BAM7

BAM7 is a direct and selective activator of proapoptotic BAX with an IC₅₀ of 3.3 μM. IC50 & Target: IC50: 3.3 μM (BAX)^[1] In Vitro: 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 Bax^-/- Bak^-/- 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 Bax^-/- Bak^-/- MEFs reconstituted with wild-type BAX but not BAXK21E , which bears the mutation that abrogates BAM7 binding^[1].