BJE6-106

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.

Signaling Pathways >> Epigenetics >> PKC

Signaling Pathways >> Apoptosis >> Apoptosis

Research Areas >> Cancer

Research Areas >> Inflammation/Immunology

Signaling Pathways >> TGF-beta/Smad >> PKC

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 Concentration: 0.2 μM, 0.5 μM Incubation Time: 24 hours, 48 hours, or 72 hours Result: Inhibited cell survival in melanoma cell lines. Apoptosis Analysis[1] Cell Line: SBcl2 cells Concentration: 0.2 μM, 0.5 μM Incubation Time: 6 hours, 12 hours, or 24 hours Result: Induced caspase 3/7 activation. Western Blot Analysis[1] Cell Line: SBcl2 cells Concentration: 0.2 μM, 0.5 μM Incubation Time: 2 hours, 5 hours, 10 hours Result: Increased phosphorylation of MKK4, JNK and H2AX.

[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.