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.
    Drug metabolism and disposition: the biological fate of chemicals, 2017, Volume: 45, Issue:2

    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.
    Anti-cancer drugs, 2017, Volume: 28, Issue:3

    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.
    Future oncology (London, England), 2017, Volume: 13, Issue:8

    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.
    Investigational new drugs, 2017, Volume: 35, Issue:5

    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.
    Investigational new drugs, 2008, Volume: 26, Issue:5

    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.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2008, Aug-01, Volume: 26, Issue:22

    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.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2008, Aug-01, Volume: 26, Issue:22

    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.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2008, Aug-01, Volume: 26, Issue:22

    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.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2008, Aug-01, Volume: 26, Issue:22

    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.
    British journal of cancer, 2008, Nov-04, Volume: 99, Issue:9

    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.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2009, Apr-10, Volume: 27, Issue:11

    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.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2009, Nov-15, Volume: 15, Issue:22

    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.
    Cancer chemotherapy and pharmacology, 2010, Volume: 66, Issue:5

    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.
    Molecular cancer therapeutics, 2010, Volume: 9, Issue:3

    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.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2010, May-01, Volume: 16, Issue:9

    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.
    Cancer chemotherapy and pharmacology, 2011, Volume: 67, Issue:4

    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.
    Cancer chemotherapy and pharmacology, 2011, Volume: 68, Issue:1

    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.
    British journal of cancer, 2010, Nov-23, Volume: 103, Issue:11

    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.
    Journal of clinical pharmacology, 2011, Volume: 51, Issue:12

    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.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2011, Apr-01, Volume: 17, Issue:7

    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.
    Cancer chemotherapy and pharmacology, 2012, Volume: 69, Issue:1

    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.
    Cancer chemotherapy and pharmacology, 2012, Volume: 69, Issue:2

    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.
    BMC cancer, 2011, Jul-26, Volume: 11

    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.
    Investigational new drugs, 2012, Volume: 30, Issue:5

    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.
    Investigational new drugs, 2012, Volume: 30, Issue:5

    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.
    Investigational new drugs, 2012, Volume: 30, Issue:6

    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.
    International journal of clinical pharmacology and therapeutics, 2012, Volume: 50, Issue:1

    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.
    Journal of clinical pharmacology, 2012, Volume: 52, Issue:5

    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.
    European journal of cancer (Oxford, England : 1990), 2012, Volume: 48, Issue:4

    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.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2012, Jun-15, Volume: 18, Issue:12

    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.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2012, Nov-01, Volume: 18, Issue:21

    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.
    Journal of drugs in dermatology : JDD, 2012, Volume: 11, Issue:11

    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.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2013, Jan-01, Volume: 19, Issue:1

    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.
    European journal of cancer (Oxford, England : 1990), 2013, Volume: 49, Issue:5

    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.
    International journal of clinical pharmacology and therapeutics, 2002, Volume: 40, Issue:12

    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.
    International journal of clinical pharmacology and therapeutics, 2003, Volume: 41, Issue:12

    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.
    International journal of clinical pharmacology and therapeutics, 2003, Volume: 41, Issue:12

    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.
    International journal of clinical pharmacology and therapeutics, 2004, Volume: 42, Issue:11

    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.
    British journal of cancer, 2005, May-23, Volume: 92, Issue:10

    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.
    Annals of oncology : official journal of the European Society for Medical Oncology, 2005, Volume: 16, Issue:10

    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.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2005, Aug-01, Volume: 11, Issue:15

    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.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2006, Jan-01, Volume: 12, Issue:1

    Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; D

2006
Mechanisms of hypertension associated with BAY 43-9006.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2006, Mar-20, Volume: 24, Issue:9

    Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Benzenesulfonates; Drug Administration Schedul

2006
Mechanisms of hypertension associated with BAY 43-9006.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2006, Mar-20, Volume: 24, Issue:9

    Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Benzenesulfonates; Drug Administration Schedul

