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However, this preservation of mitochondrial function creates a paradox: by maintaining the electron transport chain, CHAC1 inadvertently supplies the ROS that propagate iron-dependent lipid peroxidation ( via two convergent mechanisms: the direct depletion of glutathione and the indirect facilitation of mitochondrial ROS production, thereby coupling sustained metabolic activity to ferroptotic cell death under cysteine limitation

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Phase 3 trials have now initiated for overweight and obesity at this point, assessing CagriSema in larger numbers and for longer periods of time. References: Frias JP, et al

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