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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

Supports Tissue Repair and Regeneration One of the most studied benefits of BPC-157 is its potential role in accelerating tissue healing

At the molecular level, fatigue affects calcium handling within muscle fibers, disrupting excitation-contraction coupling and reducing force production

Morrow 2004)