NAD+ — nicotinamide adenine dinucleotide — is not a peptide. It is a dinucleotide coenzyme, and it does two quite different jobs that are frequently conflated.
Role one: electron carrier
The classical role. NAD+ accepts a hydride to become NADH, shuttling electrons through glycolysis, the citric acid cycle and oxidative phosphorylation. In this role it is recycled, not consumed — the NAD+/NADH ratio reports cellular energetic state.
Role two: consumed substrate
The role driving current research interest. Sirtuins, a family of NAD+-dependent deacetylases, and PARPs, involved in DNA damage response, both cleave NAD+ and consume it in the process.
This is the crux. Because these enzymes destroy NAD+ rather than recycling it, sustained DNA damage or high sirtuin activity draws down the pool, and it must be resynthesised. That consumption link is the basis of research connecting NAD+ availability to DNA repair capacity and to the sirtuin pathways associated with metabolic regulation.
A caveat on direct administration
NAD+ is a large, charged molecule that does not readily cross cell membranes. Much of the field therefore works with precursors such as nicotinamide riboside and nicotinamide mononucleotide, which enter cells and are converted intracellularly. Research designs using NAD+ directly should account for that.
Supplied lyophilised. See our reconstitution protocol for handling technique and diluent selection.
Every batch ships with a third-party certificate of analysis. View NAD+ and its current COA.
Research use only
Isla Longevity supplies this compound for laboratory research use only. It is not approved by the FDA for human or veterinary use and is not for human consumption. This article summarises published research and is not medical guidance.
