BAM7 is a direct and selective activator of proapoptotic BAX with an IC50 of 3.3 μM.
IC50&Target
Bax
3.3 μM (IC50)
体外研究
BAM7 is selective for the BH3-binding site on BAX. BAM7 activates BAX and BAX-dependent cell death. Whereas treatment with BAX or BAM7 alone has no effect on the liposomes, the combination of BAM7 and BAX yields dose-responsive liposomal release of entrapped fluorophore. BAM7 dose- and time-responsively impairs the viability of Bak MEFs that exclusively express BAX but has no effect on Bak MEFs that contain BAK but lack BAX. In contrast, standard proapoptotic stimuli such as serum withdrawal, Staurosporine and Etoposide induces an equivalent apoptotic response in Bax and Bak MEFs. As further evidence of BAM7 specificity of action, (i) BAM7 does not affect the viability of BaxBak MEFs; (ii) ANA-BAM16, which does not bind or activate BAX, has no effect on Bak MEFs; and (iii) BAM7 selectively induces cell death of BaxBak MEFs reconstituted with wild-type BAX but not BAXK21E , which bears the mutation that abrogates BAM7 binding.
分子式
C21H19N5O2S
分子量
405.47
CAS号
331244-89-4
运输条件
Room temperature in continental US; may vary elsewhere.