Lonidamine was originally investigated as an antispermatogenic agent.1 Lonidamine has been shown to decrease oxygen consumption as well as aerobic and anaerobic glycolysis in tumor cells leading to apoptosis.2 These effects have been attributed to the ability of lonidamine to inhibit mitochondrially bound hexokinase (IC50 = 90 µM for aerobic glycolysis, 45 µM for anaerobic glycolysis using Ehrlich ascites tumor cells)2. The apoptotic effects of lonidamine have also been attributed to its ability to disrupt the mitochondrial transmembrane potential3, intracellular acidification by inhibition of lactate efflux4, and inhibition of mitochondrial pyruvate (MCP) and monocarboxylate transporter (MCT)5.
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