Oligomycin A is an inhibitor of ATP synthase, which inhibits the process taking place on mitochondria coupling membrane that depended on ATP and oxidative phosphorylation [1].

Oligomycin A blocks proton channel of ATP synthase, which is necessary for transforming ADP to ATP by oxidative phosphorylation, accomplishing the inhibition of ATP synthase. The process which oligomycin A inhibits ATP synthesis can significantly reduce electron flow through the electron transport chain.

Experiments which performed in testing against 60 human cancer cell lines that from the National Cancer Institute showed that oligomycin is among the top 0.1% of the most cell line selective cytotoxic agents of 37,000 molecules. In the HeLa carcinoma cell line, the inhibitors of H+ -ATP-synthase oligomycin (5 mg/ml) was shown to strongly suppress, and the cell respiration, showing that it is tightly coupled to ATP synthesis. It was reported that Oligomycin at 100 ng/ml completely inhibits the activity of oxidative phosphorylation in 1h and induces different levels of glycolysis gains by 6 h in a group of cancer cell. As an inhibitor of the F0 part of H+-ATP-synthase, Oligomycin also suppresses the apoptosis which was induced by TNF. Treatment with different concentrations of oligomycin and rotenone severely reduced the oxygen consumption by up to 94%, indicating a major role for mitochondria in this process. And treatment with oligomycin could abolish the H2O2 increase completely [2-4].

References:
[1].  Jastroch M, Divakaruni AS, Mookerjee S, et al. Mitochondrial proton and electron leaks. Essays Biochemistry, 2010, 47:53-67.
[2].  Shchepina LA, Pletjushkina OY, Avetisyan AV, et al. Oligomycin, inhibitor of the F-0 part of H+-ATP-synthase, suppresses the TNF-induced apoptosis. Oncogene, 2002, 53: 8149-8157.
[3].  Salomon AR, Voehringer DW, Herzenberg LA, et al. Understanding and exploiting the mechanistic basis for selectivity of polyketide inhibitors of F0F1-ATPase. Proceedings of The National Academy of Sciences of The United States of America, 2000, 97(26): 14766-14771.
[4].  Alexander R, Adina V, Ivan B,　et al. Overcoming intrinsic multi-drug resistance in melanoma by blocking the mitochondrial respiratory chain of slow-cycling JARID1Bhigh cells. Cancer Cell, 2013, 23(6): 811-825.