S-8502 Sorafenib, p-Toluenesulfonate Salt, >99%

Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO at 200 mg/mL; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 10-20 µM; buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A.

BSF-106 BSF-105 BSF-104 BSF-103 BSF-102

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• More than 1,000 labs worldwide have purchased Sorafenib or its salt forms from LC Labs (either directly from us or from our many distributors, many of whom resell under their own labels).
• Sorafenib (Bay 43-9006) is a novel bi-aryl urea compound that inhibits cell proliferation by targeting the ERK pathway and angiogenesis by targeting the receptor tyrosine kinases VEGFR-2 and PDGFR-β and their associated signaling cascades.  Although sorafenib was initially developed as a Raf kinase inhibitor (IC50 = 6 nM), it has since been shown to have activity against many receptor tyrosine kinases involved in tumorigenesis and angiogenesis including FGFR-1, wt BRAF and V599E mutant BRAF, as well as members of the so-called "split kinase" family:  VEGFR-2, VEGFR-3, PDGFR-β, c-KIT, and Flt3.  However, sorafenib is not active against erbB1, erbB2, ERK-1, MEK-1, EGFR, HER-2, IGFR-1, c-MET, c-yes, PKB, PKA, cdk1/cyclinB, PKC, and pim-1.  In cellular mechanistic assays, sorafenib decreased basal phosphorylation of the ERK pathway in melanoma, breast, colon, and pancreatic tumor cell lines.  Wilhelm, S.M., et al.  "BAY 43-9006 Exhibits Broad Spectrum Oral Antitumor Activity and Targets the RAF/MEK/ERK Pathway and Receptor Tyrosine Kinases Involved in Tumor Progression and Angiogenesis."  Cancer Res. 64:  7099-7109 (2004).
• Sorafenib is more potent in a cellular system (IC50 = 20 nM) than in an enzyme assay (IC50 = 107 nM). Guo, J., et al. "Inhibition of phosphorylation of the colony-stimulating factor-1 receptor (c-Fms) tyrosine kinase in transfected cells by ABT-869 and other tyrosine kinase inhibitors." Mol. Cancer Ther. 5: 1007-1013 (2006).
• Sorafenib potently inhibited activation of the MAPK pathway and ERK phosphorylation in human cancer cell lines, irrespective of whether they harbored K-ras mutations, V599EB-Raf, or both. Wilhelm, S., et al. "The novel Raf inhibitor Bay 43-9006 blocks signaling and proliferation in BRAF mutant and wildtype melanoma and colorectal tumor cell lines." Proc. Am. Assoc. Cancer Res. 44: 106609 (2003).
• Sorafenib inhibited various nonkinase targets, including adenosine A3, dopamine D1, and muscarine M3 receptors, albeit at much higher (micromolar) concentrations than kinase targets. Carter, C., et al. "Investigators Brochure Bay 43-9006/ Raf Kinase Inhibitor." Version No. 5. West Haven, CT, Bayer Pharmaceuticals Corporation, 2004.
• Sorafenib tosylate is the active ingredient in the drug sold under the trade name Nexavar®. This drug has been approved in at least one country for use in patients with advanced renal cell cancer. NOTE: THE SORAFENIB TOSYLATE SOLD BY LC LABORATORIES FOR RESEARCH IS NOT NEXAVAR®, AND IS NOT FOR HUMAN USE.
• Sold for laboratory or manufacturing purposes only; not for human, veterinary, food, or household use.
• This product is offered for R&D use in accordance with (i) 35 USC 271(e)+A13(1) in the U.S.; (ii) Section 69.1 of Japanese Patent Law in Japan; (iii) Section 11, No. 2 of the German Patent Act of 1981 in Germany; (iv) Section 60, Paragraph 5b of the U.K. Patents Act of 1977 in the U.K.; (v) Sections 55.2(1) and 55.2(6) and other common law exemptions of Canadian patent law; (vi) Section 68B of the Patents Act of 1953 in New Zealand together with the amendment of same by the Statutes Amendment Bill of 2002; (vii) such related legislation and/or case law as may be or become applicable in the aforementioned countries; and (viii) such similar laws and rules as may apply in various other countries.
• Not available in some countries; not available to some institutions; not available for some uses.