Description
Sorafenib (BAY 43-9006, Nexavar) can inhibit VEGFR2, VEGFR3, PDGFR-beta, FLT-3 and c-kit with IC50 of 90 nM, 15 nM, 20nM, 57nM and 58 nM.
Storage
2 years at -20centigrade Powder
Targets
VEGFR2/VEGFR3, PDGFR-beta, FLT-3, c-kit, Raf/B-raf(WT)/B-raf(V599E)
Molecular Formula
C21H16CLF3N4O3.C7H803S
Chemical Name
2-Pyridinecarboxamide, 4-[4-[[[[4-chloro-3-(trifluoromethyl)phenyl]amino]carbonyl]amino]phenoxy]-N-methyl-, 4-methylbenzenesulfonate (1:1)
Solubility
DMSO 127 mg/mL Water
In vitro
Sorafenib (BAY 43-9006, Nexavar) shows inhibition to many kinases including VEGFR, PDFGR, Raf, FLT-3, Ret, and c-Kit. Sorafenib (BAY 43-9006, Nexavar) can inhibit VEGFR2, VEGFR3, PDGFR-beta, FLT-3 and c-kit with IC50 of 90 nM, 15 nM, 20nM, 57nM and 58 nM. Actually, Sorafenib (BAY 43-9006, Nexavar) is a strong Raf inhibitor which can inhibit Raf, B-raf (Wt), and B-raf (V599E) with IC50 of 6nM, 22 nM and 38 nM. Sorafenib (BAY 43-9006, Nexavar) shows its influence on RAS-MAPK signaling cascade and it can inhibit MEK and ERK weekly with IC50 more than 10 uM. Sorafenib (BAY 43-9006, Nexavar) induces mitochondrial cytochrome c and SMAC release and PARP cleavage in A375, A 2058, and SKMEL5 melanoma cells. Sorafenib (BAY 43-9006, Nexavar) also induces mitochondrial release and nuclear translocation of AIF. in sensitive cell lines, BAY 43-9006-induced apoptosis is independent of Bad dephosphorylation and caspase activation and largely mediated through the nuclear translocation of AIF. Sorafenib shows great inhibition to cell lines including hepatocellular carcinoma and renal cell carcinoma.In recent research, sorafenib shows antitumor efficacy to many types of cells including metastatic thyroid cancer cells, human neuroblastoma cells.
In vivo
Orally administered BAY 43-9006 in a representative panel of tumor xenograft models shows antitumor efficacy. Mice bearing 75 to 150 mg tumors were treated orally with BAY 43-9006 at dose levels of 7.5 to 60 mg/kg, administered daily for 9 days. During treatment with 30 to 60 mg/kg BAY 43-9006, complete tumor stasis in the HT-29, Colo-205, and DLD-1 human colon tumor models and the A549 NSCLC model was observed). Each of these tumor lines expresses a mutation in either KRAS or BRAF that would constitutively activate signaling through the RAF/MEK/ERK pathway. In another NSCLC model (NCI-H460) tumor growth was inhibited, but complete stasis during treatment was not achieved at doses up to 60 mg/kg.
Download Datasheet