Western blot analysis of extracts from NIH/3T3 cells, serum-starved overnight and untreated or treated with hPDGF-BB #8912 (100 ng/ml, 5 min) either with or without sorafenib pre-treatment (1 µM, 2 hr), using Phospho-PDGF Receptor β (Tyr1009) (42F9) Rabbit mAb #3124 (upper) or PDGF Receptor β (28E1) Rabbit mAb #3169 (lower).Learn more about how we get our images
Chemical structure of sorafenib.Learn more about how we get our images
Sorafenib is supplied as a lyophilized powder. For a 10 mM stock, reconstitute the 10 mg in 1.57 ml DMSO. Working concentrations and length of treatment can vary depending on the desired effect, but it is typically used as a pretreatment at 0.1-10 µM for 0.5-2 hr prior to treating with a stimulator. It can also be used alone, with varying treatment times lasting up to 24 hr. Soluble in DMSO at 200 mg/ml; very poorly soluble in ethanol and water with maximum solubility in water ~10-20 µM.
Store lyophilized or in solution at -20ºC. In lyophlized form, the chemical is stable for 24 months. Once in solution, use within 3 months to prevent loss of potency.
C21H16ClF3N4O3 • C7H8O3S
Sorafenib, also known as Bay 43-9006, is a novel multikinase inhibitor that targets the RAF family of serine/threonine kinases and tyrosine kinase receptors involved in tumor progression and tumor angiogenesis, including: VEGFR-2 (IC50 = 90 nM), VEGFR-3 (IC50 = 20 nM), PDGFR- (IC50 = 57 nM), c-KIT (IC50 = 68 nM), and Flt3 (IC50 = 58 nM) (1). Research studies have demonstrated that sorafenib induces apoptosis in several tumor cell lines through the down-regulation of the antiapoptotic protein myeloid cell leukemia-1 (Mcl-1). Down-regulation of Mcl-1 by sorafenib is associated with the release of cytochrome c from mitochondria into the cytosol and caspase activation, leading to apoptotic cell death (2). STAT3 inhibition by sorafenib has been observed in multiple cell types (3-5).
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