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systemic administration carries risks of off-target effects (e.g., promoting tumorigenesis via global ferroptosis inhibition), which have not been addressed in long-term safety assessments

Excess copper is reduced by FDX1 to generate Cu, which drives cell death via two primary mechanisms: (1) Cu-mediated aggregation of lipoylated TCA cycle proteins (e.g., DLAT) and loss of Fe-S clusters, and (2) Cu-induced disruption of the Npl4/p97 protein quality-control system

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Faster recovery often translates into improved training consistency, a major driver of long-term muscle growth