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This profile is consistent with the function of copper as a SOD cofactor and with the observed modulation of antioxidant defense genes Profile observed in models (synthesis): Activity at the level of fibroblasts and extracellular matrix cells – stimulation of the synthesis of structural proteins Copper transport function coupled with the activity of Cu²⁺-dependent enzymes Modulation of repair and antioxidant gene expression in transcriptomic studies Pro-angiogenic and pro-regenerative profile in wound healing models In research models, GHK-Cu is interpreted as bifunctional extracellular matrix modulator — a signal stimulating the synthesis of connective tissue components and a carrier providing copper as a cofactor for enzymes responsible for the maturation and cross-linking of this matrix

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One unexpected serious adverse reaction occurred in a NAC-treated patient caused by an erroneous iv infusion rate (1.5g-loading dose-15 min followed by 7.5 g delivered over 3h15min instead of 4 h), causing chest tightness, despite stable vital signs, which was resolved by corticosteroids and discontinuation of iv NAC