Biochemicals & reagents
1) Huang et al. (2013), B-Raf and the inhibitors: from bench to bedside; J.Hematol.Oncol. 6 1 2) Ji et al. (2016), Endoplasmic reticulum stress-induced autophagy determines the susceptibility of melanoma cells to dabrafenib; Drugs Des. Dev. Ther., 10 2491 3) Herr et al. (2015), B-Raf inhibitors induce epithelial differentiation in BRAF-mutant colorectal cancer cells; Cancer Res., 75 216
Dabrafenib is a selective inhibitor of mutant B-RafV600E (IC50 = 0.8 nM), with 4- and 6-fold reduced potency against wild type B-Raf and c-Raf (IC50 = 3.2 and 5 nM, respectively) (1). This compound has been in clinical trials in patients with B-RafV600E metastatic melanoma and other solid tumors. Endoplasmic reticulum stress and autophagy are induced in melanoma cells after treatment with dabrafenib and protect cells from dabrafenib toxicity (2). It also induces epithelial differentiation in BRAF-mutant colorectal cancer cells (3).