BAM7

Research use only, not for human use.

BAM 7 is a direct and selective activator of proapoptotic Bax with EC50 of 3.3 μM.

BAM 7 is a direct and selective activator of proapoptotic Bax with EC50 of 3.3 μM.

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.

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Bax Activator Molecule 7

Angiogenesis

Bcl-2

Bax

Cancer

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331244-89-4

405.47

C21H19N5O2S

>98% (HPLC)

DMSO: 2 mg/mL (4.93 mM)

O=C(N(C1=NC(C2=CC=CC=C2)=CS1)N=C/3C)C3=N\NC4=CC=CC=C4OCC

(E)-4-(2-(2-ethoxyphenyl)hydrazono)-5-methyl-2-(4-phenylthiazol-2-yl)-2,4-dihydro-3H-pyrazol-3-one

(-20℃)

With Ice Pack

≥ 2 years