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While copper may contribute to intracellular oxidative stress by participating in the Fenton and Haber-Weiss reactions or by interfering with iron homeostasis, either directly or indirectly through the formation of hydroxyl radicals, experimental evidence linking copper deficiency and the formation of SOD1 aggregates to the progression of PD is also discussed in terms of its therapeutic implications (119,120)

However, quantification was so far only possible for the parent compounds with EnB, showing the highest occurrence rates, followed by EnB1 (Gerding et al

GHK-Cu is a copper-bound tripeptide reference compound commonly utilized in controlled laboratory and in-vitro research environments examining peptide-mediated cellular signaling, copper-dependent biochemical pathways, and tissue-related research models

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