Drug intelligence / Profile preview

diethylammonium tetrathiomolybdate

Development stage
Preclinical
Lead developer
King's College London
Modality
Small Molecules
Administration
Intravenous
01

Overview

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.

Other names
diethyl-ammonium tetrathiomolybdate
02

Targets

COX7C (Cytochrome c oxidase subunit 7C, mitochondrial)ATP1A (Sodium/potassium-transporting ATPase)

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