PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24691568-6 2014 With subsequent molecular dynamic (MD) simulation and MM/GBSA binding free energy calculation and energy decomposition, we identified chlorhexidine and sorafenib as potential "new use" drugs targeting wild-type ABL1, while nicergoline and plerixafor targeted T315I ABL1. Sorafenib 152-161 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 211-215 24691568-6 2014 With subsequent molecular dynamic (MD) simulation and MM/GBSA binding free energy calculation and energy decomposition, we identified chlorhexidine and sorafenib as potential "new use" drugs targeting wild-type ABL1, while nicergoline and plerixafor targeted T315I ABL1. Sorafenib 152-161 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 265-269 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 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 149-152 20350535-3 2010 With the success of targeting other oncogenic kinases such as BCR-ABL, KIT or members of the epidermal-growth factor receptor (EGFR) family in other cancers, the expectations were high when the first RAF kinase-targeting drug (sorafenib) reached clinical trials. Sorafenib 227-236 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 62-69 20337484-2 2010 c-Abl and b-Raf are major targets of marketed oncology drugs Imatinib (Gleevec) and Sorafenib (Nexavar), respectively, and BIRB-796 is a p38alpha inhibitor that reached Phase II clinical trials. Sorafenib 84-93 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 0-5 20621496-3 2010 Here, we present a structural comparison of the important and similar interactions necessary for Gleevec(R), Nexavar, and BIRB-796 to bind to their respective DFG-out allosteric binding pockets and the selectivity of each with respect to c-Abl, B-Raf, and p38alpha. Sorafenib 109-116 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 238-243 20337484-2 2010 c-Abl and b-Raf are major targets of marketed oncology drugs Imatinib (Gleevec) and Sorafenib (Nexavar), respectively, and BIRB-796 is a p38alpha inhibitor that reached Phase II clinical trials. Sorafenib 95-102 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 0-5 19366808-0 2009 Sorafenib induces apoptosis specifically in cells expressing BCR/ABL by inhibiting its kinase activity to activate the intrinsic mitochondrial pathway. Sorafenib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 65-68 19366808-2 2009 Here, we show that the multikinase inhibitor sorafenib inhibits proliferation and induces apoptosis at much lower concentrations in Ton.B210 cells when driven by inducibly expressed BCR/ABL than when driven by interleukin-3. Sorafenib 45-54 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 182-189 19366808-3 2009 The increased sensitivity to sorafenib was also observed in cells inducibly expressing BCR/ABL with the imatinib-resistant E255K or T315I mutation. Sorafenib 29-38 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 87-94 19366808-5 2009 It was further revealed that sorafenib activates Bax and caspase-3 and reduces mitochondrial membrane potential specifically in BCR/ABL-driven cells. Sorafenib 29-38 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 132-135 19366808-6 2009 Sorafenib also inhibited BCR/ABL-induced tyrosine phosphorylation of its cellular substrates and its autophosphorylation in Ton.B210. Sorafenib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 29-32 19366808-7 2009 It was finally shown that sorafenib inhibits the kinase activity of BCR/ABL as well as its E255K and T315I mutants in in vitro kinase assays. Sorafenib 26-35 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 68-75 19366808-8 2009 These results indicate that sorafenib induces apoptosis of BCR/ABL-expressing cells, at least partly, by inhibiting BCR/ABL to activate the mitochondria-mediated apoptotic pathway. Sorafenib 28-37 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 63-66 19366808-8 2009 These results indicate that sorafenib induces apoptosis of BCR/ABL-expressing cells, at least partly, by inhibiting BCR/ABL to activate the mitochondria-mediated apoptotic pathway. Sorafenib 28-37 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 59-66 19366808-9 2009 Thus, sorafenib may provide an effective therapeutic measure to treat Ph+ leukemias, particularly those expressing the T315I mutant, which is totally resistant to imatinib and the second generation BCR/ABL inhibitors. Sorafenib 6-15 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 202-205 17595328-8 2007 Together, these findings suggest that sorafenib effectively induces apoptosis in highly imatinib-resistant chronic myelogenous leukemia cells, most likely by inhibiting or down-regulating targets (i.e., STAT5 and Mcl-1) downstream or independent of Bcr/Abl. Sorafenib 38-47 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 249-256 17595328-0 2007 The multikinase inhibitor sorafenib induces apoptosis in highly imatinib mesylate-resistant bcr/abl+ human leukemia cells in association with signal transducer and activator of transcription 5 inhibition and myeloid cell leukemia-1 down-regulation. Sorafenib 26-35 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 92-99 17595328-1 2007 The effects of the multikinase inhibitor sorafenib (BAY 43-9006), an agent shown previously to induce apoptosis in human leukemia cells through inhibition of myeloid cell leukemia-1 (Mcl-1) translation, have been examined in Bcr/Abl(+) leukemia cells resistant to imatinib mesylate (IM). Sorafenib 41-50 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 225-232 17595328-2 2007 When administered at pharmacologically relevant concentrations (10-15 microM), sorafenib potently induced apoptosis in imatinib mesylate-resistant cells expressing high levels of Bcr/Abl, cells exhibiting a Bcr/Abl-independent, Lyn-dependent form of resistance, and CD34(+) cells obtained from imatinib-resistant patients. Sorafenib 79-88 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 179-186 17595328-4 2007 Induction of apoptosis by sorafenib was associated with rapid and pronounced down-regulation of Mcl-1 and diminished signal transducer and activator of transcription (STAT) 5 phosphorylation and reporter activity but only very modest and delayed inactivation of the Bcr/Abl downstream target Crkl. Sorafenib 26-35 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 266-273