2006
Mechanisms of hypertension associated with BAY 43-9006.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2006, Mar-20, Volume: 24, Issue:9

    Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Benzenesulfonates; Drug Administration Schedul

2006
Mechanisms of hypertension associated with BAY 43-9006.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2006, Mar-20, Volume: 24, Issue:9

    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.
    Cytometry. Part B, Clinical cytometry, 2006, Volume: 70, Issue:3

    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.
    Cytometry. Part B, Clinical cytometry, 2006, Volume: 70, Issue:3

    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.
    Cytometry. Part B, Clinical cytometry, 2006, Volume: 70, Issue:3

    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.
    Cytometry. Part B, Clinical cytometry, 2006, Volume: 70, Issue:3

    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.
    Annals of oncology : official journal of the European Society for Medical Oncology, 2006, Volume: 17, Issue:5

    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.
    European journal of cancer (Oxford, England : 1990), 2007, Volume: 43, Issue:1

    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.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2007, Jun-10, Volume: 25, Issue:17

    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.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2007, Aug-15, Volume: 13, Issue:16

    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.
    Cancer science, 2008, Volume: 99, Issue:7

    Topics: Adult; Aged; Antineoplastic Agents; Benzenesulfonates; Extracellular Signal-Regulated MAP Kinases; F

2008
Human tumor blood flow is enhanced by nicotinamide and carbogen breathing.
    Cancer research, 1997, Dec-01, Volume: 57, Issue:23

    Topics: Administration, Inhalation; Administration, Oral; Carbon Dioxide; Female; Humans; Laser-Doppler Flow

1997

Other Studies

161 other studies available for niacinamide and Neoplasms

ArticleYear
Nicaraven prevents the fast growth of inflamed tumors by an anti-inflammatory mechanism.
    Medical oncology (Northwood, London, England), 2021, Nov-10, Volume: 39, Issue:1

    Topics: Animals; Anti-Inflammatory Agents; Biomarkers, Tumor; Cytokines; Humans; Inflammation; Macrophages;

2021
Gut microbiota severely hampers the efficacy of NAD-lowering therapy in leukemia.
    Cell death & disease, 2022, 04-08, Volume: 13, Issue:4

    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.
    Nature communications, 2022, 06-15, Volume: 13, Issue:1

    Topics: Animals; Liver; Mice; Neoplasms; Niacinamide; Nicotinamide N-Methyltransferase; Nitrogen; Uracil; Ur

2022
Autophagy-inducing nutritional interventions in experimental and clinical oncology.
    International review of cell and molecular biology, 2022, Volume: 373

    Topics: Autophagy; Carcinogenesis; Humans; Medical Oncology; Methionine; Micronutrients; Neoplasms; Niacinam

2022
Fluorescent and theranostic probes for imaging nicotinamide phosphoribosyl transferase (NAMPT).
    European journal of medicinal chemistry, 2023, Feb-15, Volume: 248

    Topics: Cell Proliferation; Cytokines; Humans; Neoplasms; Niacinamide; Nicotinamide Phosphoribosyltransferas

2023
Novel carbon skeletons activate human NicotinAMide Phosphoribosyl Transferase (NAMPT) enzyme in biochemical assay.
    PloS one, 2023, Volume: 18, Issue:3

    Topics: Cytokines; Humans; NAD; Neoplasms; Niacinamide; Nicotinamide Phosphoribosyltransferase; Sirtuins

2023
NAD
    Nature communications, 2023, 04-03, Volume: 14, Issue:1

    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.
    Radiation research, 2023, 10-01, Volume: 200, Issue:4

    Topics: Animals; Antioxidants; Mice; Neoplasms; Niacinamide; Radiation Injuries

2023
Cancer-associated variants of human NQO1: impacts on inhibitor binding and cooperativity.
    Bioscience reports, 2019, 09-30, Volume: 39, Issue:9

    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.
    Annals of nuclear medicine, 2020, Volume: 34, Issue:3

    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.
    Pain, 2020, Volume: 161, Issue:10

