Background:

Bax inhibitor peptide P5 (BIP P5) is a peptide inhibitor of Bax translocation to mitochondria [1].

Bax is a pro-apoptotic member of Bcl-2 family proteins and plays an important role in mitochondria-dependent apoptosis. Bax stays in the cytosol and transfers into mitochondria after apoptotic stimuli [1].

BIP P5 is a membrane-permeable peptide inhibitor of Bax translocation to mitochondria. In HeLa cells, BIP P5 protected cells from UVC- and STS-induced apoptosis. In U87-MG glioma cells, MCF-7 breast cancer cells and LNCaP prostate cancer cells, BIP P5 also inhibited apoptosis induced by anti-cancer drugs cisplatin, etoposide and doxorubicin. While BIP P5 did not suppress UVC- or STS-induced apoptosis in Bax-deficient cells (DU145), which suggested BIP P5 only suppressed Bax-mediated apoptosis. The caspase activation and the release of cytochrome c from mitochondria triggered by apoptotic stimuli were also significantly inhibited by BIP P5. BIP P5 inhibited the interaction of Ku70 and endogenous Bax in a dose-dependent way [1].

Reference:
[1].  Sawada M, Hayes P, Matsuyama S. Cytoprotective membrane-permeable peptides designed from the Bax-binding domain of Ku70. Nat Cell Biol, 2003, 5(4): 352-357.