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  • An orally bioavailable inhibitor of mitochondrial oxidative phosphorylation with potential antineoplastic activity. Upon administration, ATR-101 inhibits the activity of F1F0-ATP synthase, elevates the mitochondrial membrane potential and depletes ATP in adrenocortical cells. The mitochondrial dysfunction caused by the release of reactive oxygen and triggered cytochrome c release leads to caspase-mediated cell death. ATR-101 may be useful in treating certain types of adrenocortical carcinoma.
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