BJE6-106 (B106) is a potent, selective 3rd generation PKCδ inhibitor with an IC50 of 0.05 μM and targets selectivity over classical PKC isozyme PKCα (IC50=50 μM). BJE6-106 (B106) induces caspase-dependent apoptosis. BJE6-106 (B106) possesses tumor-specific effect. PKCδ|0.05 μM (IC50)|PKCα|50 μM (IC50)
BJE6-106 (B106) (0.2 μM, 0.5 μM; 24-72 hours) suppresses cell survival in melanoma cell lines with NRAS mutations[1].BJE6-106 (B106) (0.2 μM, 0.5 μM; 6-24 hours) triggers caspase-dependent apoptosis, increases the activity of caspase 3/7, the effect of B106 is greater than rottlerin (10-fold) in SBcl2 cells[1].BJE6-106 (B106) (0.5 μM; 2-10 hours) activates the MKK4-JNK-H2AX Pathway by inducing MKK4, JNK and H2AX activation at different times in SBcl2 cells[1]. Cell Viability Assay[1] Cell Line: Melanoma cell lines with NRAS mutations: SBcl2, FM6, SKMEL2, WM1366, WM1361A, and WM852 cells
[1]. Takashima A,et al. Protein kinase Cδ is a therapeutic target in malignant melanoma with NRAS mutation. ACS Chem Biol. 2014 Apr 18;9(4):1003-14.