    Topics: Animals; Female; Neoplasms; Niacinamide; Paclitaxel; Peripheral Nervous System Diseases; Pyridinium

2020
Disturbed mitochondrial dynamics in CD8
    Nature immunology, 2020, Volume: 21, Issue:12

    Topics: Biomarkers; CD8-Positive T-Lymphocytes; Epigenesis, Genetic; Epigenomics; Humans; Lymphocyte Count;

2020
Novel
    Molecular pharmaceutics, 2021, 03-01, Volume: 18, Issue:3

    Topics: Alzheimer Disease; Animals; Bipolar Disorder; Blood-Brain Barrier; Brain; Cell Line, Tumor; Diabetes

2021
The Biochemical Pathways of Nicotinamide-Derived Pyridones.
    International journal of molecular sciences, 2021, Jan-24, Volume: 22, Issue:3

    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.
    International journal of molecular sciences, 2021, Jan-30, Volume: 22, Issue:3

    Topics: Animals; Antineoplastic Agents, Alkylating; Apoptosis; Cyclophosphamide; Disease Models, Animal; DNA

2021
Rational drug design of indazole-based diarylurea derivatives as anticancer agents.
    Chemical biology & drug design, 2017, Volume: 90, Issue:4

    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.
    PloS one, 2017, Volume: 12, Issue:8

    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.
    Cancer research, 2017, 10-15, Volume: 77, Issue:20

    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.
    Anticancer research, 2017, Volume: 37, Issue:12

    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.
    Molecular medicine reports, 2018, Volume: 17, Issue:6

    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.
    Anticancer research, 2018, Volume: 38, Issue:9

    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.
    Nature chemical biology, 2013, Volume: 9, Issue:5

    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.
    Nuclear medicine and biology, 2013, Volume: 40, Issue:4

    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.
    The oncologist, 2013, Volume: 18, Issue:8

    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.
    Nature, 2013, Sep-12, Volume: 501, Issue:7466

    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.
    Bioconjugate chemistry, 2013, Sep-18, Volume: 24, Issue:9

    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.
    PloS one, 2013, Volume: 8, Issue:9

    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.
    Biomaterials, 2014, Volume: 35, Issue:4

    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.
    Therapeutic drug monitoring, 2014, Volume: 36, Issue:3

    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.
    International journal of oncology, 2014, Volume: 44, Issue:3

    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.
    Nanoscale, 2014, Mar-21, Volume: 6, Issue:6

    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.
    British journal of pharmacology, 2014, Volume: 171, Issue:13

    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.
    Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer, 2014, Volume: 22, Issue:9

    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.
    Aging cell, 2014, Volume: 13, Issue:2

    Topics: Animals; Antioxidants; Cell Line, Tumor; Cell Proliferation; Cell Respiration; Cellular Senescence;

2014
VEGF pathway inhibitors-induced hypertension: next step in therapy.
    Journal of clinical hypertension (Greenwich, Conn.), 2014, Volume: 16, Issue:8

    Topics: Antineoplastic Agents; Humans; Hypertension; Neoplasms; Niacinamide; Phenylurea Compounds

2014
Blocking lipid synthesis overcomes tumor regrowth and metastasis after antiangiogenic therapy withdrawal.
    Cell metabolism, 2014, Aug-05, Volume: 20, Issue:2

    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.
    Medical physics, 2014, Volume: 41, Issue:9

    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.
    Statistics in medicine, 2014, Dec-30, Volume: 33, Issue:30

    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.
    Anticancer research, 2014, Volume: 34, Issue:11

    Topics: Apoptosis; Biomarkers, Tumor; Blotting, Western; Cell Proliferation; Humans; L-Lactate Dehydrogenase

2014
Biological evaluation of a novel sorafenib analogue, t-CUPM.
    Cancer chemotherapy and pharmacology, 2015, Volume: 75, Issue:1

    Topics: Administration, Oral; Animals; Animals, Outbred Strains; Antineoplastic Agents; Apoptosis; Biologica

