PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22321409-5 2012 The retention behavior indicated that sorafenib had two major binding regions on VEGFR-2, and that taspine might act as a multi-target VEGFR-2 inhibitor with similar biological activity to sorafenib. Sorafenib 38-47 kinase insert domain receptor Homo sapiens 81-88 25806151-3 2012 Thus, this system has become the focus of therapeutic interventions, which led to the approval of the anti-VEGF blocking antibody bevacizumab and the VEGFR-2 pathway inhibitors pazopanib, sorafenib and sunitinib. Sorafenib 188-197 kinase insert domain receptor Homo sapiens 150-157 21979753-8 2012 Taken together, our data suggest that sorafenib exerts its cytotoxic effect likely via inhibition of the VEGFR and RAF/MEK/ERK pathways, both of which can modulate Mcl-1 expression in CLL cells. Sorafenib 38-47 kinase insert domain receptor Homo sapiens 105-110 20803052-1 2012 BACKGROUND: Sorafenib, an inhibitor of B-raf, VEGFR2, and PDGFR-beta, has activity against pancreatic cancer in preclinical models. Sorafenib 12-21 kinase insert domain receptor Homo sapiens 46-52 24451769-4 2012 Further, vascular endothelial growth factor receptor (VEGF-R) inhibitory agents including sorafenib, sunitinib, pazopanib, and axitinib that are already approved in the United States for use in advanced renal cell carcinoma have shown high response rates in treating advanced DTCs in multiple phase II trials, and have become commonly used in progressive radioiodine-refractory metastatic DTC. Sorafenib 90-99 kinase insert domain receptor Homo sapiens 9-52 24451769-4 2012 Further, vascular endothelial growth factor receptor (VEGF-R) inhibitory agents including sorafenib, sunitinib, pazopanib, and axitinib that are already approved in the United States for use in advanced renal cell carcinoma have shown high response rates in treating advanced DTCs in multiple phase II trials, and have become commonly used in progressive radioiodine-refractory metastatic DTC. Sorafenib 90-99 kinase insert domain receptor Homo sapiens 54-60 22212284-1 2012 OBJECTIVE: To assess both clinical and biological efficacy and toxicity of sorafenib in patients with metastatic renal cell carcinoma (mRCC) previously treated with an anti-angiogenic vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor. Sorafenib 75-84 kinase insert domain receptor Homo sapiens 184-227 22212284-1 2012 OBJECTIVE: To assess both clinical and biological efficacy and toxicity of sorafenib in patients with metastatic renal cell carcinoma (mRCC) previously treated with an anti-angiogenic vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor. Sorafenib 75-84 kinase insert domain receptor Homo sapiens 229-234 22212284-17 2012 CONCLUSIONS: Sorafenib at doses of 400-600 mg twice a day continuously results in acceptable and well tolerated salvage treatment after VEGFR tyrosine kinase inhibitor failure. Sorafenib 13-22 kinase insert domain receptor Homo sapiens 136-141 22214462-2 2012 Sorafenib (Nexavar), a novel bi-aryl urea BAY 43-9006, is an orally administered multikinase inhibitor with activity against RAS/RAF kinases multikinase inhibitor with activity against RAF kinases and several receptor tyrosine kinases, including vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR), FLT3, Ret, and c-Kit. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 246-289 22214462-2 2012 Sorafenib (Nexavar), a novel bi-aryl urea BAY 43-9006, is an orally administered multikinase inhibitor with activity against RAS/RAF kinases multikinase inhibitor with activity against RAF kinases and several receptor tyrosine kinases, including vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR), FLT3, Ret, and c-Kit. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 291-296 22214462-2 2012 Sorafenib (Nexavar), a novel bi-aryl urea BAY 43-9006, is an orally administered multikinase inhibitor with activity against RAS/RAF kinases multikinase inhibitor with activity against RAF kinases and several receptor tyrosine kinases, including vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR), FLT3, Ret, and c-Kit. Sorafenib 11-18 kinase insert domain receptor Homo sapiens 246-289 22214462-2 2012 Sorafenib (Nexavar), a novel bi-aryl urea BAY 43-9006, is an orally administered multikinase inhibitor with activity against RAS/RAF kinases multikinase inhibitor with activity against RAF kinases and several receptor tyrosine kinases, including vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR), FLT3, Ret, and c-Kit. Sorafenib 11-18 kinase insert domain receptor Homo sapiens 291-296 21447721-2 2011 Sorafenib and sunitinib are small molecule inhibitors of multiple kinases including VEGF receptor (VEGFR) kinases. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 84-97 20552299-2 2011 Sorafenib is an orally administered multikinase inhibitor that blocks intracellular kinases in the Raf/MEK/ERK pathway involved in tumor proliferation, and also kinases responsible for angiogenesis, including VEGFr-2, VEGFr-3, Flt-3, PDGFr-beta and c-KIT. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 209-216 22846973-1 2012 BACKGROUND: With sorafenib displaying the highest affinities for Flt3, VEGFR (vascular endothelial growth factor receptor) and Raf and dasatinib for Abl and Src kinases, the profiles of kinases targeted by these inhibitors differ strongly. Sorafenib 17-26 kinase insert domain receptor Homo sapiens 71-76 22846973-1 2012 BACKGROUND: With sorafenib displaying the highest affinities for Flt3, VEGFR (vascular endothelial growth factor receptor) and Raf and dasatinib for Abl and Src kinases, the profiles of kinases targeted by these inhibitors differ strongly. Sorafenib 17-26 kinase insert domain receptor Homo sapiens 78-121 21529991-2 2011 Therefore, research effort has focused on target-specific agents, such as sorafenib, which blocks both the RAF/MEK/ERK signalling pathways and receptors involved in neovascularization and tumor progression, including VEGFR-2 and c-Kit. Sorafenib 74-83 kinase insert domain receptor Homo sapiens 217-224 21392074-1 2011 WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: Sorafenib is a multikinase inhibitor with activity against B-raf, C-raf, VEGFR2, PDGFRbeta and FGFR1. Sorafenib 42-51 kinase insert domain receptor Homo sapiens 115-121 21212155-1 2011 BACKGROUND: Sorafenib is a small-molecule multitargeted kinase inhibitor that blocks the activation of C-RAF, B-RAF, c-KIT, FLT-3, RET, vascular endothelial growth factor receptor 2 (VEGFR-2), VEGFR-3 and platelet-derived growth factor receptor beta. Sorafenib 12-21 kinase insert domain receptor Homo sapiens 136-181 21212155-1 2011 BACKGROUND: Sorafenib is a small-molecule multitargeted kinase inhibitor that blocks the activation of C-RAF, B-RAF, c-KIT, FLT-3, RET, vascular endothelial growth factor receptor 2 (VEGFR-2), VEGFR-3 and platelet-derived growth factor receptor beta. Sorafenib 12-21 kinase insert domain receptor Homo sapiens 183-190 21486218-7 2011 Inhibition of VEGFR has emerged as a potential therapy method for cancers and it has been clinically validated with FDA-approvals of bevacizumab, sorafenib, and suntinib. Sorafenib 146-155 kinase insert domain receptor Homo sapiens 14-19 21427706-3 2011 We hypothesized that JX-594 and sorafenib, a small molecule inhibitor of B-raf and vascular endothelial growth factor receptor (VEGFR) approved for HCC, would have clinical benefit in combination given their demonstrated efficacy in HCC patients and their complementary mechanisms-of-action. Sorafenib 32-41 kinase insert domain receptor Homo sapiens 83-126 21427706-3 2011 We hypothesized that JX-594 and sorafenib, a small molecule inhibitor of B-raf and vascular endothelial growth factor receptor (VEGFR) approved for HCC, would have clinical benefit in combination given their demonstrated efficacy in HCC patients and their complementary mechanisms-of-action. Sorafenib 32-41 kinase insert domain receptor Homo sapiens 128-133 21447721-2 2011 Sorafenib and sunitinib are small molecule inhibitors of multiple kinases including VEGF receptor (VEGFR) kinases. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 99-104 21407223-7 2011 Sorafenib-induced growth suppression was associated with not only inhibition of angiogenic targets p-PDGFR-beta, p-VEGFR-2, and their downstream signalling pathways p-Akt and p-ERK, cell cycle, and anti-apoptotic proteins that include cyclin D1, cyclin B1, and survivin but also upregulation of proapoptotic Bim. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 115-122 21224376-1 2011 PURPOSE: Sorafenib, a multikinase inhibitor targeting Raf and VEGFR, has shown activity in unselected patients with non-small-cell lung cancer (NSCLC). Sorafenib 9-18 kinase insert domain receptor Homo sapiens 62-67 22130231-14 2011 VEGFR tyrosine kinase inhibitors such as sunitinib and sorafenib are also effective in antiangiogenic tumor therapy by inhibiting VEGFR signaling. Sorafenib 55-64 kinase insert domain receptor Homo sapiens 0-5 22130231-14 2011 VEGFR tyrosine kinase inhibitors such as sunitinib and sorafenib are also effective in antiangiogenic tumor therapy by inhibiting VEGFR signaling. Sorafenib 55-64 kinase insert domain receptor Homo sapiens 130-135 20443129-1 2011 Sorafenib, an oral VEGFR-2, Raf, PDGFR, c-KIT and Flt-3 inhibitor, is active against renal cell and hepatocellular carcinomas, and has recently demonstrated promising activity for lung and breast cancers. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 19-26 21098323-1 2011 PURPOSE Sorafenib is a kinase inhibitor targeting Raf and other kinases (ie, vascular endothelial growth factor receptor [VEGFR], platelet-derived growth factor receptor [PDGFR], Flt3, and c-KIT). Sorafenib 8-17 kinase insert domain receptor Homo sapiens 77-120 21098323-1 2011 PURPOSE Sorafenib is a kinase inhibitor targeting Raf and other kinases (ie, vascular endothelial growth factor receptor [VEGFR], platelet-derived growth factor receptor [PDGFR], Flt3, and c-KIT). Sorafenib 8-17 kinase insert domain receptor Homo sapiens 122-127 20736856-2 2010 Sorafenib is a potent inhibitor of the ras/raf/MEK pathway and also targets VEGFR and cKIT. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 76-81 21220499-2 2011 Sorafenib, a VEGFR inhibitor with activity against RAF kinase, is active against hepatocellular carcinoma (HCC); however, the possible involvement of sorafenib in the EMT remains unclear. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 13-18 22212931-4 2011 Molecular therapies such as sorafenib, a BRAF/ VEGFR/PDGFR tyrosine kinase inhibitor, have shown to improve survival in patients with advanced HCC. Sorafenib 28-37 kinase insert domain receptor Homo sapiens 47-52 22174910-0 2011 Antitumor activity of sorafenib in human cancer cell lines with acquired resistance to EGFR and VEGFR tyrosine kinase inhibitors. Sorafenib 22-31 kinase insert domain receptor Homo sapiens 96-101 22174910-4 2011 Considering the role of RAS and RAF as downstream signals of both the EGFR and VEGFR pathways, we treated resistant cells with sorafenib, an inhibitor of C-RAF, B-RAF, c-KIT, FLT-3, RET, VEGFR-2, VEGFR-3, and PDGFR-beta. Sorafenib 127-136 kinase insert domain receptor Homo sapiens 79-84 22174910-4 2011 Considering the role of RAS and RAF as downstream signals of both the EGFR and VEGFR pathways, we treated resistant cells with sorafenib, an inhibitor of C-RAF, B-RAF, c-KIT, FLT-3, RET, VEGFR-2, VEGFR-3, and PDGFR-beta. Sorafenib 127-136 kinase insert domain receptor Homo sapiens 187-194 21045832-1 2010 BACKGROUND: The combination of sorafenib (vascular endothelial growth factor receptor 2 inhibitor) and sirolimus (mammalian target of rapamycin inhibitor) might work synergistically. Sorafenib 31-40 kinase insert domain receptor Homo sapiens 42-87 20698202-10 2010 Sorafenib, a multikinase inhibitor, which can competitively inhibit RAF/MEK/ERK pathway, human vascular endothelial growth factor receptors (VEGFR2, VEGFR3) platelet-derived growth factor receptor beta (PDGFR), Flt3, and C-kit receptors, has been successfully applied for solid tumors such as renal cancer and hepatocellular carcinoma. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 141-147 19890601-4 2010 The sole systemic therapy that has shown efficacy in improving the survival of HCC patients is sorafenib, an oral kinase inhibitor that blocks the Raf/MEK/ERK pathway and the receptor for VEGFR 2 and PDGFR-beta. Sorafenib 95-104 kinase insert domain receptor Homo sapiens 188-195 20368568-2 2010 Sorafenib, a multikinase inhibitor targeting Ret and VEGFR, showed antitumor activity in preclinical studies of MTC. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 53-58 20204367-1 2010 PURPOSE: Sorafenib is a novel oral anticancer agent targeting signal transduction and angiogenic pathways through inhibitory effects against MAP kinases and vascular endothelial growth factor receptor-2. Sorafenib 9-18 kinase insert domain receptor Homo sapiens 157-202 20351323-1 2010 PURPOSE: Sunitinib and sorafenib are oral vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs) used in a vast range of cancers. Sorafenib 23-32 kinase insert domain receptor Homo sapiens 42-85 20351323-1 2010 PURPOSE: Sunitinib and sorafenib are oral vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs) used in a vast range of cancers. Sorafenib 23-32 kinase insert domain receptor Homo sapiens 87-92 20351323-11 2010 CONCLUSION: Treatment with VEGFR TKIs sunitinib and sorafenib is associated with a significant increase in the risk of ATEs. Sorafenib 52-61 kinase insert domain receptor Homo sapiens 27-32 20630084-0 2010 Hypertension and hand-foot skin reactions related to VEGFR2 genotype and improved clinical outcome following bevacizumab and sorafenib. Sorafenib 125-134 kinase insert domain receptor Homo sapiens 53-59 20658715-5 2010 On the other hand, sorafenib not only inhibits VEGF receptor (VEGFR) but is also a B-Raf inhibitor (a component of the ras - MAPK pathway) and this leads to downregulation of immune responses. Sorafenib 19-28 kinase insert domain receptor Homo sapiens 47-60 20658715-5 2010 On the other hand, sorafenib not only inhibits VEGF receptor (VEGFR) but is also a B-Raf inhibitor (a component of the ras - MAPK pathway) and this leads to downregulation of immune responses. Sorafenib 19-28 kinase insert domain receptor Homo sapiens 62-67 19652055-1 2009 PURPOSE: Sorafenib is an oral multikinase inhibitor that targets the Ras/Raf/MEK/ERK mitogenic signaling pathway and the angiogenic receptor tyrosine kinases, vascular endothelial growth factor receptor 2 and platelet-derived growth factor receptor beta. Sorafenib 9-18 kinase insert domain receptor Homo sapiens 159-253 20149262-15 2010 Therefore, Sorafenib-mediated blockade of the Raf/MAPK and VEGFR pathways might enhance the efficacy of radiation, when Sorafenib is followed sequentially as a maintenance modality. Sorafenib 11-20 kinase insert domain receptor Homo sapiens 59-64 20103668-4 2010 It is likely that the multikinase inhibitors, sorafenib, sunitinib, axitinib, and motesanib, whose targets include VEGFR-2, exert their effects primarily through inhibition of endothelial cells. Sorafenib 46-55 kinase insert domain receptor Homo sapiens 115-122 20721275-2 2010 These include the immunotherapeutics, alfa-interferon, and interleukin-2, and agents that target the vascular endothelial growth factor receptor (VEGFR) via its tyrosine kinase, such as sorafenib, sunitinib, and pazopanib, or the mammalian target of rapamycin (mTOR), such as temsirolimus and everolimus. Sorafenib 186-195 kinase insert domain receptor Homo sapiens 146-151 20714148-5 2010 Sorafenib reduced c-Kit, ERK and VEGFR2 activation and on the other hand, gemcitabine inhibited Akt phosphorylation. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 33-39 20215359-3 2010 These include the vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors sunitinib and sorafenib, which inhibit angiogenic signaling in endothelial cells and vascular pericytes predominantly through VEGFR and platelet-derived growth factor receptor beta. Sorafenib 111-120 kinase insert domain receptor Homo sapiens 18-61 20215359-3 2010 These include the vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors sunitinib and sorafenib, which inhibit angiogenic signaling in endothelial cells and vascular pericytes predominantly through VEGFR and platelet-derived growth factor receptor beta. Sorafenib 111-120 kinase insert domain receptor Homo sapiens 63-68 20215359-3 2010 These include the vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors sunitinib and sorafenib, which inhibit angiogenic signaling in endothelial cells and vascular pericytes predominantly through VEGFR and platelet-derived growth factor receptor beta. Sorafenib 111-120 kinase insert domain receptor Homo sapiens 223-228 19811659-9 2009 The potential targets for other kinase inhibitors (sunitinib and sorafenib) in ChRCC seem to be VEGFR and PDGFR. Sorafenib 65-74 kinase insert domain receptor Homo sapiens 96-101 19767240-0 2009 Risk of bleeding with vascular endothelial growth factor receptor tyrosine-kinase inhibitors sunitinib and sorafenib: a systematic review and meta-analysis of clinical trials. Sorafenib 107-116 kinase insert domain receptor Homo sapiens 22-65 19767240-1 2009 BACKGROUND: Sunitinib and sorafenib are oral vascular endothelial growth factor receptor (VEGFR) tyrosine-kinase inhibitors used in various cancers. Sorafenib 26-35 kinase insert domain receptor Homo sapiens 45-88 19767240-1 2009 BACKGROUND: Sunitinib and sorafenib are oral vascular endothelial growth factor receptor (VEGFR) tyrosine-kinase inhibitors used in various cancers. Sorafenib 26-35 kinase insert domain receptor Homo sapiens 90-95 19767240-11 2009 INTERPRETATION: Treatment with the VEGFR tyrosine-kinase inhibitors sunitinib and sorafenib is associated with a significant increase in risk of bleeding. Sorafenib 82-91 kinase insert domain receptor Homo sapiens 35-40 20109071-1 2010 Sorafenib is a small molecule inhibitor of RAF kinase, VEGFR-2, c-KIT, and FLT3. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 55-62 19935794-2 2010 Sorafenib, a multikinase inhibitor of VEGFR-2/-3, PDGFR-beta, B-Raf, and C-Raf, has shown to be active in preclinical models of cholangiocarcinoma. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 38-48 19112807-4 2008 In addition, in vitro studies have shown sorafenib to be a potent multikinase inhibitor, targeting receptor tyrosine kinases associated with tumor angiogenesis (VEGFR-2, VEGFR-3, and PDGFR-beta) and progression. Sorafenib 41-50 kinase insert domain receptor Homo sapiens 161-168 19220580-9 2009 Treatment of 10-0505 tumours with sorafenib plus rapamycin resulted in growth inhibition, inhibition of vascular endothelial growth factor receptor-2 phosphorylation, increased apoptosis and completely blocked sorafenib-induced phosphorylation of mTOR targets and cyclin B1 expression. Sorafenib 34-43 kinase insert domain receptor Homo sapiens 104-149 19542731-1 2009 Sorafenib(Nexavar)is a multikinase inhibitor, with disruptive activity at intracellular C-RAF, B-RAF and mutant BRAF receptors, and extracellular C-KIT, FLT-3, VEGFR-2, VEGFR-3 and PDGFRb receptors. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 160-167 19209155-3 2009 This knowledge is important because inhibitors of VEGF, including bevacizumab (anti-VEGF antibodies) and sorafenib (Braf/VEGFR2 kinase inhibitor), have already entered the clinic. Sorafenib 105-114 kinase insert domain receptor Homo sapiens 121-127 19228742-1 2009 PURPOSE: Sorafenib, a vascular endothelial growth factor (VEGF) receptor-2 and RAF kinase inhibitor, commonly causes skin toxicity. Sorafenib 9-18 kinase insert domain receptor Homo sapiens 22-74 19258226-1 2009 Sorafenib (Nexavar) is a targeted therapy acting as VEGFR and PDGFR tyrosine-kinase inhibitor that has been approved in France in the treatment of metastatic renal cell carcinoma and hepatocarcinoma. Sorafenib 11-18 kinase insert domain receptor Homo sapiens 52-57 19188183-1 2009 BACKGROUND: Sorafenib, a multitarget kinase inhibitor, inhibits members of the mitogen-activated protein kinase (MAPK) pathway and receptor tyrosine kinases, including vascular endothelial growth factor receptor 2 (VEGF-R2). Sorafenib 12-21 kinase insert domain receptor Homo sapiens 168-213 19188183-1 2009 BACKGROUND: Sorafenib, a multitarget kinase inhibitor, inhibits members of the mitogen-activated protein kinase (MAPK) pathway and receptor tyrosine kinases, including vascular endothelial growth factor receptor 2 (VEGF-R2). Sorafenib 12-21 kinase insert domain receptor Homo sapiens 215-222 19155200-8 2009 Recently, a large, randomised, placebo-controlled trial has shown that a multikinase inhibitor targeting Ras-kinase and VEGFR-2, sorafenib, improves survival of patients with advanced HCC. Sorafenib 129-138 kinase insert domain receptor Homo sapiens 120-127 19672141-1 2009 The approval of a multitargeted receptor tyrosine kinase inhibitor, sorafenib, with activity against vascular endothelial growth factor receptor-2 and -3, Raf-1 and B-Raf, platelet-derived growth factor receptor-alpha and -beta, and other kinases, has ushered in the era of molecular targeted agents in advanced hepatocellular carcinoma (HCC). Sorafenib 68-77 kinase insert domain receptor Homo sapiens 101-153 19212337-3 2009 However, resistance mediated by a T674I mutation in the ATP-binding pocket of PDGFRA has been reported in advanced disease, and sorafenib, a potent inhibitor of RAF-1, B-RAF, VEGFR and PDGFR, is active against this mutant in vitro. Sorafenib 128-137 kinase insert domain receptor Homo sapiens 175-180 19258226-1 2009 Sorafenib (Nexavar) is a targeted therapy acting as VEGFR and PDGFR tyrosine-kinase inhibitor that has been approved in France in the treatment of metastatic renal cell carcinoma and hepatocarcinoma. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 52-57 19296866-16 2009 Sorafenib, originally developed as RAF inhibitor, is now in clinical use as a VEGFR inhibitor. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 78-83 19707458-2 2008 Sorafenib is an oral multi-kinase inhibitor that mainly targets Raf kinases and receptor tyrosine kinases associated with angiogenesis (VEGFR-2/-3, PDGFR-beta). Sorafenib 0-9 kinase insert domain receptor Homo sapiens 136-146 19296000-5 2008 Multi-kinase ihibitors (sorafenib and sunitinib) are orally administered small-molecules, that inhibit different receptors (essentials in the neoplastic angiogenesis), such as the VEGFR or PDGFR. Sorafenib 24-33 kinase insert domain receptor Homo sapiens 180-185 18474019-5 2008 Sorafenib is an oral multikinase inhibitor (VEGFR and PDGFR) showing also inhibitors effect on the Raf system. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 44-49 18423135-3 2008 The development of anti-VEGF/VEGFR agents and the latest clinical data are reviewed, including bevacizumab as a monoclonal antibody to VEGF, sunitinib and sorafenib as VEGFR tyrosine kinase inhibitors, and IMC-1C11 as VEGFR monoclonal antibody. Sorafenib 155-164 kinase insert domain receptor Homo sapiens 168-173 18423135-3 2008 The development of anti-VEGF/VEGFR agents and the latest clinical data are reviewed, including bevacizumab as a monoclonal antibody to VEGF, sunitinib and sorafenib as VEGFR tyrosine kinase inhibitors, and IMC-1C11 as VEGFR monoclonal antibody. Sorafenib 155-164 kinase insert domain receptor Homo sapiens 168-173 17935273-7 2007 Sorafenib and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and platelet-derived growth factor receptor beta (PDGFR-beta), while temsirolimus is an mTOR inhibitor. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 86-140 17962201-1 2008 BACKGROUND: Sorafenib is an orally bioavailable vascular endothelial growth factor receptor (VEGFR) inhibitor with antitumor activity in metastatic renal cell carcinoma (RCC). Sorafenib 12-21 kinase insert domain receptor Homo sapiens 48-91 17962201-1 2008 BACKGROUND: Sorafenib is an orally bioavailable vascular endothelial growth factor receptor (VEGFR) inhibitor with antitumor activity in metastatic renal cell carcinoma (RCC). Sorafenib 12-21 kinase insert domain receptor Homo sapiens 93-98 17935273-7 2007 Sorafenib and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and platelet-derived growth factor receptor beta (PDGFR-beta), while temsirolimus is an mTOR inhibitor. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 142-149 17846009-10 2007 Sorafenib (BAY43-9006) was found to inhibit Raf1, but also VEGFR2 and 3, Flt3, PDGFR-a and b and c-kit, has been tested in a phase III study against placebo after one prior systemic therapy. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 59-71 17846009-10 2007 Sorafenib (BAY43-9006) was found to inhibit Raf1, but also VEGFR2 and 3, Flt3, PDGFR-a and b and c-kit, has been tested in a phase III study against placebo after one prior systemic therapy. Sorafenib 11-21 kinase insert domain receptor Homo sapiens 59-71 17229632-2 2007 Sorafenib (BAY43-9006, Nexavar) is a small molecule B-RAF inhibitor that is used for the treatment of renal cell carcinoma, and has been shown to have activity against receptor tyrosine kinases from the platelet-derived growth factor receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR) families. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 255-298 17619763-3 2007 Sutent and sorafenib are orally available inhibitors of the VEGFR and platelet derived growth factor receptor (PDGFR). Sorafenib 11-20 kinase insert domain receptor Homo sapiens 60-65 17296815-6 2007 Sorafenib is a multikinase inhibitor that inhibits the kinase activity of both C-RAF and B-RAF and targets the vascular endothelial growth factor receptor family (VEGFR-2 and VEGFR-3) and platelet-derived growth factor receptor family (PDGFR-beta and stem cell factor receptor [KIT]). Sorafenib 0-9 kinase insert domain receptor Homo sapiens 163-170 17229632-2 2007 Sorafenib (BAY43-9006, Nexavar) is a small molecule B-RAF inhibitor that is used for the treatment of renal cell carcinoma, and has been shown to have activity against receptor tyrosine kinases from the platelet-derived growth factor receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR) families. Sorafenib 11-21 kinase insert domain receptor Homo sapiens 255-298 17229632-2 2007 Sorafenib (BAY43-9006, Nexavar) is a small molecule B-RAF inhibitor that is used for the treatment of renal cell carcinoma, and has been shown to have activity against receptor tyrosine kinases from the platelet-derived growth factor receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR) families. Sorafenib 11-21 kinase insert domain receptor Homo sapiens 300-305 17229632-2 2007 Sorafenib (BAY43-9006, Nexavar) is a small molecule B-RAF inhibitor that is used for the treatment of renal cell carcinoma, and has been shown to have activity against receptor tyrosine kinases from the platelet-derived growth factor receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR) families. Sorafenib 23-30 kinase insert domain receptor Homo sapiens 255-298 17229632-2 2007 Sorafenib (BAY43-9006, Nexavar) is a small molecule B-RAF inhibitor that is used for the treatment of renal cell carcinoma, and has been shown to have activity against receptor tyrosine kinases from the platelet-derived growth factor receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR) families. Sorafenib 23-30 kinase insert domain receptor Homo sapiens 300-305 17229632-2 2007 Sorafenib (BAY43-9006, Nexavar) is a small molecule B-RAF inhibitor that is used for the treatment of renal cell carcinoma, and has been shown to have activity against receptor tyrosine kinases from the platelet-derived growth factor receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR) families. