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With advancing age, cellular NAD levels decline significantly through three main mechanisms: reduced synthesis (decreased NAMPT), increased catabolism (CD38 hyperactivation under inflammaging conditions) and excessive consumption by DNA repair systems. Intravenous administration of NAD or its precursors such as NR (nicotinamide riboside) and NMN (nicotinamide mononucleotide) aims to restore a more youthful biosynthetic and reparative capacity to ageing cells
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In the GHK-Cu complex, the Cu (II) ion is coordinated by the nitrogen from the imidazole side chain of the histidine, another nitrogen from the alpha-amino group of glycine, and the deprotonated amide nitrogen of the glycine-histidine peptide bond (Figure 1)
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