2015
Multifunctional porous silicon nanoparticles for cancer theranostics.
    Biomaterials, 2015, Volume: 48

    Topics: Angiogenesis Inhibitors; Animals; Cell Line, Tumor; Humans; Male; Mice, Nude; Nanoparticles; Neoplas

2015
Nexavar/Stivarga and viagra interact to kill tumor cells.
    Journal of cellular physiology, 2015, Volume: 230, Issue:9

    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.
    PloS one, 2015, Volume: 10, Issue:3

    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.
    Journal of cellular physiology, 2015, Volume: 230, Issue:10

    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.
    Oncotarget, 2015, Sep-08, Volume: 6, Issue:26

    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.
    PloS one, 2015, Volume: 10, Issue:6

    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.
    International journal of cancer, 2016, Feb-15, Volume: 138, Issue:4

    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.
    Oncotarget, 2015, Sep-29, Volume: 6, Issue:29

    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.
    Journal of immunology (Baltimore, Md. : 1950), 2015, Oct-01, Volume: 195, Issue:7

    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.
    BMJ open, 2016, Jan-27, Volume: 6, Issue:1

    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.
    International journal of dermatology, 2016, Volume: 55, Issue:4

    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.
    International journal of pharmaceutics, 2016, Apr-30, Volume: 503, Issue:1-2

    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.
    PloS one, 2016, Volume: 11, Issue:4

    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.
    Oncotarget, 2016, 06-28, Volume: 7, Issue:26

    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.
    Clinical pharmacology in drug development, 2015, Volume: 4, Issue:6

    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.
    Hypertension research : official journal of the Japanese Society of Hypertension, 2017, Volume: 40, Issue:8

    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.
    Journal of medicinal chemistry, 2017, 04-13, Volume: 60, Issue:7

    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.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2008, Aug-01, Volume: 26, Issue:22

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic C

2008
Vorinostat and sorafenib synergistically kill tumor cells via FLIP suppression and CD95 activation.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2008, Sep-01, Volume: 14, Issue:17

    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?
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2008, Nov-10, Volume: 26, Issue:32

    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.
    Cancer science, 2009, Volume: 100, Issue:1

    Topics: Animals; Benzamides; Benzenesulfonates; Cell Line, Tumor; Extravasation of Diagnostic and Therapeuti

2009
Cutaneous drug eruptions induced by sorafenib: a case series.
    Journal of drugs in dermatology : JDD, 2008, Volume: 7, Issue:9

    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.
    Molecular cancer therapeutics, 2009, Volume: 8, Issue:2

    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.
    Journal of pharmaceutical and biomedical analysis, 2009, May-01, Volume: 49, Issue:4

    Topics: Aged; Angiogenesis Inhibitors; Antineoplastic Agents; Benzenesulfonates; Calibration; Chromatography

2009
Selecting promising treatments in randomized Phase II cancer trials with an active control.
    Journal of biopharmaceutical statistics, 2009, Volume: 19, Issue:3

    Topics: Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Clinical Trials, Phase II as Topi

2009
VEGF inhibition and metastasis: possible implications for antiangiogenic therapy.
    Cancer biology & therapy, 2009, Volume: 8, Issue:13

    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.
    Journal of chromatography. B, Analytical technologies in the biomedical and life sciences, 2009, Jul-15, Volume: 877, Issue:22

    Topics: Antineoplastic Agents; Benzamides; Benzenesulfonates; Chromatography, Liquid; Dasatinib; Drug Monito

2009
How well do angiogenesis inhibitors work? Biomarkers of response prove elusive.
    Journal of the National Cancer Institute, 2009, Jun-16, Volume: 101, Issue:12

    Topics: Angiogenesis Inhibitors; Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzene

2009
Multiple Histology Phase II Trials.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2009, Jul-01, Volume: 15, Issue:13

    Topics: Antineoplastic Agents; Benzenesulfonates; Clinical Trials, Phase II as Topic; Computer Simulation; H