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 300-305 19089671-11 2007 Sorafenib is an oral-targeted agent that acts as a multikinase inhibitor and competitively inhibits the Raf, vascular endothelial growth factor receptor 2 (VEGFR2), VEGFR3, platelet-derived growth factor receptor beta, Flt3, and C-KIT receptors (Chabner BA et al. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 109-154 19089671-11 2007 Sorafenib is an oral-targeted agent that acts as a multikinase inhibitor and competitively inhibits the Raf, vascular endothelial growth factor receptor 2 (VEGFR2), VEGFR3, platelet-derived growth factor receptor beta, Flt3, and C-KIT receptors (Chabner BA et al. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 156-162 16503817-1 2006 Sorafenib is a small molecule inhibitor of several kinases involved in tumour proliferation and tumour angiogenesis including Raf, VEGFR and platelet derived growth factor receptor. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 131-136 16824050-3 2006 The novel, oral treatment sorafenib (BAY 43-9006), has been shown to be an inhibitor of VEGFR, Raf and platelet-derived growth factor in clinical trials against a variety of cancers, with the greatest activity to date observed in metastatic renal cancer. Sorafenib 26-35 kinase insert domain receptor Homo sapiens 88-93 16824050-3 2006 The novel, oral treatment sorafenib (BAY 43-9006), has been shown to be an inhibitor of VEGFR, Raf and platelet-derived growth factor in clinical trials against a variety of cancers, with the greatest activity to date observed in metastatic renal cancer. Sorafenib 37-48 kinase insert domain receptor Homo sapiens 88-93 16988583-3 2006 RECENT FINDINGS: Sorafenib was initially developed as an inhibitor of Raf kinase; however, it has broad spectrum activity against multiple tyrosine kinases, including angiogenic factors VEGFR and PDGFR. Sorafenib 17-26 kinase insert domain receptor Homo sapiens 186-191 16890795-6 2006 Sorafenib is the first oral multi-kinase inhibitor to be developed that targets Raf kinases (Raf-1, wild-type B-Raf, and b-raf V600E), in addition to receptor tyrosine kinases associated with angiogenesis (vascular endothelial growth factor receptor [VEGFR]-2/-3, platelet-derived growth factor receptor [PDGFR]-beta) or tumor progression (Flt-3, c-kit). Sorafenib 0-9 kinase insert domain receptor Homo sapiens 206-249 16890795-6 2006 Sorafenib is the first oral multi-kinase inhibitor to be developed that targets Raf kinases (Raf-1, wild-type B-Raf, and b-raf V600E), in addition to receptor tyrosine kinases associated with angiogenesis (vascular endothelial growth factor receptor [VEGFR]-2/-3, platelet-derived growth factor receptor [PDGFR]-beta) or tumor progression (Flt-3, c-kit). Sorafenib 0-9 kinase insert domain receptor Homo sapiens 251-256 18087180-6 2007 Several agents have entered clinical trials in HCC patients, and recent data indicated that a multikinase inhibitor targeting Ras kinase and VEGFR-2, sorafenib, is effective in prolonging survival of patients with advanced HCC. Sorafenib 150-159 kinase insert domain receptor Homo sapiens 141-148 17178882-2 2006 Sorafenib (BAY 43-9006, Nexavar) is a multikinase inhibitor with activity against Raf kinase and several receptor tyrosine kinases, including vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor (PDGFR), FLT3, Ret, and c-Kit. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 142-187 17178882-2 2006 Sorafenib (BAY 43-9006, Nexavar) is a multikinase inhibitor with activity against Raf kinase and several receptor tyrosine kinases, including vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor (PDGFR), FLT3, Ret, and c-Kit. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 189-195 17178882-2 2006 Sorafenib (BAY 43-9006, Nexavar) is a multikinase inhibitor with activity against Raf kinase and several receptor tyrosine kinases, including vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor (PDGFR), FLT3, Ret, and c-Kit. Sorafenib 11-22 kinase insert domain receptor Homo sapiens 142-187 17178882-2 2006 Sorafenib (BAY 43-9006, Nexavar) is a multikinase inhibitor with activity against Raf kinase and several receptor tyrosine kinases, including vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor (PDGFR), FLT3, Ret, and c-Kit. Sorafenib 24-31 kinase insert domain receptor Homo sapiens 142-187 17178882-11 2006 These results suggest that the antitumor activity of sorafenib in HCC models may be attributed to inhibition of tumor angiogenesis (VEGFR and PDGFR) and direct effects on tumor cell proliferation/survival (Raf kinase signaling-dependent and signaling-independent mechanisms). Sorafenib 53-62 kinase insert domain receptor Homo sapiens 132-137 16850127-3 2006 To date, the vascular endothelial growth factor receptor (VEGFR) pathway has been the most promising target, and two agents (BAY 43-9006 and SU 11248) that inhibit not only VEGFR but also other receptors, including platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), KIT, and Raf kinase, were recently approved by the FDA for advanced RCC. Sorafenib 125-136 kinase insert domain receptor Homo sapiens 173-178 16133532-1 2006 Sorafenib is a novel, small-molecule anticancer compound that inhibits tumor cell proliferation by targeting Raf in the Raf/MEK/ERK signalling pathway, and inhibits angiogenesis by targeting tyrosine kinases such as vascular-endothelial growth factor receptor (VEGFR-2 and VEGFR-3) and platelet-derived growth factor receptor (PDGFR). Sorafenib 0-9 kinase insert domain receptor Homo sapiens 261-268 16240452-7 2005 In addition to inhibiting VEGFR and PDGFR-mediated angiogenic pathways, BAY 43-9006 has been shown to inhibit the Raf/MEK/ERK pathway at the level of Raf kinase. Sorafenib 72-83 kinase insert domain receptor Homo sapiens 26-31 16757355-8 2006 Further characterization of sorafenib revealed that this molecule was a multikinase inhibitor that targeted the vascular endothelial growth factor receptor family (VEGFR-2 and VEGFR-3) and platelet-derived growth factor receptor family (PDGFR-beta and Kit), which play key roles in tumor progression and angiogenesis. Sorafenib 28-37 kinase insert domain receptor Homo sapiens 164-171 16757355-9 2006 Thus, sorafenib may inhibit tumor growth by a dual mechanism, acting either directly on the tumor (through inhibition of Raf and Kit signaling) and/or on tumor angiogenesis (through inhibition of VEGFR and PDGFR signaling). Sorafenib 6-15 kinase insert domain receptor Homo sapiens 196-201 16425993-2 2005 Significant advances in the treatment of clear-cell RCC have been derived from agents that target these pathways, including the multiple-kinase inhibitors (MKIs) sorafenib, sunitinib, and AG013736, which target multiple VEGFRs as well as PDGFR-beta. Sorafenib 162-171 kinase insert domain receptor Homo sapiens 220-226 16425993-3 2005 Sorafenib has the added advantage of inhibiting multiple different Raf isoforms, which enables it to target TGF-alpha/EGFR signaling and may also enhance its inhibition of VEGFR and PDGFR-beta. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 172-177 15466206-4 2004 In addition, BAY 43-9006 demonstrated significant activity against several receptor tyrosine kinases involved in neovascularization and tumor progression, including vascular endothelial growth factor receptor (VEGFR)-2, VEGFR-3, platelet-derived growth factor receptor beta, Flt-3, and c-KIT. Sorafenib 13-24 kinase insert domain receptor Homo sapiens 165-208 16869784-7 2005 One of these, the Raf kinase/VEGF-R2 inhibitor Sorafenib, has already been approved for treatment of renal cancer and is being tested in other indications. Sorafenib 47-56 kinase insert domain receptor Homo sapiens 29-36 16006586-0 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. Sorafenib 103-114 kinase insert domain receptor Homo sapiens 87-92 15870716-1 2005 BAY 43-9006 is a novel dual-action Raf kinase and vascular endothelial growth factor receptor (VEGFR) inhibitor that targets tumour cell proliferation and tumour angiogenesis. Sorafenib 0-11 kinase insert domain receptor Homo sapiens 50-93 15870716-1 2005 BAY 43-9006 is a novel dual-action Raf kinase and vascular endothelial growth factor receptor (VEGFR) inhibitor that targets tumour cell proliferation and tumour angiogenesis. Sorafenib 0-11 kinase insert domain receptor Homo sapiens 95-100 15466206-4 2004 In addition, BAY 43-9006 demonstrated significant activity against several receptor tyrosine kinases involved in neovascularization and tumor progression, including vascular endothelial growth factor receptor (VEGFR)-2, VEGFR-3, platelet-derived growth factor receptor beta, Flt-3, and c-KIT. Sorafenib 13-24 kinase insert domain receptor Homo sapiens 210-215 15466206-6 2004 Potent inhibition of VEGFR-2, platelet-derived growth factor receptor beta, and VEGFR-3 cellular receptor autophosphorylation was also observed for BAY 43-9006. Sorafenib 148-159 kinase insert domain receptor Homo sapiens 21-28 15466206-10 2004 These data demonstrate that BAY 43-9006 is a novel dual action RAF kinase and VEGFR inhibitor that targets tumor cell proliferation and tumor angiogenesis. Sorafenib 28-39 kinase insert domain receptor Homo sapiens 78-83 34862634-1 2022 Twelve new triazolo(4,3-a)quinoxaline-based compounds are reported as anticancer agents with potential effects against vascular endothelial growth factor receptor-2 (VEGFR-2), using sorafenib as a reference molecule. Sorafenib 182-191 kinase insert domain receptor Homo sapiens 166-173 15448036-1 2004 BAY 43-9006 is an oral inhibitor of CRAF, wild-type BRAF, mutant V599E BRAF, vascular endothelial growth factor receptor (VEGFR) 2, VEGFR3, mVEGFR2, FLT-3, platelet-derived growth factor receptor, p38, and c-kit among other kinases. Sorafenib 0-11 kinase insert domain receptor Homo sapiens 122-130 33944931-0 2021 Study on novel PtNP-Sorafenib and its interaction with VEGFR2. Sorafenib 20-29 kinase insert domain receptor Homo sapiens 55-61 34862634-3 2022 The most powerful VEGFR-2 inhibitor was compound 14a, which had an IC50 value of 3.2 nM, which is very close to that of sorafenib (IC50 = 3.12 nM). Sorafenib 120-129 kinase insert domain receptor Homo sapiens 18-25 34862655-5 2022 Compounds 18, 13, and 10 were more potent than sorafenib, inhibiting vascular endothelial growth factor receptor-2 (VEGFR-2) at GI50 values of 0.05, 0.06, and 0.08 microM, respectively. Sorafenib 47-56 kinase insert domain receptor Homo sapiens 69-114 34862655-5 2022 Compounds 18, 13, and 10 were more potent than sorafenib, inhibiting vascular endothelial growth factor receptor-2 (VEGFR-2) at GI50 values of 0.05, 0.06, and 0.08 microM, respectively. Sorafenib 47-56 kinase insert domain receptor Homo sapiens 116-123 34862655-6 2022 Compound 11 inhibited VEGFR-2 at an IC50 value of 0.10 microM, which is equipotent to sorafenib. Sorafenib 86-95 kinase insert domain receptor Homo sapiens 22-29 34862655-7 2022 Compound 14 inhibited VEGFR-2 at an IC50 value of 0.11 microM, which is nearly equipotent to sorafenib. Sorafenib 93-102 kinase insert domain receptor Homo sapiens 22-29 34876355-11 2021 Levels of a CD34+KDR+ are higher at baseline in patients responding to sorafenib. Sorafenib 71-80 kinase insert domain receptor Homo sapiens 17-20 34596910-5 2022 Compound 7f was found to be the most potent derivative that inhibited VEGFR-2 at an IC50 value of 0.08 microM, which is more potent than sorafenib (IC50 = 0.10 microM). Sorafenib 137-146 kinase insert domain receptor Homo sapiens 70-77 34596910-6 2022 Compound 8c inhibited VEGFR-2 at an IC50 value of 0.10 microM, which is equipotent to sorafenib. Sorafenib 86-95 kinase insert domain receptor Homo sapiens 22-29 34655447-2 2021 Initially designed as a Raf inhibitor, Sorafenib was later shown to also block key molecules in tumour progression such as VEGFR and PDGFR. Sorafenib 39-48 kinase insert domain receptor Homo sapiens 123-128 34325596-9 2021 Moreover, 11b, 11f, 11g, 12e, 12f, 12g, and 12k showed the highest VEGFR-2 inhibitory activities (IC50 range is 2.9 - 5.4 microM), comparing to sorafenib (IC50 = 3.07 nM). Sorafenib 144-153 kinase insert domain receptor Homo sapiens 67-74 34340610-7 2021 Compound 27a was the most potent VEGFR-2 inhibitor with IC50 of 3.2 nM very close to positive control sorafenib (IC50 = 3.12 nM). Sorafenib 102-111 kinase insert domain receptor Homo sapiens 33-40 34411344-7 