Oligomycin B is a mitochondrial F1FO ATP synthase inhibitor.

The mitochondrial F1F0 ATP synthase is responsible for the ATP production in mammals via a rotary catalytic mechanism. Studies also show that the F1F0 ATP synthase can switch to an ATP hydrolase, which occurs under conditions during myocardial ischemia.

In vitro: Previous study found that oligomycin B and aurovertin B were able to inhibit both the synthase and the hydrolase function, which not only rendered them difficult to be experimentally used, but also precluded them from being therapeutics. Aurovertin B bound between the subunits catalytic F1 domain of the F1F0 ATPase, where it prevented the conformational changes required for the catalytic cycle of this enzyme, whereas oligomycin bound to the F0 domain and blocked proton flow [1].

In vivo: In a previous animal study, intracranial pressure measurements were performed in SD rats treated by intraperitoneal injection of vehicle, cyclosporine A, or oligomycin B. It was found that cerebral edema and mitochondrial impairment could be significantly worsened by treatment with oligomycin B, whereas a noticeable improvement could be observed in animals that received injections of cyclosporine A [2].

Clinical trial: Up to now, oligomycin B is still in the preclinical development stage.

References:
[1] G.  J. Grover and J. Malm. Pharmacological profile of the selective mitochondrial F1F0 ATP hydrolase inhibitor BMS-199264 in myocardial ischemia. Cardiovasc.Ther. 26, 287-296 (2008).
[2] Vlodavsky E, Palzur E, Shehadeh M, Soustiel JF.  Post-traumatic cytotoxic edema is directly related to mitochondrial function. J Cereb Blood Flow Metab. 2017 Jan;37(1):166-177.