NAD+

Nicotinamide Adenine Dinucleotide (NAD+; CAS 53-84-9; MW 663.4 g/mol; C21H27N7O14P2) is a dinucleotide coenzyme present in every living cell — central to cellular energy metabolism, DNA repair, and cellular signaling. Its inclusion in the General Peptide research catalog reflects the central position NAD+ holds in current aging biology and metabolic research.

NAD+ serves as the electron carrier in the TCA cycle and oxidative phosphorylation, shuttling electrons as NADH to fuel the mitochondrial electron transport chain for ATP production. The discovery of NAD+ as the rate-limiting substrate for three major enzyme families elevated it to a central position in aging biology: Sirtuins (SIRT1-7) — class III histone deacetylases regulating chromatin remodeling, DNA repair, metabolic gene expression, circadian rhythm maintenance, and mitochondrial biogenesis. SIRT1 and SIRT3 are particularly well-characterized, with loss-of-function associated with accelerated aging phenotypes. Poly(ADP-ribose) polymerases (PARPs) — enzymes that detect DNA damage and initiate repair, consuming NAD+ in the process. DNA damage-induced PARP activation can rapidly deplete cellular NAD+ pools. CD38 and CD157 ADP-ribosyl cyclases — NAD+-consuming enzymes involved in calcium signaling and inflammatory signaling whose expression increases with age and inflammatory states.

The critical observation is that NAD+ levels decline substantially with age across tissues and species — skeletal muscle, liver, and brain NAD+ content in old animals is 40-60% lower than in young animals. This decline is now understood to be mechanistically linked to multiple aging phenotypes including mitochondrial dysfunction, impaired DNA repair, metabolic syndrome, neurodegeneration, and immunosenescence.

The 750mg vial format reflects NAD+ use in large-animal and multi-protocol research designs where substantial total quantities are required.