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Product Details
Sorafenib,284461-73-0,IC-0234167
Sorafenib acts as a multi-kinase inhibitor, targeting Raf-1 and B-Raf with IC50 values of 6 nM and 22 nM, respectively. Additionally, Sorafenib demonstrates inhibitory effects on VEGFR-2, VEGFR-3, PDGFR-β, Flt-3, and c-KIT, displaying corresponding IC50 values of 90 nM, 20 nM, 57 nM, 59 nM, and 68 nM. Beyond these kinase activities, Sorafenib is capable of inducing autophagy and apoptosis while triggering ferroptosis activation, resulting in its notable antitumor efficacy [1-3]. Sorafenib(5-40μM; 24 h) had a dose-dependent inhibitory effect on HSC-T6 cells viability [4]. Sorafenib(25mM;0-42h) alters the lipid composition in Huh7.5 cells[5]. Sorafenib(2.5, 5, 10 mg/kg; i.p; twice a week for 8 weeks) attenuated liver injury and extracellular matrix (ECM) accumulation in CCl4 -induced fibrotic livers, accompanied by reduction of SLC7A11 and GPX4 proteins[4]. Treatment with erastin and sorafenib(10 mg/kg; i.p; once every other day) alleviated liver fibrosis in mice by inducing hepatic stellate cells(HSCs) ferroptosis in mice[6].The synergism of sorafenib and T cells is mediated via reduced ATF4 expression, causing activation of the IRF7-IL-15 axis in leukemia cells and thereby leading to metabolic reprogramming of leukemia-reactive T cells in humans[7].
Sorafenib acts as a multi-kinase inhibitor, targeting Raf-1 and B-Raf with IC50 values of 6 nM and 22 nM, respectively. Additionally, Sorafenib demonstrates inhibitory effects on VEGFR-2, VEGFR-3, PDGFR-β, Flt-3, and c-KIT, displaying corresponding IC50 values of 90 nM, 20 nM, 57 nM, 59 nM, and 68 nM. Beyond these kinase activities, Sorafenib is capable of inducing autophagy and apoptosis while triggering ferroptosis activation, resulting in its notable antitumor efficacy [1-3]. Sorafenib(5-40μM; 24 h) had a dose-dependent inhibitory effect on HSC-T6 cells viability [4]. Sorafenib(25mM;0-42h) alters the lipid composition in Huh7.5 cells[5]. Sorafenib(2.5, 5, 10 mg/kg; i.p; twice a week for 8 weeks) attenuated liver injury and extracellular matrix (ECM) accumulation in CCl4 -induced fibrotic livers, accompanied by reduction of SLC7A11 and GPX4 proteins[4]. Treatment with erastin and sorafenib(10 mg/kg; i.p; once every other day) alleviated liver fibrosis in mice by inducing hepatic stellate cells(HSCs) ferroptosis in mice[6].The synergism of sorafenib and T cells is mediated via reduced ATF4 expression, causing activation of the IRF7-IL-15 axis in leukemia cells and thereby leading to metabolic reprogramming of leukemia-reactive T cells in humans[7].