2009
Array of cutaneous adverse effects associated with sorafenib.
    Journal of the American Academy of Dermatology, 2009, Volume: 61, Issue:2

    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.
    Cancer letters, 2010, Feb-01, Volume: 288, Issue:1

    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.
    Laboratory investigation; a journal of technical methods and pathology, 2009, Volume: 89, Issue:9

    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.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2009, Oct-01, Volume: 15, Issue:19

    Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Benzenesulfonates; Blood Pressure; Blood Pres

2009
Rapid development of hypertension by sorafenib: toxicity or target?
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2009, Oct-01, Volume: 15, Issue:19

    Topics: Angiogenesis Inhibitors; Animals; Benzenesulfonates; Blood Pressure; Drug Delivery Systems; Drug Dos

2009
Tyrosine kinase inhibitor-induced macrocytosis.
    Anticancer research, 2009, Volume: 29, Issue:12

    Topics: Anemia, Macrocytic; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Benzenesulfonates; E

2009
Risk of bleeding not increased by sorafenib or sunitinib.
    The Lancet. Oncology, 2010, Volume: 11, Issue:2

    Topics: Antineoplastic Agents; Benzenesulfonates; Hemorrhage; Humans; Indoles; Neoplasms; Niacinamide; Pheny

2010
[Correction of metabolic disturbances in cancer patients in the early postanesthesia period].
    Khirurgiia, 2010, Issue:4

    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.
    Investigational new drugs, 2011, Volume: 29, Issue:5

    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.
    International journal of oncology, 2010, Volume: 37, Issue:2

    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.
    Journal of experimental & clinical cancer research : CR, 2010, Jul-14, Volume: 29

    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.
    Pediatric blood & cancer, 2010, Dec-01, Volume: 55, Issue:6

    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.
    Journal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners, 2011, Volume: 17, Issue:3

    Topics: Aged; Antineoplastic Agents; Benzamides; Benzenesulfonates; Blood Glucose; Dasatinib; Diabetes Melli

2011
Spiny follicular hyperkeratosis eruption: a new cutaneous adverse effect of sorafenib.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2010, Nov-01, Volume: 28, Issue:31

    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.
    Acta crystallographica. Section C, Crystal structure communications, 2011, Volume: 67, Issue:Pt 1

    Topics: Antineoplastic Agents; Benzenesulfonates; Crystallography, X-Ray; Enzyme Inhibitors; Humans; Hydroge

2011
An approach to meta-analysis of dose-finding studies.
    Statistics in medicine, 2011, Jul-30, Volume: 30, Issue:17

    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.
    Archiv der Pharmazie, 2011, Volume: 344, Issue:6

    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.
    Molecular cancer therapeutics, 2011, Volume: 10, Issue:7

    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.
    Cancer research, 2011, Jul-15, Volume: 71, Issue:14

    Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Autophagy; Benzenesulfonates; Cell Line, Tu

2011
99mTc-HYNIC-spermine for imaging polyamine transport system-positive tumours: preclinical evaluation.
    European journal of nuclear medicine and molecular imaging, 2011, Volume: 38, Issue:10

    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.
    Pharmaceutical research, 2011, Volume: 28, Issue:12

    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.
    Journal of microencapsulation, 2011, Volume: 28, Issue:6

    Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Cattle; Cell Line, Tumor; Drug Carriers; Female;

2011
[Antioxidant protection as a component of anesthetic management cancer patients].
    Khirurgiia, 2011, Issue:6

    Topics: Adaptation, Physiological; Aged; Anesthetics, Combined; Antioxidants; Balanced Anesthesia; Drug Comb

2011
[Adverse effects of new oncologic therapies].
    Praxis, 2011, Jul-27, Volume: 100, Issue:15

    Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Antineoplastic Com

2011
Sorafenib enhances pemetrexed cytotoxicity through an autophagy-dependent mechanism in cancer cells.
    Autophagy, 2011, Volume: 7, Issue:10

    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.
    European journal of medicinal chemistry, 2011, Volume: 46, Issue:12

