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Diethylammonium tetrathiomolybdate (DEATTM) is a slow-release hydrogen sulfide (H2S) donor under preclinical investigation for the treatment of ischemia-reperfusion injury (IRI), particularly in the context of hemorrhage-reperfusion. By releasing sulfide, DEATTM reversibly inhibits the mitochondrial electron transport chain, specifically targeting cytochrome c oxidase (Complex IV), which reduces metabolic activity and limits the excessive generation of reactive oxygen species (ROS) during reperfusion. Additionally, DEATTM exhibits short-term diuretic and natriuretic effects, likely mediated through the inhibition of renal tubular Na+/K+-ATPase.
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