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NAD+ (Nicotinamide Adenine Dinucleotide)

≥99% Purity
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Categories: Anti-aging Peptides, Metabolic Peptides

NAD+ is the essential coenzyme for 500+ enzymatic reactions and the obligate substrate for sirtuins, PARPs, and CD38. Central to aging research — NAD+ decline is recognized as a hallmark of biological aging.


Nicotinamide Adenine Dinucleotide (NAD+, oxidized form) is a dinucleotide coenzyme composed of nicotinamide mononucleotide (NMN) linked to adenosine monophosphate (AMP) via a pyrophosphate bond. As an electron carrier, NAD+ participates in over 500 enzymatic redox reactions across glycolysis, the tricarboxylic acid (TCA) cycle, oxidative phosphorylation, and fatty acid beta-oxidation, making it arguably the single most important metabolic cofactor in mammalian biochemistry.

Beyond its classical role as a redox shuttle, NAD+ serves as the obligate co-substrate for three enzyme families that are central to aging biology research. Sirtuins (SIRT1-7) are NAD+-dependent protein deacylases that regulate gene expression, DNA repair, mitochondrial biogenesis, inflammation, and stress response — SIRT1 and SIRT3 in particular are considered longevity-promoting enzymes whose activity is directly limited by NAD+ availability. Poly(ADP-ribose) polymerases (PARPs), particularly PARP1, consume NAD+ during DNA damage repair, competing with sirtuins for the shared substrate pool. CD38/cADPR cyclases are ecto-enzymes that hydrolyze NAD+ on immune cells, functioning in calcium signaling and immune regulation while also being major NAD+ consumers that increase with age and inflammation.

The age-related decline of NAD+ is now recognized as a conserved hallmark of biological aging across species and tissues. Published research from the laboratories of David Sinclair (Harvard), Shin-ichiro Imai (Washington University), and others has documented progressive NAD+ depletion in aging tissues correlated with mitochondrial dysfunction, impaired DNA repair capacity, sirtuin hypoactivity, and chronic low-grade inflammation (“inflammaging”). This decline is driven by increased CD38 expression and PARP activity with aging, combined with reduced NAD+ biosynthesis. Strategies to replenish NAD+ levels — including direct supplementation and precursor-based approaches (NMN, NR) — represent one of the most active areas of contemporary longevity research.

Supplied as a lyophilized powder (oxidized form) with ≥99% purity. NAD+ is sensitive to light, moisture, and oxidation — store at -20°C desiccated under inert atmosphere. Reconstitute immediately before use. For cellular metabolism and aging research only.

⚠ Supplied strictly for research and experimental purposes only.