    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.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2012, Jan-01, Volume: 18, Issue:1

    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.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2012, Apr-01, Volume: 18, Issue:7

    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.
    Annals of oncology : official journal of the European Society for Medical Oncology, 2012, Volume: 23, Issue:4

    Topics: Antineoplastic Agents; Camellia sinensis; Drug Therapy, Combination; ErbB Receptors; Humans; Neoplas

2012
RAIN-Droplet: a novel 3D in vitro angiogenesis model.
    Laboratory investigation; a journal of technical methods and pathology, 2012, Volume: 92, Issue:7

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal, Humanized; Benzenesulfonates; Bevacizumab; Cells, C

2012
Variability of sorafenib toxicity and exposure over time: a pharmacokinetic/pharmacodynamic analysis.
    The oncologist, 2012, Volume: 17, Issue:9

    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.
    PloS one, 2012, Volume: 7, Issue:8

    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.
    Acta pharmacologica Sinica, 2012, Volume: 33, Issue:10

    Topics: Antineoplastic Agents; Blotting, Western; Cell Culture Techniques; Cell Line, Tumor; Cell Proliferat

2012
No end in sight for telomerase-targeted cancer drugs.
    Nature medicine, 2013, Volume: 19, Issue:1

    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.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2013, Mar-15, Volume: 19, Issue:6

    Topics: Animals; Antineoplastic Agents; Glucuronic Acid; HEK293 Cells; Humans; Liver-Specific Organic Anion

2013
Taking cancer-drug toxicity to heart.
    Cancer discovery, 2013, Volume: 3, Issue:2

    Topics: Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Bevacizumab; Doxorubicin; Heart Failure; H

2013
Nicotinamide-containing sunscreens for use in Australasian countries and cancer-provoking conditions.
    Medical hypotheses, 2003, Volume: 60, Issue:4

    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.
    Cancer research, 1952, Volume: 12, Issue:12

    Topics: Epidermis; Neoplasms; Niacin; Niacinamide; Nicotinic Acids

1952
Significance of enzymatically catalyzed exchange reactions in chemotherapy.
    Science (New York, N.Y.), 1954, Sep-17, Volume: 120, Issue:3116

    Topics: Animals; Coenzymes; Liver; Mice; Neoplasms; Niacin; Niacinamide; Nicotinic Acids; Pyridines; Tryptop

1954
[Methylated nicotinamide in the liver in neoplasms in rats].
    Voprosy onkologii, 1955, Volume: 1, Issue:6

    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.
    British journal of cancer, 1961, Volume: 15

    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].
    Bollettino della Societa italiana di biologia sperimentale, 1960, Dec-31, Volume: 36

    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].
    Biochemische Zeitschrift, 1960, Volume: 333

    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.
    Nature, 1961, Feb-25, Volume: 189

    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.
    Nature, 1961, Dec-09, Volume: 192

    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].
    Biochimica et biophysica acta, 1961, Aug-19, Volume: 51

    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.
    The Journal of biological chemistry, 1963, Volume: 238

    Topics: Ascites; In Vitro Techniques; NAD; Neoplasms; Neoplasms, Experimental; Niacin; Niacinamide; Nicotini

1963
6-AMINONICOTINAMIDE AND THE RADIOSENSITIVITY OF HUMAN LIVER CELLS IN CULTURE.
    Nature, 1963, Dec-21, Volume: 200

    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.
    Nature, 1964, Mar-14, Volume: 201

    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].
    Zeitschrift fur Krebsforschung, 1964, May-08, Volume: 66

    Topics: Animals; Carbohydrate Metabolism; Carcinoma, Ehrlich Tumor; DNA; DNA, Neoplasm; NAD; Neoplasm Protei

1964
THE EFFECT OF CIGARETTE SMOKING ON BLADDER CARCINOGENS IN MAN.
    Canadian Medical Association journal, 1965, Jul-03, Volume: 93

    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].
    International journal of radiation biology and related studies in physics, chemistry, and medicine, 1965, Volume: 9

