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387 Recent studies have further emphasized the role of mitochondrial dysfunction in promoting the pathology of PD, with various regulatory mechanisms being uncovered

Artemisinin (ART) derivatives, e.g., are activated via reductive cleavage of their peroxide bond by intracellular iron (Fe 2+ ) or heme generating, carbon-centered free radicals [9], [10] with the potential to alkylate vital cellular components including the tripeptide glutathione (-Glu-Cys-Gly, GSH)

Paradoxically, combining the FAO inhibitor etomoxir (ETO) with MAPKi significantly increased tumor growth compared with MAPKi alone [59]

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