Small molecules capable of uncoupling respiration and ATP synthesis in mitochondria are protective towards various cell malfunctions. Recently (2-fluorophenyl){6-[(2-fluorophenyl)amino](1,2,5-oxadiazolo[3,4-e]pyrazin-5-yl)}amine (BAM15), a new compound of this type, has become popular as a potent mitochondria-selective depolarizing agent producing minimal adverse effects. To validate protonophoric mechanism of BAM15 action, we examined its behavior in bilayer lipid membranes (BLM). BAM15 proved to be a typical anionic protonophore with the activity on planar membranes being suppressed upon decreasing membrane dipole potential. In both planar BLM and liposomes, BAM15 induced proton conductance with the potency close to that of the classical protonophoric uncoupler carbonyl cyanide m-chlorophenyl hydrazone (CCCP). In isolated rat liver mitochondria (RLM), BAM15 caused membrane potential collapse, increased respiration rate and induced Ca²⁺ efflux at concentrations slightly higher than those for CCCP. Surprisingly, the uncoupling action of BAM15 on isolated RLM, in contrast to that of CCCP, was partially reversed by carboxyatractyloside (CATR), an inhibitor of adenine nucleotide translocase, thereby indicating involvement of this protein in the BAM15-induced uncoupling. BAM15 inhibited growth of Bacillus subtilis at micromolar concentrations. In electrophysiological experiments on molluscan neurons, BAM15 caused plasma membrane depolarization and suppression of electrical activity, but the effect developed more slowly than that of CCCP.

能够解脱线粒体中的呼吸作用和ATP合成的小分子可防止各种细胞功能异常。最近，（2-氟苯基）{6-[（（2-氟苯基）氨基]（1,2,5-恶二唑并[3,4-e]吡嗪-5-基）}胺（BAM15），这种新化合物作为一种有效的线粒体选择性去极化剂，其产生的不良影响极小，已广受欢迎。为了验证BAM15作用的质子机制，我们检查了其在双层脂质膜（BLM）中的行为。BAM15被证明是一种典型的阴离子质子体，当降低膜的偶极电位时，其对平面膜的活性受到抑制。在平面BLM和脂质体中，BAM15诱导的质子传导均接近于经典的质子解偶联羰基氰化物间氯苯基（CCCP）。浓度略高于CCCP的²⁺外排。出乎意料的是，与CCCP相反，BAM15对分离的RLM的解偶联作用被腺嘌呤核苷酸转位酶的抑制剂羧基白术苷（CATR）部分逆转，从而表明该蛋白质参与了BAM15诱导的解偶联。BAM15以微摩尔浓度抑制枯草芽孢杆菌的生长。在软体动物神经元的电生理实验中，BAM15引起质膜去极化并抑制电活动，但其作用比CCCP慢。