2021 The enzyme assay results of the new compounds were compared with those of sorafenib as a reference VEGFR-2 inhibitor. Sorafenib 74-83 kinase insert domain receptor Homo sapiens 99-106 34534755-7 2021 Evaluation of growth inhibitory activity of the synthesized compounds against hepatocellular carcinoma (HepG2), that overexpresses VEGFR2, showed superior activity of compounds 8, 10a and 10c with IC50 in sub micromolar concentrations of 0.84, 0.79 and 0.69 muM, respectively, which is better than that of the reference drug, Sorafenib (IC50 = 3.99 microM). Sorafenib 326-335 kinase insert domain receptor Homo sapiens 131-137 34534755-9 2021 The results of VEGFR2 kinase inhibition assay demonstrate that, compounds 8 and 10a are the most active inhibitors with IC50 = 25.7 and 28.2 nM, respectively, (Sorafenib IC50 = 28.1 nM). Sorafenib 160-169 kinase insert domain receptor Homo sapiens 15-21 34534755-10 2021 Molecular docking of the synthesized derivatives to VEGFR2 (PDB: 3WZE) showed similar binding modes to that of the co-crystallized ligand, sorafenib. Sorafenib 139-148 kinase insert domain receptor Homo sapiens 52-58 34582293-5 2021 Alpha-fetoprotein, des-carboxyprothrombin, vascular endothelial growth factor, angiopoietin-2, and dysregulated MTOR, VEGFR2, c-KIT, RAF1, PDGFRbeta have the potential of proteomic/genomic biomarkers for sorafenib treatment. Sorafenib 204-213 kinase insert domain receptor Homo sapiens 118-124 33349069-8 2021 Additionally, molecular docking study was performed against VEGFR (PDB ID: 4ASD) using MOE 2015.10 software and Sorafenib as a reference ligand. Sorafenib 112-121 kinase insert domain receptor Homo sapiens 60-65 34056992-7 2021 Furthermore, compounds 23a, 23d, 23h, 23i, 23j, 23l, 23 m, and 23n showed the highest VEGFR-2 inhibitory activities with IC50 values ranging from 3.7 to 11.8 nM, comparing to sorafenib (IC50 = 3.12 nM). Sorafenib 175-184 kinase insert domain receptor Homo sapiens 86-93 34691254-4 2021 Sorafenib is a tyrosine kinase inhibitor, whose targets include c-Kit, platelet derived growth factor receptor (PDGFR), VEGFR and RAF. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 120-125 34691254-12 2021 Mechanistically, sorafenib inhibited c-Kit, PDGFR, VEGFR, B-Raf and c-Raf phosphorylation both in vitro and in vivo. Sorafenib 17-26 kinase insert domain receptor Homo sapiens 51-56 34591285-1 2021 Donafenib (Zepsun , ), a deuterium derivative of sorafenib, is an oral small molecule multikinase inhibitor of multiple receptor kinases, including vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR) and Raf kinases. Sorafenib 50-59 kinase insert domain receptor Homo sapiens 149-192 34089726-0 2021 Sorafenib derivatives-functionalized gold nanoparticles confer protection against tumor angiogenesis and proliferation via suppression of EGFR and VEGFR-2. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 147-154 34175720-4 2021 Doxorubicin as a universal anticancer drug and sorafenib as a potent VEGFR-2 inhibitor were used as positive controls. Sorafenib 47-56 kinase insert domain receptor Homo sapiens 69-76 34175720-12 2021 Compounds 15 and 17b potently inhibited VEGFR-2 at lower IC50 values of 1.09 and 1.19 microM, respectively, compared to sorafenib (IC50 = 1.27 microM). Sorafenib 120-129 kinase insert domain receptor Homo sapiens 40-47 35489270-13 2022 Enzymatic evaluation showed that both derivatives were potent dual MMP-2/VEGFR-2 inhibitors, particularly 8d (MMP-2; IC50 = 5.66 nM and VEGFR-2; IC50 = 6.65 nM), relative to the reference MMP-2 inhibitor NNGH (IC50 = 299.50 nM) and VEGFR-2 inhibitor sorafenib (IC50 = 4.92 nM). Sorafenib 250-259 kinase insert domain receptor Homo sapiens 73-80 34463438-7 2022 Interestingly, they were able to suppress Caco-2 colon cancer cells migration at 5.8 mug/mL and potently inactivate the VEGFR2 angiogenic enzyme (1.5-fold relative to sorafenib. Sorafenib 167-176 kinase insert domain receptor Homo sapiens 120-126 34108938-6 2021 Apoptosis was observed after sorafenib treatment, and coimmunoprecipitation data suggested that the drug prevents formation VEGFR-VE-cadherin and beta-catenin proteins complex. Sorafenib 29-38 kinase insert domain receptor Homo sapiens 124-129 34909649-0 2021 Reversal of TGF-beta-induced epithelial-mesenchymal transition in hepatocellular carcinoma by sorafenib, a VEGFR-2 and Raf kinase inhibitor. Sorafenib 94-103 kinase insert domain receptor Homo sapiens 107-114 34909649-2 2021 Sorafenib, a RAF kinase and VEGFR-2 inhibitor, exhibits efficacy against advanced hepatocellular carcinoma (HCC), renal carcinoma, and thyroid cancer. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 28-35 34853223-5 2021 We assessed 24 cases who received VEGFR-TKI monotherapy (sunitinib, sorafenib, pazopanib, axitinib) with left ventricular ejection fraction (LVEF) above 50% during the therapy at the Osaka University Hospital from January 2008 to June 2019. Sorafenib 68-77 kinase insert domain receptor Homo sapiens 34-39 34460053-8 2021 Such derivative showed the best VEGFR-2 inhibitory activity with an IC50 value of 3.9 nM, which is very close to that of sorafenib (IC50 = 3.13 nM). Sorafenib 121-130 kinase insert domain receptor Homo sapiens 32-39 35189405-1 2022 Hand-foot skin reaction (HFSR) is the most debilitating and prevalent side effect caused by multikinase inhibitors (MKIs) that share vascular endothelial growth factor receptor (VEGFR) as the common inhibition target, such as sorafenib, regorafenib, axitinib, etc. Sorafenib 226-235 kinase insert domain receptor Homo sapiens 133-176 35189405-1 2022 Hand-foot skin reaction (HFSR) is the most debilitating and prevalent side effect caused by multikinase inhibitors (MKIs) that share vascular endothelial growth factor receptor (VEGFR) as the common inhibition target, such as sorafenib, regorafenib, axitinib, etc. Sorafenib 226-235 kinase insert domain receptor Homo sapiens 178-183 35445315-2 2022 Vascular endothelial growth factor receptor (VEGFR) inhibitors like sorafenib may cause proteinuria. Sorafenib 68-77 kinase insert domain receptor Homo sapiens 0-43 35445315-2 2022 Vascular endothelial growth factor receptor (VEGFR) inhibitors like sorafenib may cause proteinuria. Sorafenib 68-77 kinase insert domain receptor Homo sapiens 45-50 35245519-1 2022 AIMS: Hepatocellular carcinoma (HCC) is the most common liver malignancy,characterized by dysregulation of multiple oncogenic signaling pathways, including the VEGF/PI3K/NF-kappaB and p38 MAPK axes.Sorafenib is a multikinase inhibitor that targets Raf kinases and receptor tyrosine kinases,which mediate HCC angiogenesis.Rhamnazin is a VEGFR2 signaling inhibitor, which inhibits the phosphorylation of Vascular endothelial growth factor receptor 2(VEGFR2) and its downstream signaling regulators. Sorafenib 198-207 kinase insert domain receptor Homo sapiens 336-342 35245519-1 2022 AIMS: Hepatocellular carcinoma (HCC) is the most common liver malignancy,characterized by dysregulation of multiple oncogenic signaling pathways, including the VEGF/PI3K/NF-kappaB and p38 MAPK axes.Sorafenib is a multikinase inhibitor that targets Raf kinases and receptor tyrosine kinases,which mediate HCC angiogenesis.Rhamnazin is a VEGFR2 signaling inhibitor, which inhibits the phosphorylation of Vascular endothelial growth factor receptor 2(VEGFR2) and its downstream signaling regulators. Sorafenib 198-207 kinase insert domain receptor Homo sapiens 402-447 35245519-1 2022 AIMS: Hepatocellular carcinoma (HCC) is the most common liver malignancy,characterized by dysregulation of multiple oncogenic signaling pathways, including the VEGF/PI3K/NF-kappaB and p38 MAPK axes.Sorafenib is a multikinase inhibitor that targets Raf kinases and receptor tyrosine kinases,which mediate HCC angiogenesis.Rhamnazin is a VEGFR2 signaling inhibitor, which inhibits the phosphorylation of Vascular endothelial growth factor receptor 2(VEGFR2) and its downstream signaling regulators. Sorafenib 198-207 kinase insert domain receptor Homo sapiens 448-454 35245519-8 2022 The sorafenib-rhamnazin combination also showed significant inhibition of the angiogenicVEGF/VEGFR2/PI3K/NF-kappaBsignaling axis associated with significant upregulation of the apoptotic p38MAPK/caspase-3 axis and inhibition of Ki67, a proliferation marker in HepG2 and HUH-7 cells. Sorafenib 4-13 kinase insert domain receptor Homo sapiens 93-99 35245519-9 2022 SIGNIFICANCE: Rhamnazin potentiates the chemotherapeutic effect of sorafenib via modulation ofthe VEGF/PI3K/NF-kappaBsignaling axis, downregulation of VEGFR2 expression, and upregulation of the p38MAPK/caspase-3 axis in human HCC cell lines. Sorafenib 67-76 kinase insert domain receptor Homo sapiens 151-157 35484400-0 2022 KDR genetic predictor of toxicities induced by sorafenib and regorafenib. Sorafenib 47-56 kinase insert domain receptor Homo sapiens 0-3 35457095-3 2022 Neutralizing VEGF with avastin and polyclonal goat anti-VEGF antibody and inhibiting VEGFR2 with sorafenib and vatalanib resulted in the formation of HUVEC clusters of variable sizes as a result of inhibited EC differentiation. Sorafenib 97-106 kinase insert domain receptor Homo sapiens 85-91 35496328-7 2022 Derivatives 5g, 4g and 4f were observed to be the highest effective derivatives that inhibited VEGFR-2 at the submicromolar level (IC50 = 0.080, 0.083 and 0.095 muM respectively) in comparison to sorafenib (IC50 = 0.084 muM). Sorafenib 196-205 kinase insert domain receptor Homo sapiens 95-102 35337128-2 2022 It is vital to uncover novel chemical candidates of VEGFR inhibitors to develop more potent anti-breast and anti-liver cancer agents than the currently available candidates, sorafenib and regorafenib, that face resistance obstacles and severe side effects. Sorafenib 174-183 kinase insert domain receptor Homo sapiens 52-57 35337128-5 2022 Stunningly, compound 7 showed the best significant inhibition of the VEGFR-2 protein expression level (72.3%) as compared to the control and even higher than that produced with sorafenib and regorafenib (70.4% and 55.6%, respectively). Sorafenib 177-186 kinase insert domain receptor Homo sapiens 69-76 35091289-3 2022 Sorafenib is an FDA approved cancer therapeutic with activity against many protein kinases, including VEGFR. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 102-107 35123995-6 2022 In addition, compounds 4a and 4b exhibited comparable inhibitory activity on tyrosine kinase receptors EGFR and VEGFR-2 kinases to that of the reference protein kinases inhibitor Sorafenib. Sorafenib 179-188 kinase insert domain receptor Homo sapiens 112-119 33831675-4 2021 The molecular docking studies revealed that the analogue 2m bound B-RAF near the binding position of Sorafenib, while it interacted VEGFR2 efficiently at the same binding position of Sorafenib. Sorafenib 183-192 kinase insert domain receptor Homo sapiens 132-138 33962153-10 2021 In a similar manner to Sorafenib, docking of target compounds with VEGFR-2 protein 4ASD showed HB with Cys919 in hinge region of enzyme and HB with both Glu885 and Asp1046 in gate area. Sorafenib 23-32 kinase insert domain receptor Homo sapiens 67-74 33948974-7 2021 Hormonal pharmaceuticals, including melatonin, exerts proapoptotic via regulating matrix metallopeptidase activity while nonhormonal pharmaceutical sorafenib exerts antiproliferative effect via MAPK/ERK pathway and antiangiogenesis activity via VEGF/VEGFR pathway. Sorafenib 148-157 kinase insert domain receptor Homo sapiens 250-255 33917617-5 2021 Compounds 16 and 23 (Z) and (E)-styryl p-bromophenyl urea, respectively, showed better results than sorafenib in down-regulation of VEGFR-2 and also improved the effect of the anti-PD-L1 compound BMS-8 on both targets, PD-L1 and c-Myc proteins. Sorafenib 100-109 kinase insert domain receptor Homo sapiens 132-139 33667419-8 2021 A combinatorial screen of the positive and negative regulators of sorafenib-induced apoptosis revealed ROS knockdown coupled with overexpression of FLT3, FGFR, PDGFR, VEGFR, or KIT as a particularly potent combination in reducing sorafenib-induced apoptosis Network simulations of combinatorial treatment with sorafenib and the antioxidant N-acetyl cysteine (NAC) suggest that NAC may protect cardiomyocytes from sorafenib-induced apoptosis. Sorafenib 66-75 kinase insert domain receptor Homo sapiens 167-172 33334586-4 2021 Compounds 29b, 29c and 29a exhibited potent inhibitory activities towards VEGFR-2 at IC50 values of 3.1 +- 0.04, 3.4 +- 0.05 and 3.7 +- 0.06 microM, respectively, comparing sorafenib (IC50 = 2.4 +- 0.05 microM). Sorafenib 173-182 kinase insert domain receptor Homo sapiens 74-81 33628103-1 2021 Background: Sorafenib, an oral multi-kinase inhibitor of rapidly accelerated fibrosarcoma; vascular endothelial growth factor receptor-2/3, platelet-derived growth factor receptor, c-Kit, and Flt-3 signaling, is approved for treatment of advanced hepatocellular carcinoma (HCC). Sorafenib 12-21 kinase insert domain receptor Homo sapiens 91-138 32653608-8 2020 Among them, compounds 8f was found to be the most potent derivative that inhibited VEGFR-2 at IC50 value of 0.22 +- 0.02 microM, which is nearly the half as that of sorafenib IC50 value (0.10 +- 0.02 microM). Sorafenib 165-174 kinase insert domain receptor Homo sapiens 83-90 33142416-11 2020 Also, compounds 7c and 7b possessed good VEGFR-2 inhibition with IC50 values of 0.16 +- 0.06 and 0.17 +- 0.06 microM respectively which are more than the half activity of that of sorafenib. Sorafenib 179-188 kinase insert domain receptor Homo sapiens 41-48 32747013-1 2020 OBJECTIVE: To examine whether blocking multiple points of the angiogenesis pathway by addition of sorafenib, a multi-kinase inhibitor against VEGFR2/3, Raf, c-Kit, and PDGFR, to bevacizumab would yield clinical activity in ovarian cancer (OvCa). Sorafenib 98-107 kinase insert domain receptor Homo sapiens 142-150 32683176-5 2020 VEGFR-2-kinase was tested against 3a, 3b, 3e, 4b and sorafenib was used as a reference. Sorafenib 53-62 kinase insert domain receptor Homo sapiens 0-7 32683176-7 2020 The results of the docking study showed a good fitting of the new compounds to the active site of VEGFR-2 with binding free energies in the range of -9.80 to -11.25 kcal/mol compared to -12.12 kcal/mol for sorafenib. Sorafenib 206-215 kinase insert domain receptor Homo sapiens 98-105 32510731-6 2020 Compounds 11b, 11e, and 11c potently inhibited VEGFR-2 at IC50 values of 0.12 +- 0.02, 0.12 +- 0.02, and 0.13 +- 0.02 microM, respectively, which are nearly equipotent as sorafenib IC50 value (0.10 +- 0.02 microM). Sorafenib 171-180 kinase insert domain receptor Homo sapiens 47-54 32663641-1 2020 To develop inhibitors blocking VEGFR2 and the Raf/MEK/ERK mitogen-activated protein kinase signaling pathway new compounds based on sorafenib were designed, synthesized and biologically evaluated. Sorafenib 132-141 kinase insert domain receptor Homo sapiens 31-37 32882995-6 2020 Sorafenib is a tyrosine kinase inhibitor that targets RAF kinase, KIT, VEGFR, PDGFR1beta, FLT3, and RET. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 71-76 32399432-4 2020 Methods: Through quantitative real-time reverse transcription PCR, we analyzed the expression levels of seven actionable genes (VEGFR2, PDGFRB, c-KIT, c-RAF, EGFR, mTOR, and FGFR1) in tumors versus noncancerous tissues from 220 HCC patients treated with sorafenib. Sorafenib 254-263 kinase insert domain receptor Homo sapiens 128-134 32549224-3 2020 Molecular targeted therapy with sorafenib, a dual-target inhibitor targeting the serine-threonine kinase Raf and the tyrosine kinases VEGFR/PDGFR, is at present the main treatment for advanced-stage HCC, either in a single or combinatory regimen. Sorafenib 32-41 kinase insert domain receptor Homo sapiens 134-139 32480170-2 2020 Five quinazoline -2-carboxamide derivatives (5d, 5e, 5 h, 5i, 5j) revealed potent nanomolar VEGFR-2 inhibition with IC50 values of 12.1, 40.3, 15.5, 13.1 and 57.4 nM, respectively, superior to that of the reference drug sorafenib (IC50 78.9 nM). Sorafenib 220-229 kinase insert domain receptor Homo sapiens 92-99 32480170-5 2020 Furthermore, molecular modeling study was administered to realize any clarification of the binding mode in the inactive VEGFR-2 conformation that demonstrates compatible binding modes similar to those of sorafenib and regorafenib. Sorafenib 204-213 kinase insert domain receptor Homo sapiens 120-127 32399432-8 2020 With an area under the curve of 0.779, a TBS combining mTOR with VEGFR2, c-KIT, and c-RAF was the most significant predictor of response to sorafenib. Sorafenib 140-149 kinase insert domain receptor Homo sapiens 65-71 32065066-6 2020 Sorafenib (BAY 43-9006; Nexavar), a multikinase inhibitor acting on Raf kinase and receptor tyrosine kinases-including vascular endothelial growth factor receptors 2 and 3-was administered daily (60 mg/kg, per os). Sorafenib 0-9 kinase insert domain receptor Homo sapiens 119-171 31586713-6 2019 Compound 5j was specially promising as it exhibited inhibitory activity of VEGFR2 close to sorafenib (IC50 0.11 +- 0.01 muM), most potent B-RAF activity inhibition (IC50 0.178 +- 0.004 muM) and MMP9 inhibition (IC50 0.08 +- 0.004 muM). Sorafenib 91-100 kinase insert domain receptor Homo sapiens 75-81 31391334-9 2019 The immune modulation resulted from sorafenib-mediated blockade of signaling through the VEGF/VEGFR/flt-3 pathway, affecting ERK phosphorylation. Sorafenib 36-45 kinase insert domain receptor Homo sapiens 94-99 31448458-8 2019 Our design was based on the essential pharmacophoric features of the VEGFR-2 inhibitor sorafenib. Sorafenib 87-96 kinase insert domain receptor Homo sapiens 69-76 31755336-13 2019 Interestingly, these hits retains 90% similarity with standard VEGFR2 inhibitor (Sorafenib). Sorafenib 81-90 kinase insert domain receptor Homo sapiens 63-69 31146197-4 2019 First, sorafenib was docked in the binding site of VEGFR 2 to study its binding orientation and affinity, followed by the generation of a valid 3D QSAR pharmacophore model for use in the virtual screening of different 3D databases. Sorafenib 7-16 kinase insert domain receptor Homo sapiens 51-58 31046582-7 2019 Sorafenib is an oral multikinase inhibitor with activity against Raf-1 serine/threonine kinase, B-Raf, vascular endothelial growth factor receptor-2 (VEGFR-2), platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT-3), and c-KIT. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 103-148 31181647-8 2019 Additional inhibition of Vascular Endothelial Growth Factor Receptor (VEGFR) or Insulin-like Growth Factor 1 Receptor (IGF1R) enhanced effects on AFP and DCP levels, cell growth inhibition and MAPK and PI3K/Akt signaling inhibition due to sorafenib/regorafenib combination. Sorafenib 239-248 kinase insert domain receptor Homo sapiens 25-68 31181647-8 2019 Additional inhibition of Vascular Endothelial Growth Factor Receptor (VEGFR) or Insulin-like Growth Factor 1 Receptor (IGF1R) enhanced effects on AFP and DCP levels, cell growth inhibition and MAPK and PI3K/Akt signaling inhibition due to sorafenib/regorafenib combination. Sorafenib 239-248 kinase insert domain receptor Homo sapiens 70-75 31046582-7 2019 Sorafenib is an oral multikinase inhibitor with activity against Raf-1 serine/threonine kinase, B-Raf, vascular endothelial growth factor receptor-2 (VEGFR-2), platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT-3), and c-KIT. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 150-157 30689282-0 2019 Exploring binding mechanisms of VEGFR2 with three drugs lenvatinib, sorafenib, and sunitinib by molecular dynamics simulation and free energy calculation. Sorafenib 68-77 kinase insert domain receptor Homo sapiens 32-38 30689282-1 2019 Lenvatinib (LEN), sorafenib (SOR), and sunitinib (SUN) are drugs targeting vascular endothelial growth factor receptor 2 (VEGFR2). Sorafenib 18-27 kinase insert domain receptor Homo sapiens 75-120 30689282-1 2019 Lenvatinib (LEN), sorafenib (SOR), and sunitinib (SUN) are drugs targeting vascular endothelial growth factor receptor 2 (VEGFR2). Sorafenib 18-27 kinase insert domain receptor Homo sapiens 122-128 30973909-0 2019 Expression of Concern: Antitumor Activity of Sorafenib in Human Cancer Cell Lines with Acquired Resistance to EGFR and VEGFR Tyrosine Kinase Inhibitors. Sorafenib 45-54 kinase insert domain receptor Homo sapiens 119-124 30826508-3 2019 Compounds 7h, 9a and 9l showed potent inhibitory activity against VEGFR-2 kinase with IC50 values of 87, 27 and 94 nM, respectively in comparison to sorafenib (IC50 = 180 nM) as a reference. Sorafenib 149-158 kinase insert domain receptor Homo sapiens 66-73 30641320-4 2019 Moreover, in vitro studies of the VEGFR-2 inhibition in human breast cancer MCF-7 cell line for the promising cytotoxic compounds showed that compounds 7a, 8c, 9b, 9c and 9d were potent inhibitors at low micromolar concentrations (IC50 = 0.034-0.582 muM) compared to the reference drug, sorafenib (IC50 = 0.019 muM). Sorafenib 287-296 kinase insert domain receptor Homo sapiens 34-41 30393973-3 2019 Six of the synthesized compounds were screened against vascular endothelial growth factor receptor 2 (VEGFR-2) where compounds 8, 9, 12, and 15 exhibited an outstanding potency in comparison with sorafenib, with IC50 values of 6.7-8.9 nM. Sorafenib 196-205 kinase insert domain receptor Homo sapiens 55-100 30393973-3 2019 Six of the synthesized compounds were screened against vascular endothelial growth factor receptor 2 (VEGFR-2) where compounds 8, 9, 12, and 15 exhibited an outstanding potency in comparison with sorafenib, with IC50 values of 6.7-8.9 nM. Sorafenib 196-205 kinase insert domain receptor Homo sapiens 102-109 29628325-6 2018 Molecular docking for the most potent compounds was performed to predict their possible binding mode within VEGFR2 active site and they showed binding affinity in a similar way to sorafenib. Sorafenib 180-189 kinase insert domain receptor Homo sapiens 108-114 30502686-8 2019 Ortho-chloro substituted urea 5 and ortho-bromo substituted urea 8 were the most active ones in both down-regulation of VEGFR-2 and inhibition of the kinase activity of this receptor, with better results than those obtained with sunitinib and sorafenib. Sorafenib 243-252 kinase insert domain receptor Homo sapiens 120-127 29739298-11 2018 CONCLUSIONS: Overall, our data may suggest that polymorphism analysis of the VEGF, VEGFR-2, HIF and eNOS genes can identify HCC patients who are more likely to benefit from sorafenib. Sorafenib 173-182 kinase insert domain receptor Homo sapiens 83-90 30194077-6 2018 For example, in glioblastoma multiforme, two target genes (FLT1, FLT3) of the experimental drug sorafenib were recurrently deleted, whereas another target (KDR) of sorafenib was recurrently amplified. Sorafenib 96-105 kinase insert domain receptor Homo sapiens 156-159 30194077-6 2018 For example, in glioblastoma multiforme, two target genes (FLT1, FLT3) of the experimental drug sorafenib were recurrently deleted, whereas another target (KDR) of sorafenib was recurrently amplified. Sorafenib 164-173 kinase insert domain receptor Homo sapiens 156-159 29527631-0 2018 Phase II trial of ifosfamide in combination with the VEGFR inhibitor sorafenib in advanced soft tissue sarcoma: a Spanish group for research on sarcomas (GEIS) study. Sorafenib 69-78 kinase insert domain receptor Homo sapiens 53-58 29631788-0 2018 Design and discovery of thioether and nicotinamide containing sorafenib analogues as multikinase inhibitors targeting B-Raf, B-RafV600E and VEGFR-2. Sorafenib 62-71 kinase insert domain receptor Homo sapiens 140-147 29631788-1 2018 New sorafenib derivatives containing thioether and nicotinamide moiety were designed and synthesized as B-Raf, B-RafV600E and VEGFR-2 multikinase inhibitors. Sorafenib 4-13 kinase insert domain receptor Homo sapiens 126-133 29328399-0 2018 miR-378a enhances the sensitivity of liver cancer to sorafenib by targeting VEGFR, PDGFRbeta and c-Raf. Sorafenib 53-62 kinase insert domain receptor Homo sapiens 76-81 29881824-4 2018 Although sorafenib is an inhibitor of multiple kinases, including serine/threonine-protein kinase c-Raf, serine/threonine-protein kinase B-Raf, vascular endothelial growth factor receptor (VEGFR)-1, VEGFR-2, VEGFR-3, and platelet-derived growth factor receptor beta, HCC cells are able to escape from sorafenib treatment using other pathways that the drug insufficiently inhibits. Sorafenib 9-18 kinase insert domain receptor Homo sapiens 199-206 29313954-2 2018 In the current study, the authors conducted a phase 1/2 study of sorafenib (an inhibitor of Raf kinase and vascular endothelial growth factor receptor 2 [VEGFR-2]) and the mTOR inhibitor temsirolimus in patients with recurrent glioblastoma. Sorafenib 65-74 kinase insert domain receptor Homo sapiens 107-152 29313954-2 2018 In the current study, the authors conducted a phase 1/2 study of sorafenib (an inhibitor of Raf kinase and vascular endothelial growth factor receptor 2 [VEGFR-2]) and the mTOR inhibitor temsirolimus in patients with recurrent glioblastoma. Sorafenib 65-74 kinase insert domain receptor Homo sapiens 154-161 29554654-9 2018 This article reviews the literature behind the preclinical and clinical data of the combination of RT with VEGFR-TKIs currently approved for RCC (sunitinib, sorafenib, pazopanib, and axitinib), with a focus on dose schedules as well as efficacy and toxicity. Sorafenib 157-166 kinase insert domain receptor Homo sapiens 107-112 29323750-2 2018 Additionally, molecular docking was carried out to study their binding pattern and binding affinity in the VEGFR-2 active site using sorafenib as a reference VEGFR-2 inhibitor. Sorafenib 133-142 kinase insert domain receptor Homo sapiens 107-114 29323750-2 2018 Additionally, molecular docking was carried out to study their binding pattern and binding affinity in the VEGFR-2 active site using sorafenib as a reference VEGFR-2 inhibitor. Sorafenib 133-142 kinase insert domain receptor Homo sapiens 158-165 29323750-5 2018 Moreover, compound 18b was the most potent VEGFR-2 inhibitor with an IC50 value of 0.07 muM, which is more potent than that of sorafenib (0.09 muM). Sorafenib 127-136 kinase insert domain receptor Homo sapiens 43-50 29295519-0 2017 Design and Discovery of Quinazoline- and Thiourea-Containing Sorafenib Analogs as EGFR and VEGFR-2 Dual TK Inhibitors. Sorafenib 61-70 kinase insert domain receptor Homo sapiens 91-98 29289530-9 2018 This model enables the study of anti-angiogenic drugs which target a specific factor/receptor pathway, as demonstrated by the use of the clinically approved sorafenib and sunitinib for targeting the VEGF-A/VEGFR-2 pathway. Sorafenib 157-166 kinase insert domain receptor Homo sapiens 206-213 29651967-4 2018 The objective of present research work is the synthesis of new agents with the same essential pharmacophoric features of the reported and clinically used VEGFR-2 inhibitors (e.g vatalanib and sorafenib). Sorafenib 192-201 kinase insert domain receptor Homo sapiens 154-161 29651967-10 2018 Sorafenib as a highly potent VEGFR-2 inhibitor was used as a reference drug with IC50 of 5.47+-0.3 and 7.26+-0.3 microM respectively. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 29-36 29651967-12 2018 Compounds 6o, 6m, 6d and 9b emerged as the most active counterparts against VEGFR-2 with IC50 values of 0.1+-0.01, 0.15+-0.02, 0.28+-0.03 and 0.38+-0.04 microM, respectively comparable to that of sorafenib (IC50 = 0.1+-0.02) microM. Sorafenib 196-205 kinase insert domain receptor Homo sapiens 76-83 29295519-2 2017 In this work, a series of novel quinazoline- and thiourea-containing sorafenib analogs (10a-v) were designed and synthesized as EGFR and VEGFR-2 dual TK inhibitors. Sorafenib 69-78 kinase insert domain receptor Homo sapiens 137-144 30050861-1 2017 Sorafenib is a multi-target small molecule inhibitor of the RAF kinase family and VEGFR-2/PDGFR. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 82-89 29131379-3 2017 Eleven compounds in this series were further evaluated for their inhibitory activity against VEGFR-2, where compounds 7a, 7b, 8c, and 8b also showed the highest VEGFR-2 inhibition with IC50 of 0.11 +- 0.01, 0.31 +- 0.03, 0.72 +- 0.08, and 0.91 +- 0.08 muM, respectively, in comparison to sorafenib as reference ligand with IC50 of 0.1 +- 0.02. Sorafenib 288-297 kinase insert domain receptor Homo sapiens 93-100 27981515-0 2017 Preliminary data of VEGF-A and VEGFR-2 polymorphisms as predictive factors of radiological response and clinical outcome in iodine-refractory differentiated thyroid cancer treated with sorafenib. Sorafenib 185-194 kinase insert domain receptor Homo sapiens 31-38 28817373-1 2017 Purpose Sorafenib and lenvatinib are oral multikinase inhibitors targeting vascular endothelial growth factor receptor (VEGFR) and approved for radioiodine (RAI)-refractory differentiated thyroid cancer (DTC). Sorafenib 8-17 kinase insert domain receptor Homo sapiens 75-118 28817373-1 2017 Purpose Sorafenib and lenvatinib are oral multikinase inhibitors targeting vascular endothelial growth factor receptor (VEGFR) and approved for radioiodine (RAI)-refractory differentiated thyroid cancer (DTC). Sorafenib 8-17 kinase insert domain receptor Homo sapiens 120-125 28925739-8 2017 In addition, these compounds revealed good binding within VEGFR2 tyrosine kinase enzyme in comparison with sorafenib reference. Sorafenib 107-116 kinase insert domain receptor Homo sapiens 58-64 28243971-0 2017 Erratum to: Preliminary data of VEGF-A and VEGFR-2 polymorphisms as predictive factors of radiological response and clinical outcome in iodine-refractory differentiated thyroid cancer treated with sorafenib. Sorafenib 197-206 kinase insert domain receptor Homo sapiens 43-50 28276433-5 2017 However, over the past decade, marked advances in the treatment of metastatic RCC have been made, with targeted agents including sorafenib, sunitinib, bevacizumab, pazopanib and axitinib, which inhibit vascular endothelial growth factor (VEGF) and its receptor (VEGFR), and everolimus and temsirolimus, which inhibit mechanistic target of rapamycin complex 1 (mTORC1), being approved. Sorafenib 129-138 kinase insert domain receptor Homo sapiens 262-267 29029413-1 2017 Sorafenib is a multiple kinase inhibitor which targets Raf kinases, VEGFR, and PDGFR and is approved for the treatment of hepatocellular carcinoma (HCC). Sorafenib 0-9 kinase insert domain receptor Homo sapiens 68-73 27936391-3 2017 The anti-proliferative effects and differential expressions of 8 genes related to sorafenib anti-cancer mechanisms (tyrosine kinase receptor genes: KDR, PDGFRB; RAF cascade: RAF1, BRAF, MAP2K1, MAP2K2, MAPK1, MAPK3) were investigated in primary cultured hepatocellular carcinoma cells collected from 8 patients using clinically applied sorafenib concentrations (5, 10mug/mL). Sorafenib 82-91 kinase insert domain receptor Homo sapiens 148-151 27936391-4 2017 The anti-proliferative effects of sorafenib at either 5 or 10mug/mL, which were related to down-regulations of KDR, PDGFRB and/or genes in the RAF cascade, were achieved only in one patient (HCC38/KMUH). Sorafenib 34-43 kinase insert domain receptor Homo sapiens 111-114 27936391-7 2017 Increase the sorafenib concentration to 10mug/mL paradoxically up-regulated and/or obliterated the previously down-regulated genes in the RAF cascade and/or KDR in 4 patients (HCC29/KMUH, HCC76/KMUH, HCC87/KMUH, HCC98/KMUH). Sorafenib 13-22 kinase insert domain receptor Homo sapiens 157-160 27936391-10 2017 The responses of KDR, PDGFRB and the RAF cascade to sorafenib among patients are diverse or even contrary. Sorafenib 52-61 kinase insert domain receptor Homo sapiens 17-20 28352319-1 2017 The aim of the current study was to demonstrate the distribution of VEGFR-2 on glioma microvascular endothelial cells on a nanoscale and investigate changes in VEGFR-2 activity following treatment with the VEGFR-2 inhibitor and agonist sorafenib and bradykinin, respectively. Sorafenib 236-245 kinase insert domain receptor Homo sapiens 68-75 28352319-3 2017 Changes in the activity of VEGFR-2 on the glioma microvascular endothelial cell membranes following treatment with sorafenib and bradykinin were characterized by atomic force microscopy (AFM). Sorafenib 115-124 kinase insert domain receptor Homo sapiens 27-34 28352319-10 2017 The distribution and activity of VEGFR-2 on glioma microvascular endothelial cell membranes treated with sorafenib and bradykinin suggested that the activity of VEGFR-2 could be regulated by its inhibitor or agonist. Sorafenib 105-114 kinase insert domain receptor Homo sapiens 33-40 28352319-10 2017 The distribution and activity of VEGFR-2 on glioma microvascular endothelial cell membranes treated with sorafenib and bradykinin suggested that the activity of VEGFR-2 could be regulated by its inhibitor or agonist. Sorafenib 105-114 kinase insert domain receptor Homo sapiens 161-168 27082062-1 2016 UNLABELLED: Angiogenesis inhibition by the vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR) inhibitor sorafenib provides survival benefit in hepatocellular carcinoma (HCC); however, angiogenic escape from sorafenib may occur due to angiogenesis-associated fibroblast growth factor receptor (FGFR) pathway activation. Sorafenib 260-269 kinase insert domain receptor Homo sapiens 43-86 27855595-1 2017 BACKGROUND: Sorafenib is an important VEGFR2/KDR inhibitor which is widely used for the treatment of cancer. Sorafenib 12-21 kinase insert domain receptor Homo sapiens 38-44 27855595-1 2017 BACKGROUND: Sorafenib is an important VEGFR2/KDR inhibitor which is widely used for the treatment of cancer. Sorafenib 12-21 kinase insert domain receptor Homo sapiens 45-48 27777009-1 2016 Two series of sorafenib derivatives (N-methylpicolinamide-4-oxy) chalcones (5a-o, 7a-e) were synthesized and characterized by NMR and MS. All of the target compounds were evaluated for the cytotoxicity against A549, HepG2, MCF-7, and PC-3 cancer cell lines and some selected compounds were further evaluated for the activity against VEGFR-2/KDR and BRAF kinases. Sorafenib 14-23 kinase insert domain receptor Homo sapiens 333-340 27777009-1 2016 Two series of sorafenib derivatives (N-methylpicolinamide-4-oxy) chalcones (5a-o, 7a-e) were synthesized and characterized by NMR and MS. All of the target compounds were evaluated for the cytotoxicity against A549, HepG2, MCF-7, and PC-3 cancer cell lines and some selected compounds were further evaluated for the activity against VEGFR-2/KDR and BRAF kinases. Sorafenib 14-23 kinase insert domain receptor Homo sapiens 341-344 27082062-1 2016 UNLABELLED: Angiogenesis inhibition by the vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR) inhibitor sorafenib provides survival benefit in hepatocellular carcinoma (HCC); however, angiogenic escape from sorafenib may occur due to angiogenesis-associated fibroblast growth factor receptor (FGFR) pathway activation. Sorafenib 260-269 kinase insert domain receptor Homo sapiens 88-93 27558799-6 2016 Then, the binding energy of the four molecules to VEGFR-2 tyrosine kinase was calculated using molecular docking, and their values were found to be lower than that of Sorafenib. Sorafenib 167-176 kinase insert domain receptor Homo sapiens 50-57 26723100-7 2016 ORR was improved with selective VEGFR inhibitors, with 91% increased odds over sorafenib (odds ratio 1.91; 95% confidence interval 1.35-2.69). Sorafenib 79-88 kinase insert domain receptor Homo sapiens 32-37 27030639-4 2016 Here we report the first case of a patient with perivascular epithelioid cell tumor whose disease had a rapid progression after surgery and had a rapid remarkable response of combination therapy of a VEGFR inhibitor, sorafenib, with an mTOR inhibitor, sirolimus. Sorafenib 217-226 kinase insert domain receptor Homo sapiens 200-205 27089255-7 2016 Since sorafenib has an anti-angiogenic effect by its inhibitory targeting VEGFR, we hypothesized that sorafenib could complement the anti-cancer effect of iron depletion. Sorafenib 6-15 kinase insert domain receptor Homo sapiens 74-79 27089255-7 2016 Since sorafenib has an anti-angiogenic effect by its inhibitory targeting VEGFR, we hypothesized that sorafenib could complement the anti-cancer effect of iron depletion. Sorafenib 102-111 kinase insert domain receptor Homo sapiens 74-79 27058899-1 2016 Sorafenib may reduce endothelial nitric oxide synthase (eNOS) activity by inhibiting vascular endothelial growth factor receptors (VEGF-R), leading to a decrease in nitric oxide production. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 85-129 27058899-1 2016 Sorafenib may reduce endothelial nitric oxide synthase (eNOS) activity by inhibiting vascular endothelial growth factor receptors (VEGF-R), leading to a decrease in nitric oxide production. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 131-137 26723100-10 2016 CONCLUSION: Although selective VEGFR inhibitors are associated with similar overall survival as multikinase inhibitor sorafenib, they show significant improvement in progression-free survival, regardless of first-line or later use, and ORR compared with sorafenib. Sorafenib 254-263 kinase insert domain receptor Homo sapiens 31-36 27160228-5 2016 The patient was initially treated with sorafenib, an inhibitor of VEGFR2, and developed progressive disease. Sorafenib 39-48 kinase insert domain receptor Homo sapiens 66-72 26439451-1 2016 BACKGROUND: Sorafenib and sunitinib are oral vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs) approved in 2005 and 2006, respectively, for the treatment of patients with renal cell carcinoma (RCC). Sorafenib 12-21 kinase insert domain receptor Homo sapiens 45-88 26830973-8 2016 Our results suggest that polymorphisms in VEGF and VEGFR2 are associated with sorafenib clinical outcomes, and polymorphisms in VEGF and ABCB1 are associated with sorafenib-related toxicities. Sorafenib 78-87 kinase insert domain receptor Homo sapiens 51-57 26350096-7 2016 Recent clinical studies have revealed that sorafenib, a pan-RAF and VEGFR inhibitor, has impressive benefits for KRAS mutant lung cancer patients. Sorafenib 43-52 kinase insert domain receptor Homo sapiens 68-73 26861740-2 2016 Sorafenib works synergistically with radiation and inhibits Ras/Raf, PDFGR, and VEGFR. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 80-85 26439451-1 2016 BACKGROUND: Sorafenib and sunitinib are oral vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs) approved in 2005 and 2006, respectively, for the treatment of patients with renal cell carcinoma (RCC). Sorafenib 12-21 kinase insert domain receptor Homo sapiens 90-95 26237499-3 2015 Sorafenib is a small molecule that blocks the activation of C-RAF, B-RAF, c-KIT, FLT-3, RET, VEGFR-2, VEGFR-3 and PDGFR approved for advanced renal cell and hepatocellular carcinoma (b, c). Sorafenib 0-9 kinase insert domain receptor Homo sapiens 93-100 26482392-3 2015 Since the approval of sorafenib, an inhibitor of vascular endothelial growth factor receptor (VEGFR), in December 2005, 7 drugs have been introduced that have provided a high level of clinical efficacy in patients with mRCC, with a median survival of ~30 months in an unselected patient population that generally fits trials eligibility. Sorafenib 22-31 kinase insert domain receptor Homo sapiens 49-92 26482392-3 2015 Since the approval of sorafenib, an inhibitor of vascular endothelial growth factor receptor (VEGFR), in December 2005, 7 drugs have been introduced that have provided a high level of clinical efficacy in patients with mRCC, with a median survival of ~30 months in an unselected patient population that generally fits trials eligibility. Sorafenib 22-31 kinase insert domain receptor Homo sapiens 94-99 26648069-1 2016 Sorafenib is a small molecular inhibitor of intracellular tyrosine and serine/threonine protein kinases (VEGFR, PDGFR, CRAF and BRAF), and is thought also to induce autophagy, a chief mechanism influencing tumor growth. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 105-110 25861837-13 2015 CONCLUSION: We report the results of a trial that combined cetuximab and sorafenib for the treatment of KRAS-mutated mCRC, with correlative imaging studies and pharmacodynamic angiogenic cytokine profiling as downstream markers of EGFR and VEGF receptor (VEGFR) signaling. Sorafenib 73-82 kinase insert domain receptor Homo sapiens 240-253 25861837-13 2015 CONCLUSION: We report the results of a trial that combined cetuximab and sorafenib for the treatment of KRAS-mutated mCRC, with correlative imaging studies and pharmacodynamic angiogenic cytokine profiling as downstream markers of EGFR and VEGF receptor (VEGFR) signaling. Sorafenib 73-82 kinase insert domain receptor Homo sapiens 255-260 26042424-1 2015 Inhibitors of VEGF receptor (VEGFR) signaling such as sorafenib and sunitinib that are currently used in the treatment of malignant diseases have been shown to affect immunological responses by inhibition of the function of antigen presenting cells and T lymphocytes. Sorafenib 54-63 kinase insert domain receptor Homo sapiens 14-27 26497860-1 2015 Sorafenib is a tyrosine kinase inhibitor (TKI) of the vascular endothelial growth factor receptor (VEGFR) used for advanced renal cell carcinoma. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 54-97 26497860-1 2015 Sorafenib is a tyrosine kinase inhibitor (TKI) of the vascular endothelial growth factor receptor (VEGFR) used for advanced renal cell carcinoma. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 99-104 26169036-0 2015 Inhibition of MAPK and VEGFR by Sorafenib Controls the Progression of Endometriosis. Sorafenib 32-41 kinase insert domain receptor Homo sapiens 23-28 26169036-1 2015 INTRODUCTION: Sorafenib is a strong multikinase inhibitor targeting 2 different pathways of endometriosis pathogenesis: RAF kinase and vascular endothelial growth factor receptor (VEGFR). Sorafenib 14-23 kinase insert domain receptor Homo sapiens 135-178 26169036-1 2015 INTRODUCTION: Sorafenib is a strong multikinase inhibitor targeting 2 different pathways of endometriosis pathogenesis: RAF kinase and vascular endothelial growth factor receptor (VEGFR). Sorafenib 14-23 kinase insert domain receptor Homo sapiens 180-185 26169036-7 2015 In addition, this study highlights the antiangiogenic role of Sorafenib which translates as a decreased phosphorylated VEGFR-2-VEGFR-2 ratio in endometriosis. Sorafenib 62-71 kinase insert domain receptor Homo sapiens 119-126 26169036-7 2015 In addition, this study highlights the antiangiogenic role of Sorafenib which translates as a decreased phosphorylated VEGFR-2-VEGFR-2 ratio in endometriosis. Sorafenib 62-71 kinase insert domain receptor Homo sapiens 127-134 26314892-4 2015 The increase in endothelial activation was associated with an increase in the VEGFR2 to VEGFR1 ratio, which neutralized the tumor-suppressive effect of VEGFR-targeting sorafenib. Sorafenib 168-177 kinase insert domain receptor Homo sapiens 78-84 26314892-4 2015 The increase in endothelial activation was associated with an increase in the VEGFR2 to VEGFR1 ratio, which neutralized the tumor-suppressive effect of VEGFR-targeting sorafenib. Sorafenib 168-177 kinase insert domain receptor Homo sapiens 78-83 25816720-9 2015 In sorafenib-treated patients, VEGFR2 rs2071559 (G/G vs. A/A) was associated with longer OS (26.8 vs. 13.8 months; HR, 0.41; Padjusted = .030). Sorafenib 3-12 kinase insert domain receptor Homo sapiens 31-37 25816720-10 2015 In multivariate analyses, no SNP predicted axitinib efficacy; VEGFR2 rs2071559 predicted PFS (P = .0053) and OS (P = .0027) for sorafenib. Sorafenib 128-137 kinase insert domain receptor Homo sapiens 62-68 25816720-13 2015 Although VEGFR2 rs2071559 predicted sorafenib efficacy in patients with mRCC, sensitivity/specificity limitations preclude its use for selecting individual patients for sorafenib treatment. Sorafenib 36-45 kinase insert domain receptor Homo sapiens 9-15 25559745-0 2015 Expression of pERK and VEGFR-2 in advanced hepatocellular carcinoma and resistance to sorafenib treatment. Sorafenib 86-95 kinase insert domain receptor Homo sapiens 23-30 25559745-9 2015 CONCLUSIONS: Elevated tissue expression of pERK and VEGFR-2 was predictive of poor outcome in advanced HCC treated with sorafenib. Sorafenib 120-129 kinase insert domain receptor Homo sapiens 52-59 26187792-7 2015 Furthermore, the expression of VEGF-A, VEGF-C, VEGF-D, VEGFR-2 and VEGFR-3 at protein/mRNA levels in the process of lymphatic tube formation in vitro and tumor lymphangiogenesis in vivo was downregulated; NCTD in combination with mF4-31C1 or Sorafenib enhanced these effects. Sorafenib 242-251 kinase insert domain receptor Homo sapiens 55-62 25823619-4 2015 Sorafenib blocks angiogenesis and tumor cell proliferation through inhibition of kinases, such as VEGFR2, PDGFR, or the serine/threonine kinases RAF. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 98-104 26275293-3 2015 We evaluated the efficacy of sorafenib, a broad spectrum tyrosine kinase inhibitor targeting VEGFR2 and PDGFR as well as RET and RAF1, in patients with metastatic chemotherapy refractory esophageal and GE junction cancer. Sorafenib 29-38 kinase insert domain receptor Homo sapiens 93-99 26042424-1 2015 Inhibitors of VEGF receptor (VEGFR) signaling such as sorafenib and sunitinib that are currently used in the treatment of malignant diseases have been shown to affect immunological responses by inhibition of the function of antigen presenting cells and T lymphocytes. Sorafenib 54-63 kinase insert domain receptor Homo sapiens 29-34 25551444-0 2014 NSK-01105, a novel sorafenib derivative, inhibits human prostate tumor growth via suppression of VEGFR2/EGFR-mediated angiogenesis. Sorafenib 19-28 kinase insert domain receptor Homo sapiens 97-103 25413440-3 2015 We previously performed a structure-activity relationship study on a series of sorafenib analogues designed to investigate the inhibition overlap between the major targets of sorafenib Raf-1 kinase and VEGFR-2, and an enzyme shown to be a potent off-target of sorafenib, soluble epoxide hydrolase. Sorafenib 79-88 kinase insert domain receptor Homo sapiens 202-209 25605317-1 2015 INTRODUCTION: Sorafenib (Nexavar) is an oral multi-kinase inhibitor targeting B-type Raf kinase (BRAF) (both wild type and BRAF(V600E)), VEGFR1, VEGFR2, VEGFR3, PDGFRbeta and RET (also RET/PTC) influencing both differentiated thyroid cancer (DTC) cell proliferation and angiogenesis. Sorafenib 14-23 kinase insert domain receptor Homo sapiens 145-151 25605317-1 2015 INTRODUCTION: Sorafenib (Nexavar) is an oral multi-kinase inhibitor targeting B-type Raf kinase (BRAF) (both wild type and BRAF(V600E)), VEGFR1, VEGFR2, VEGFR3, PDGFRbeta and RET (also RET/PTC) influencing both differentiated thyroid cancer (DTC) cell proliferation and angiogenesis. Sorafenib 25-32 kinase insert domain receptor Homo sapiens 145-151 25363205-2 2015 Sorafenib, a tyrosine kinase inhibitor of vascular endothelial growth factor receptor (VEGFR), combined with bevacizumab, a monoclonal antibody to vascular endothelial growth factor (VEGF-A), would vertically inhibit VEGF/VEGFR signaling. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 42-85 25363205-2 2015 Sorafenib, a tyrosine kinase inhibitor of vascular endothelial growth factor receptor (VEGFR), combined with bevacizumab, a monoclonal antibody to vascular endothelial growth factor (VEGF-A), would vertically inhibit VEGF/VEGFR signaling. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 87-92 25336977-9 2014 Among different VEGFR-TKIs, sorafenib and sunitinib had significant risk of death when compared with control arms, respectively. Sorafenib 28-37 kinase insert domain receptor Homo sapiens 16-21 24927771-1 2014 We performed a systematic review and meta-analysis of thyroid function abnormalities associated with seven vascular endothelial growth factor receptor (VEGFR) targeted tyrosine kinase inhibitors (sorafenib, sunitinib, axitinib, cediranib, pazopanib, regorafenib and vandetanib). Sorafenib 196-205 kinase insert domain receptor Homo sapiens 107-150 24927771-1 2014 We performed a systematic review and meta-analysis of thyroid function abnormalities associated with seven vascular endothelial growth factor receptor (VEGFR) targeted tyrosine kinase inhibitors (sorafenib, sunitinib, axitinib, cediranib, pazopanib, regorafenib and vandetanib). Sorafenib 196-205 kinase insert domain receptor Homo sapiens 152-157 25087655-5 2014 Although 4 cases received bevacizumab (anti-VEGF-A), one was given sorafenib (small molecule tyrosine kinase inhibitor affecting VEGF-R2). Sorafenib 67-76 kinase insert domain receptor Homo sapiens 129-136 24510746-4 2014 The aim of our study was to evaluate the role of VEGF and VEGFR polymorphisms in determining the clinical outcome of HCC patients receiving sorafenib. Sorafenib 140-149 kinase insert domain receptor Homo sapiens 58-63 24510746-9 2014 Once prospectively validated, the analysis of VEGF and VEGFR SNPs may represent a clinical tool to better identify HCC patients more likely to benefit from sorafenib. Sorafenib 156-165 kinase insert domain receptor Homo sapiens 55-60 25299731-1 2014 A detailed atomistic description of the unbinding process of sorafenib and sunitinib, two known VEGFR2 inhibitors clinically used to treat renal cell carcinoma, was unraveled by using steered molecular dynamics (SMD) simulations. Sorafenib 61-70 kinase insert domain receptor Homo sapiens 96-102 24849467-7 2014 In high VEGFR1/2-expressing HepG2 cells, sorafenib treatment inhibited cell proliferation, reduced VEGFR2 mRNA expression in vitro, and delayed xenograft tumor growth in vivo. Sorafenib 41-50 kinase insert domain receptor Homo sapiens 99-105 25182707-0 2014 The relationship of kinase insert domain receptor gene polymorphisms and clinical outcome in advanced hepatocellular carcinoma patients treated with sorafenib. Sorafenib 149-158 kinase insert domain receptor Homo sapiens 20-49 25182707-2 2014 Our aim was to determine whether single-nucleotide polymorphisms (SNPs) in KDR gene are associated with clinical outcomes after first-line sorafenib therapy in advanced hepatocellular carcinoma (HCC). Sorafenib 139-148 kinase insert domain receptor Homo sapiens 75-78 25182707-3 2014 The SNPs in KDR were tested in 78 advanced HCC patients receiving first-line sorafenib. Sorafenib 77-86 kinase insert domain receptor Homo sapiens 12-15 25182707-8 2014 Our results suggest that SNPs in KDR gene can predict clinical outcome in advanced HCC patients receiving first-line sorafenib. Sorafenib 117-126 kinase insert domain receptor Homo sapiens 33-36 24803676-2 2014 Sorafenib is a multikinase inhibitor targeting BRAF, VEGFR, PDGFR, and c-kit. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 53-58 24127298-11 2014 Treatment with VEGFR TKIs sorafenib, sunitinib and pazopanib is associated with a significant increase in the risk of GI events in patients with cancer, and frequent clinical monitoring should be emphasized when managing these three and newer VEGFR TKIs. Sorafenib 26-35 kinase insert domain receptor Homo sapiens 15-20 24127298-11 2014 Treatment with VEGFR TKIs sorafenib, sunitinib and pazopanib is associated with a significant increase in the risk of GI events in patients with cancer, and frequent clinical monitoring should be emphasized when managing these three and newer VEGFR TKIs. Sorafenib 26-35 kinase insert domain receptor Homo sapiens 243-248 24661286-4 2014 Inhibition of VEGFR was associated with tumor activity in preclinical models of synovial sarcoma and drugs such as sorafenib, pazopanib and bevacizumab have been employed in synovial sarcoma in monotherapy and in combination with chemotherapy. Sorafenib 115-124 kinase insert domain receptor Homo sapiens 14-19 24773940-2 2014 Sorafenib (Nexavar), a multi-kinase inhibitor targeting Raf kinase, vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor, has shown promising results in the treatment of malignancies. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 68-111 24773940-2 2014 Sorafenib (Nexavar), a multi-kinase inhibitor targeting Raf kinase, vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor, has shown promising results in the treatment of malignancies. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 113-118 24773940-2 2014 Sorafenib (Nexavar), a multi-kinase inhibitor targeting Raf kinase, vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor, has shown promising results in the treatment of malignancies. Sorafenib 11-18 kinase insert domain receptor Homo sapiens 68-111 24773940-2 2014 Sorafenib (Nexavar), a multi-kinase inhibitor targeting Raf kinase, vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor, has shown promising results in the treatment of malignancies. Sorafenib 11-18 kinase insert domain receptor Homo sapiens 113-118 24773940-5 2014 In this case, VEGFR inhibition caused by sorafenib alone may have contributed to the development of psychosis. Sorafenib 41-50 kinase insert domain receptor Homo sapiens 14-19 24817603-16 2014 CONCLUSIONS: Combined VEGF/VEGFR blockade using bevacizumab with sorafenib shows clinical activity. Sorafenib 65-74 kinase insert domain receptor Homo sapiens 27-32 24714776-1 2014 PURPOSE: Sorafenib is an inhibitor of VEGF receptor (VEGFR), platelet-derived growth factor receptor (PDGFR), and RAF kinases, amongst others. Sorafenib 9-18 kinase insert domain receptor Homo sapiens 38-51 24687604-5 2014 Sorafenib-the first-line drug in advanced HCC-targets multiple kinases, including VEGFRs, but has only an overall mild beneficial effect. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 82-88 24375110-0 2014 VEGFR, RET, and RAF/MEK/ERK pathway take part in the inhibition of osteosarcoma MG63 cells with sorafenib treatment. Sorafenib 96-105 kinase insert domain receptor Homo sapiens 0-5 24375110-5 2014 In the present study, we performed assays of cell proliferation, RT-PCR, and western blot to investigate the effect of sorafenib on OS MG63 cells and to elucidate the molecular actions of sorafenib against RTKs VEGFR2 and RET, as well as MEK/ERK signaling pathway. Sorafenib 188-197 kinase insert domain receptor Homo sapiens 211-217 24375110-6 2014 The present study confirmed that sorafenib could inhibit the proliferation of OS MG63 cells and caused a series of biomolecule effects, including the change of VEGFR2 and ERK gene expression, and the phosphorylation alteration of VEGFR2, RET, and MEK1 proteins. Sorafenib 33-42 kinase insert domain receptor Homo sapiens 160-166 24375110-6 2014 The present study confirmed that sorafenib could inhibit the proliferation of OS MG63 cells and caused a series of biomolecule effects, including the change of VEGFR2 and ERK gene expression, and the phosphorylation alteration of VEGFR2, RET, and MEK1 proteins. Sorafenib 33-42 kinase insert domain receptor Homo sapiens 230-236 24375110-7 2014 VEGFR2, RET, and MEK/ERK signaling pathway are involved in the pharmacological mechanism of sorafenib. Sorafenib 92-101 kinase insert domain receptor Homo sapiens 0-6 24714776-1 2014 PURPOSE: Sorafenib is an inhibitor of VEGF receptor (VEGFR), platelet-derived growth factor receptor (PDGFR), and RAF kinases, amongst others. Sorafenib 9-18 kinase insert domain receptor Homo sapiens 53-58 24420556-1 2014 OBJECTIVES: Sorafenib is a multi-tyrosine kinase inhibitor of Raf kinase, VEGFR, and PDGFR. Sorafenib 12-21 kinase insert domain receptor Homo sapiens 74-79 24460304-2 2013 Sorafenib is an oral multi-kinase inhibitor exerting its effects via the RAF/ MEK/ERK pathway, vascular endothelial growth factor receptor (VEGFR) and platelet derived growth factor receptor beta (PDGFR-beta) tyrosine kinases. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 95-138 24743196-3 2014 Sorafenib, sunitinib, axitinib, and pazopanib are kinase inhibitors that block vascular endothelial growth factor receptor(VEGFR). Sorafenib 0-9 kinase insert domain receptor Homo sapiens 123-128 24416138-1 2014 PURPOSE: Sorafenib, an oral inhibitor of B-raf, VEGFR2, and PDGFR2-beta, acts against pancreatic cancer in preclinical models. Sorafenib 9-18 kinase insert domain receptor Homo sapiens 48-54 24096267-2 2014 The anti-tumor effect of sorafenib is thought to be mediated through its inhibition of the RAS-Raf-Erk pathway, as well as its inhibition of VEGFR and PDGFR. Sorafenib 25-34 kinase insert domain receptor Homo sapiens 141-146 24309512-3 2014 (2) Some of the anti-tumor effects of sorafenib have been ascribed to anti-angiogenic actions of this agent on endothelial associated kinases such as VEGFR2. Sorafenib 38-47 kinase insert domain receptor Homo sapiens 150-156 24549815-2 2014 In the present study, we selected sorafenib (SOR), a VEGFR inhibitor, in combination with celecoxib (CXB), a COX-2 inhibitor, for suppressing tumor growth and simultaneously for reducing doses of both drugs for the treatment of NSCLC. Sorafenib 34-43 kinase insert domain receptor Homo sapiens 53-58 24297950-11 2014 The longer OS observed with sorafenib suggests sequenced VEGFR inhibition may benefit patients with mRCC. Sorafenib 28-37 kinase insert domain receptor Homo sapiens 57-62 23887852-1 2013 BACKGROUND: Sorafenib (a VEGFR and multi-targeted kinase inhibitor) and Bortezomib (a proteasome inhibitor) have clinical antineoplastic activities as single agents, and combine synergistically in preclinical models. Sorafenib 12-21 kinase insert domain receptor Homo sapiens 25-30 23542751-5 2013 Molecular profiling of two of the proposed targets of sorafenib, platelet-derived growth factor receptor beta and vascular endothelial growth factor receptor 2, of the patient"s tumour lesion showed high and intermediate expression levels in the tumour as compared with the surrounding non-neoplastic tissue. Sorafenib 54-63 kinase insert domain receptor Homo sapiens 114-159 23601669-2 2013 Sunitinib, sorafenib and pazopanib were the first generation of vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs) to have significant clinical activity in metastatic clear cell RCC. Sorafenib 11-20 kinase insert domain receptor Homo sapiens 64-107 23601669-2 2013 Sunitinib, sorafenib and pazopanib were the first generation of vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs) to have significant clinical activity in metastatic clear cell RCC. Sorafenib 11-20 kinase insert domain receptor Homo sapiens 109-114 23591401-1 2013 OBJECTIVES: Sorafenib, an oral multikinase inhibitor of the VEGFR/PDGFR/Raf/MEK/ERK pathway, has shown potential activity in patients with recurrent ovarian cancer (OC). Sorafenib 12-21 kinase insert domain receptor Homo sapiens 60-65 23142289-4 2013 Sorafenib selectively inhibited radiation-induced activation of vascular endothelial growth factor receptor-2 (VEGFR2) and downstream extracellular signal-regulated kinase (ERK) pathway, induced DNA damage and suppressed DNA repair capacity, decreased radiation-activated NF-kappaB and increased radiation-induced apoptosis. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 64-109 23142289-4 2013 Sorafenib selectively inhibited radiation-induced activation of vascular endothelial growth factor receptor-2 (VEGFR2) and downstream extracellular signal-regulated kinase (ERK) pathway, induced DNA damage and suppressed DNA repair capacity, decreased radiation-activated NF-kappaB and increased radiation-induced apoptosis. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 111-117 23399884-7 2013 Some antiangiogenic drugs inhibiting the VEGFR2 receptor are successfully used in clinics for the treatment of several types of tumours in synergy with chemotherapy (e.g., Nexavar( ) from Bayer, Sutent( ) from Pfizer and Votrient( ) from GlaxoSmithKline, approved by the FDA in 2005, 2006 and 2009, respectively). Sorafenib 172-179 kinase insert domain receptor Homo sapiens 41-47 23143218-12 2013 Inhibition of serum VEGF receptor 2 (VEGFR2) was inversely correlated with sorafenib steady-state concentrations (P = 0.019). Sorafenib 75-84 kinase insert domain receptor Homo sapiens 20-35 23143218-12 2013 Inhibition of serum VEGF receptor 2 (VEGFR2) was inversely correlated with sorafenib steady-state concentrations (P = 0.019). Sorafenib 75-84 kinase insert domain receptor Homo sapiens 37-43 22973961-9 2013 No direct drug interaction was detected by LC-MS/MS measurement, while lysates from A549 and H1975 cells exposed to erlotinib+sorafenib showed a significant inhibition in the phosphorylation of 16 overlapping peptides, including sites from RAF, VEGFR2, PDGFR, CDK2 and SRC, suggesting new markers to identify NSCLC patients who are likely to respond to this treatment. Sorafenib 126-135 kinase insert domain receptor Homo sapiens 245-251 24460304-2 2013 Sorafenib is an oral multi-kinase inhibitor exerting its effects via the RAF/ MEK/ERK pathway, vascular endothelial growth factor receptor (VEGFR) and platelet derived growth factor receptor beta (PDGFR-beta) tyrosine kinases. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 140-145 22651902-8 2012 All exploratory subgroup analyses indicated a trend toward an increase risk of FAEs with VEGFR TKI treatment, though the subgroup analyses reached statistical significance for renal carcinoma studies, studies utilizing placebo as the control arm, and studies evaluating sorafenib. Sorafenib 270-279 kinase insert domain receptor Homo sapiens 89-94 22006587-7 2013 Sorafenib and nutlin-3 decreased the phosphorylation of vascular endothelial growth factor receptor-2 (VEGFR-2) and ERK along with inducing p53 activity. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 56-101 22006587-7 2013 Sorafenib and nutlin-3 decreased the phosphorylation of vascular endothelial growth factor receptor-2 (VEGFR-2) and ERK along with inducing p53 activity. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 103-110 24640739-7 2013 Currently, a number of VEGFR2 inhibitors are under clinical trials (ramucirumab, cediranib) and several were approved (sunitinib, sorafenib). Sorafenib 130-139 kinase insert domain receptor Homo sapiens 23-29 23036118-9 2012 Initial efficacy of sorafenib (an inhibitor of the intracellular domain of VEGFR, PDGFR and c-Kit) and afatinib (an irreversible inhibitor of pan-HER tyrosine kinase) have been demonstrated. Sorafenib 20-29 kinase insert domain receptor Homo sapiens 75-80 22941289-0 2012 The important roles of RET, VEGFR2 and the RAF/MEK/ERK pathway in cancer treatment with sorafenib. Sorafenib 88-97 kinase insert domain receptor Homo sapiens 28-34 22941289-1 2012 AIM: To elucidate the roles of receptor tyrosine kinases RET and VEGFR2 and the RAF/MEK/ERK signaling cascade in cancer treatment with sorafenib. Sorafenib 135-144 kinase insert domain receptor Homo sapiens 65-71 22941289-7 2012 RESULTS: Sorafenib potently suppressed the activities of cRAF, VEGFR2, and RET with IC(50) values of 20.9, 4 and 0.4 nmol/L, respectively. Sorafenib 9-18 kinase insert domain receptor Homo sapiens 63-69 22941289-8 2012 Sorafenib inhibited cRAF, VEGFR2, and RET via non-ATP-competitive, ATP-competitive and mixed-type modes, respectively. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 26-32 22941289-12 2012 CONCLUSION: This study provides novel evidence that protein kinases RET and VEGFR2 play crucial roles in cancer treatment with sorafenib. Sorafenib 127-136 kinase insert domain receptor Homo sapiens 76-82 22297207-6 2012 Several multitargeted receptor tyrosine kinase inhibitors (TKIs) such as sorafenib, cediranib, and BIBF 1120, with activity against vascular endothelial growth factor receptor (VEGFR) and other proangiogenic pathways (eg, fibroblast growth factor [FGF] and platelet-derived growth factor [PDGF] pathways) are in clinical development for NSCLC. Sorafenib 73-82 kinase insert domain receptor Homo sapiens 132-175 23227538-1 2012 Sorafenib, the first oral multikinase inhibitor, can inhibit several kinases involved in tumor proliferation and angiogenesis including Raf, VEGFR, PDGFR, kit and so on. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 141-146 22641227-10 2012 Sorafenib/AZD6244 potently inhibited angiogenesis and phosphorylation of VEGFR-2, PDGFR-beta and ERK, p90RSK, p70S6K, cdk-2 and retinoblastoma. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 85-92 22665524-2 2012 Because sorafenib targets both angiogenesis-related kinases (VEGFR) and the pathogenetic kinases found in GIST (KIT or PDGFRA), the molecular basis for sorafenib efficacy in this setting remains unknown. Sorafenib 8-17 kinase insert domain receptor Homo sapiens 61-66 22711876-10 2012 We also show that beta-TRCP inhibits cell migration and decreases sensitivity to the VEGFR2 inhibitor sorafenib in poorly differentiated PTC cells. Sorafenib 102-111 kinase insert domain receptor Homo sapiens 85-91 22572725-3 2012 RECENT FINDINGS: Recent studies with oral vascular endothelial growth factor receptor (VEGFR) inhibitors such as sunitinib, sorafenib and cediranib have shown disease stabilization in patients with advanced synovial sarcoma. Sorafenib 124-133 kinase insert domain receptor Homo sapiens 42-85 22572725-3 2012 RECENT FINDINGS: Recent studies with oral vascular endothelial growth factor receptor (VEGFR) inhibitors such as sunitinib, sorafenib and cediranib have shown disease stabilization in patients with advanced synovial sarcoma. Sorafenib 124-133 kinase insert domain receptor Homo sapiens 87-92 22357220-4 2012 Sorafenib tosylate (Bay 54-9085) is an oral, small-molecule multikinase inhibitor of several targets including RAF/MEK/ERK MAP kinase signalling, VEGFR-2, VEGFR-3 and platelet-derived growth factor receptor-beta. Sorafenib 0-9 kinase insert domain receptor Homo sapiens 146-153 22483592-5 2012 Compounds 9g, 9m, 9o and 9p demonstrated competitive antiproliferative activities to sorafenib, the reference standard, while compounds 9d, 9m, and 9p showed significant inhibitory activities against the phosphorylation of VEGFR. Sorafenib 85-94 kinase insert domain receptor Homo sapiens 223-228 22519770-2 2012 sorafenib is an oral multikinase inhibitor that targets Raf/mitogen-activated protein (MAP) kinase/extracellular signal-regulated kinase (ERK) (Raf/MEK/ERK) and several tyrosine kinases (VEGFR-2, VEGFR-3, PDGFR-beta) that has shown efficacy in hepatocellular carcinoma (HCC). Sorafenib 0-9 kinase insert domain receptor Homo sapiens 187-194 23983378-12 2012 The IC50 value of KDR of BB1-10 is less than sorafenib. Sorafenib 45-54 kinase insert domain receptor Homo sapiens 18-21 22394203-1 2012 INTRODUCTION: Sorafenib is an orally available multi-kinase inhibitor that inhibits tumor proliferation by targeting multiple kinases including the vascular endothelial growth factor receptors VEGFR1, VEGFR2, VEGFR3 and the platelet-derived growth factor receptor PDGFR, and it targets tumor progression by inhibiting FLT3, C-Kit and BRAF. Sorafenib 14-23 kinase insert domain receptor Homo sapiens 201-207 22190165-4 2012 Here, we report the in vitro antilymphoma activity of sorafenib, an inhibitor of VEGFR and Raf kinase. Sorafenib 54-63 kinase insert domain receptor Homo sapiens 81-86