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Under hypoxic conditions, Hb binding to band 3 causes the release of glycolytic enzymes into the cytosol, thereby promoting glycolysis and 2,3-biphosphoglycerate synthesis via the Rapoport–Luebering shunt [54,55]

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Further mechanistic investigations have implicated GHK-Cu in the activation of the Nrf2/ARE antioxidant response pathway in cultured cells, where it appears to reduce reactive oxygen species (ROS) burden independently of direct radical scavenging—suggesting an indirect, gene-regulatory mode of action rather than purely stoichiometric antioxidant chemistry