M109S is a novel small molecule that shields cells from mitochondria-dependent apoptosis, demonstrating effectiveness both in vitro and in vivo. It shows promise as a research tool for probing cell death mechanisms and could lead to the development of therapeutics that target the mitochondria-dependent cell death pathway. M109S possesses oral bioactivity and excellent brain permeability [1].

M109S, at concentrations ranging from 0.1 to 10,000 nM over 24 to 48 hours, inhibits Bax- and Bak-induced apoptosis [1]. Additionally, M109S at 0 to 10 μM for 4 hours suppresses Staurosporine-induced apoptosis in MEF cells. It also prevents apoptosis in Neuro2a cells initiated by Etoposide when applied at 0 to 10μM for 24 hours [1]. At a concentration of 500 nM for 24 hours, M109S inhibits Obatoclax-induced apoptosis in ARPE19 cells [1]. Furthermore, at 500 nM for 48 hours, M109S inhibits Bax conformational change (N-terminus exposure) and mitochondrial translocation [1]. At 1.0 μM for 4 hours, M109S reduces mitochondrial oxygen consumption and reactive oxygen species, while M109S at 0.1 to 1 nM for 4 hours increases glycolysis [1].

M109S, administered at a dose of 10 mg/kg through oral gavage three times within 48 hours, protects the retina from photoreceptor cell death induced by intense light exposure [1]. As an orally bioactive cell death inhibitor that penetrates the blood-brain/retinal barrier, M109S can be delivered via intraperitoneal injection at 1 mg/kg, intravenous injection at 5 mg/kg, or oral gavage at 10 mg/kg in a single dose [1].