sorafenib is a small molecular inhibitor of several tyrosineprotein kinases including vegfr (vascular endothelial growth factorreceptors) and pdgfr (platelet-derived growth factor receptors) andraf kinases. sorafenib prevents mouse vegfr-2, vegfr-3 and pdgfr-βwith ic50 of 15, 20 and 57 nm, respectively. sorafenib inhibitswild-type b-raf and mutant b-rafv599ewithic50 of 22 and 38 nm, respectively. sorafenib inhibits raf-1 withan ic50 of 6 nm. [1] sorafenibinhibits oncogenic ret kinase activity with an ic50 of 50 nm.sorafenib arrests the growth of nih3t3 and rat1 fibroblaststransformed by oncogenic ret and of thyroid carcinoma cells thatharbor spontaneous oncogenic ret alleles. sorafenib inhibits thegrowth of cells carrying retv804l orretv804m withic50 of 0.11 and 0.15 µm, respectively. [2] sorafenibpotently inhibits flt3-wt (wild type fms-like tyrosyl kinase-3),flt3-itd (internal tandem duplication) and flt3d835y withic50 of 32.6, 2.8 and 103.5 nm. the kivaluesof sorafenib for flt3-wt, flt3-itd and flt3d835y are18.7, 1.5 and 44 nm, respectively. [3] oncedaily oral dosing of sorafenib reveals broad-spectrum antitumoractivity in colon, breast, and non–small-cell lung cancer xenograftmodels.[1] after3 weeks of oral treatment with sorafenib (60 mg/kg/day), the volumeof tt cell xenografts is reduced from 72.5 to 44 mm3, whereas invehicle-treated mice, mean tumor volume increases to 408mm3. [2] sorafenibinduces regression of subcutaneous flt3-itd tumors in athymicmice. [3] sorafenibproduces significant tumor growth inhibition (tgi) and a reductionin tumor vasculature of both ectopic and orthotopic renca and 786-otumors, at a dose as low as 15 mg/kg when administereddaily.[4]

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