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It inhibits NNMT (nicotinamide N-methyltransferase), an enzyme regulating metabolism, fat storage, and NAD+ consumption.[4][27][6] NNMT methylates nicotinamide, a NAD+ breakdown product, diverting it from recycling and reducing available NAD+

P53 phosphorylation at Ser15 enhances the affinity of both FOXO4 and FOXO4-DRI for p53 TAD2 explaining the preferential engagement of FOXO4-DRI with the hyperphosphorylated p53 characteristic of senescent cells

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That decline is one reason GHK-Cu supplementation tends to produce more visible results in patients over 3540

There are two types of peptides you may benefit from: endogenous and exogenous