NAD+

Nicotinamide adenine dinucleotide (NAD+; CAS 53-84-9; molecular formula C21H27N7O14P2; molecular weight 663.43) is a small-molecule pyridine dinucleotide cofactor that functions in three biologically distinct roles: as the dominant cellular electron-transfer cofactor in oxidative metabolism (where it cycles between the oxidized NAD+ and reduced NADH forms), as the substrate for the sirtuin family of NAD+-dependent deacetylases (which hydrolyze NAD+ to nicotinamide and ADP-ribose), and as the substrate for poly-ADP-ribose polymerases (PARPs) and the CD38 ecto-enzyme (both of which also consume NAD+). Cellular NAD+ concentrations are tightly regulated and decline substantially with age in humans and other mammals; the age-related decline correlates with reduced sirtuin activity, impaired DNA damage repair, and a constellation of metabolic dysfunctions that has motivated substantial research interest in NAD+ supplementation as a geroprotective intervention. The research-grade product supplied as "NAD+" is the oxidized free acid form, which has poor oral bioavailability but is suitable for parenteral administration in research models. Better-characterized parenteral approaches use NAD+ precursors (nicotinamide riboside NR and nicotinamide mononucleotide NMN), which are more efficiently absorbed orally and converted intracellularly to NAD+. Direct NAD+ administration in research-grade dosing has been used in study of cellular bioenergetics, neurological function, and metabolic endpoints. The compound is not approved by any regulatory authority for human or veterinary use as a therapeutic; NAD+ is also widely available as a food supplement under separate regulatory frameworks.