BMS-191264 decreases cardiac necrosis and improves the recovery of contractile activities after reperfusion.[1]
BMS-199624 is a potent inhibitor of the ATP hydrolase activity of mitochondrial F1F0 ATP synthase.
BMS-199624 is a potent inhibitor of the ATP hydrolase activity of mitochondrial F1F0 ATP synthase. The compound BMS-199624 has no affect on the ATP synthase function of F1F0. In isolated rat hearts, BMS-199624 blocks depletion of ATP levels, and blocks necrosis during ischemia.
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BMS-199264 is available through a partnership with Bristol-Myers Squibb (BMS). To learn more and view other BMS compounds, visit sigma.com/BMS.
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Sold for research purposes only under agreement from BMS.
The mitochondrial F1F0 ATP synthase is responsible for the majority of ATP production in mammals and does this through a rotary catalytic mechanism. Studies show that the F1F0 ATP synthase can switch to an ATP hydrolase, and this occurs under
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