WEHI-3773

WEHI-3773 inhibits BAX-mediated apoptosis in BAK-deficient cells by blocking the conformational activation, mitochondrial redistribution and cytochrome c release of BAX. In BAX-deficient cells, WEHI-3773 promotes BAK-mediated apoptosis by inducing the conformational activation of BAK, cytochrome c release and VDAC2 dissociation^[1].
WEHI-3773 (0.1-10000 nM; pre-incubated for 2 h followed by co-incubation with BH3 mimetics for 22 h) dose-dependently enhances BAK-mediated apoptosis in Bax^-/- Vdac2^-/- mouse embryonic fibroblasts (MEFs) expressing VDAC2 or a chimeric VDAC protein containing the β7 to β10 region of VDAC2, but exerts no such effect in cells expressing VDAC1 or a chimeric protein lacking this region^[1].
WEHI-3773 (200 nM; 48 h) enhances BH3 mimetic-induced cell death in BAX^-/- MV4;11 acute myeloid leukemia (AML) cells and reverses venetoclax resistance caused by BAX deletion^[1].
WEHI-3773 (200 nM; 48 h) enhances BH3 mimetic-induced cell death in venetoclax-resistant OCI-AML3 acute myeloid leukemia cells harboring BAX mutations, thereby overcoming acquired venetoclax resistance^[1].
WEHI-3773 (80-10000 nM) dose-dependently promotes BAK conformational activation and cytochrome c release in BAK^-/- HeLa cells treated with ABT-737 + S63845^[2].
WEHI-3773 (200 nM; 48 h) restores the sensitivity of BAX^-/- MV4;11 human acute myeloid leukemia (AML) cells to venetoclax, S63845, and their combination following 48 h of co-treatment^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.