BAM15 increases mitochondrial respiration rate and is also found to be less cytotoxic compared to other protonophore uncouplers such as carbonyl cyanide p-trifluoromethoxyphenylhydrazone. Hindered oncogenic MAPK (mitogen-activated protein kinase ) signaling leads to BAM15 induced mitochondrial apoptotic pathway activation.
Enzyminhibitor
This novel mitochondrial uncoupler (FW = 340.29 g/mol), also named (2- fluorophenyl)-{6-[(2-fluorophenyl)amino]-(1,2,5-oxadiazolo[3,4-e]pyrazin- 5-yl)}amine, exhibits a broad effective range of H+ gradient-dissipating action without affecting plasma membrane electrophysiology. With FCCP as an equipotent positive control, BAM15 was found to be fully able to increase mitochondrial respiration in the presence of oligomycin over a broader concentration range than FCCP in both myoblasts and hepatocytes. BAM15 and FCCP had similar effects on mitochondrial depolarization in L6 myoblasts treated with concentrations of each uncoupler at 1 and 10 μM, as measured by tetramethylrhodamine (TMRM) fluorescence. Neither FCCP nor BAM15 donates electrons to the Electron Transport Chain. Although some non-protonophoric uncouplers increase proton transport into the matrix via interaction with the mitochondrial inner membrane adenine nucleotide translocase (ANT), neither BAM15 nor FCCP requires the ANT to increase mitochondrial respiration.
BAM15 Upstream-Materialien And Downstream Produkte