    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.
    Life sciences (1962), 1965, Volume: 4

    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.
    Biochemical pharmacology, 1961, Volume: 8

    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.
    International journal of radiation oncology, biology, physics, 2004, Nov-01, Volume: 60, Issue:3

    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.
    Cancer research, 2004, Oct-01, Volume: 64, Issue:19

    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.
    Cancer research, 2004, Oct-01, Volume: 64, Issue:19

    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.
    Cancer research, 2004, Oct-01, Volume: 64, Issue:19

    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.
    Cancer research, 2004, Oct-01, Volume: 64, Issue:19

    Topics: Administration, Oral; Animals; Benzenesulfonates; Cell Line, Tumor; Disease Progression; Female; Hum

2004
In vivo modulation of signaling factors involved in cell survival.
    Journal of radiation research, 2004, Volume: 45, Issue:4

    Topics: Animals; Blotting, Western; Cell Line, Tumor; Cell Survival; Curcumin; Cytosol; Extracellular Signal

2004
Cancer. Encouraging results for second-generation antiangiogenesis drugs.
    Science (New York, N.Y.), 2005, May-27, Volume: 308, Issue:5726

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzenesulfonate

2005
Clinical trials referral resource. Current clinical trials of BAY 43-9006, Part 1.
    Oncology (Williston Park, N.Y.), 2005, Volume: 19, Issue:4

    Topics: Angiogenesis Inhibitors; Benzenesulfonates; Clinical Trials as Topic; Humans; Neoplasms; Niacinamide

2005
Clinical trials referral resource.
    Oncology (Williston Park, N.Y.), 2005, Volume: 19, Issue:6

    Topics: Antineoplastic Agents; Benzenesulfonates; Clinical Trials as Topic; Humans; Neoplasms; Niacinamide;

2005
Drug approval triggers debate on future direction for cancer treatments.
    Nature reviews. Drug discovery, 2006, Volume: 5, Issue:2

    Topics: Antineoplastic Agents; Benzenesulfonates; Drug Approval; Drug Design; Enzyme Inhibitors; Neoplasms;

2006
Pharmacy benefit spending on oral chemotherapy drugs.
    Journal of managed care pharmacy : JMCP, 2006, Volume: 12, Issue:7

    Topics: Administration, Oral; Ambulatory Care; Antineoplastic Agents; Benzamides; Benzenesulfonates; Capecit

2006
Speeding up cancer-drug development.
    The Lancet. Oncology, 2006, Volume: 7, Issue:10

    Topics: Benzenesulfonates; Carcinoma, Hepatocellular; Carcinoma, Renal Cell; Clinical Trials, Phase II as To

2006
A tale of two drugs.
    Nature reviews. Drug discovery, 2006, Volume: 5, Issue:10

    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.
    The Journal of pharmacology and experimental therapeutics, 2007, Volume: 323, Issue:1

    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.
    IDrugs : the investigational drugs journal, 2007, Volume: 10, Issue:8

    Topics: Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Benzenesu

2007
ASCO 2007: plenary top 5.
    Oncology (Williston Park, N.Y.), 2007, Volume: 21, Issue:7

    Topics: Antineoplastic Agents; Benzenesulfonates; Carcinoma, Hepatocellular; Carcinoma, Renal Cell; Carcinom

2007
Examining heterogeneity in phase II trial designs may improve success in phase III.
    Journal of the National Cancer Institute, 2008, Feb-06, Volume: 100, Issue:3

    Topics: Antineoplastic Agents; Benzenesulfonates; Clinical Trials, Phase II as Topic; Clinical Trials, Phase

2008
Quantifying hypertension in patients with cancer treated with sorafenib.
    The Lancet. Oncology, 2008, Volume: 9, Issue:2

    Topics: Antineoplastic Agents; Benzenesulfonates; Humans; Hypertension; Neoplasms; Niacinamide; Phenylurea C

2008
Carbogen breathing with nicotinamide improves the oxygen status of tumours in patients.
    British journal of cancer, 1995, Volume: 72, Issue:1

    Topics: Adult; Aged; Aged, 80 and over; Carbon Dioxide; Female; Humans; Male; Middle Aged; Neoplasms; Niacin

1995
ARCON.
    Clinical oncology (Royal College of Radiologists (Great Britain)), 1994, Volume: 6, Issue:5

    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.
    British journal of cancer, 1993, Volume: 67, Issue:1

    Topics: Animals; Cardiac Output; Colonic Neoplasms; Male; Mammary Neoplasms, Experimental; Metoclopramide; M

1993
Nicotinamide pharmacokinetics in patients.
    Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 1995, Volume: 36, Issue:3

    Topics: Administration, Oral; Combined Modality Therapy; Humans; Hyperthermia, Induced; Neoplasms; Niacinami

1995
Nicotinamide pharmacokinetics in normal volunteers and patients undergoing palliative radiotherapy.
    Acta oncologica (Stockholm, Sweden), 1996, Volume: 35, Issue:2

    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.
    The British journal of cancer. Supplement, 1996, Volume: 27

    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.
    Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al], 1996, Volume: 172 Suppl 2

    Topics: Animals; Carbon Dioxide; Cell Hypoxia; Cells, Cultured; Humans; Mice; Neoplasms; Neoplasms, Experime

1996
ARCON.
    Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al], 1996, Volume: 172 Suppl 2

    Topics: Animals; Carbon Dioxide; Cell Hypoxia; Humans; Mice; Neoplasms; Neoplasms, Experimental; Niacinamide

1996
Comments on hyperbaric oxygen and carbogen/nicotinamide with fractionated radiation.
    Radiation research, 1997, Volume: 148, Issue:5

    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.
    Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 1997, Volume: 45, Issue:2

    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.
    Teratogenesis, carcinogenesis, and mutagenesis, 2001, Volume: 21, Issue:2

    Topics: Acetaldehyde; Alcohol Drinking; Allopurinol; Animals; Antimetabolites; Caffeine; Carcinogens; Chroma

2001
Negative control of p53 by Sir2alpha promotes cell survival under stress.
    Cell, 2001, Oct-19, Volume: 107, Issue:2

    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.
    Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 2002, Volume: 62, Issue:1

    Topics: Administration, Inhalation; Administration, Oral; Adult; Aged; Carbon Dioxide; Female; Humans; Laser

2002
ARCON: accelerated radiotherapy with carbogen and nicotinamide.
    BJR supplement, 1992, Volume: 24

    Topics: Carbon Dioxide; Cell Hypoxia; Humans; Neoplasms; Niacinamide; Oxygen Consumption; Radiation Toleranc

1992
Carbogen and nicotinamide: expectations too high? (response to J. Martin Brown)
    Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 1992, Volume: 24, Issue:2

    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.
    Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 1992, Volume: 24, Issue:2

    Topics: Animals; Carbon Dioxide; Humans; Mice; Neoplasms; Neoplasms, Experimental; Niacinamide; Oxygen; Radi

1992
Carbogen and nicotinamide: expectations too high?
    Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 1992, Volume: 24, Issue:2

    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.
    Journal of medicinal chemistry, 1987, Volume: 30, Issue:5

    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.
    Mutation research, 1985, Volume: 143, Issue:4

    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].
    Vrachebnoe delo, 1968, Volume: 7

    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.
    Indian journal of biochemistry, 1971, Volume: 8, Issue:2

    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.
    European journal of cancer, 1973, Volume: 9, Issue:7

    Topics: Aged; Humans; Hydroxyindoleacetic Acid; Middle Aged; Neoplasms; Niacinamide; Tryptophan

1973
From protozoa to bacteria and viruses. Fifty years with microbes (André Lwoff).
    Annual review of microbiology, 1971, Volume: 25

    Topics: Bibliographies as Topic; Ciliophora; Crustacea; Eukaryota; Eye; Fever; France; Growth Substances; He

1971