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- Test date
- 2026-06-05
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In stock
NAD+
500mg · Single vial · Lyophilized powder
Single vial44.99CAD
Longevity & metabolic research
NAD+ (nicotinamide adenine dinucleotide) is a coenzyme central to cellular energy metabolism and mitochondrial function, used in longevity, metabolic and DNA-repair research.
- Studied in mitochondrial function and cellular energy research
- Referenced in sirtuin pathway and DNA repair research
- Appears in menopausal metabolic decline and cellular aging research contexts
Order
1
- Dose
- 500mg
- Pack size
- Single vial
- Form
- Lyophilized powder
- Storage
- 2–8°C
In vitro laboratory research use only · Not for human or veterinary use · Batch documented · Third-party tested · Ships from Canada
§ Verification — Batch 2026-05
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§ Research
Research · NAD+
Overview
NAD+ (nicotinamide adenine dinucleotide, oxidized form) is a ubiquitous dinucleotide cofactor composed of nicotinamide mononucleotide and adenosine monophosphate joined by a pyrophosphate bridge. It functions as a central electron carrier in cellular energy metabolism and as a consumed substrate for several enzyme families. It is a standard reagent in enzymology and metabolic research, and tissue NAD+ levels are widely measured in studies of cellular aging. It is supplied as a reagent for dehydrogenase assays and for studies of sirtuin and PARP enzymology.
Mechanism of action
As a hydride acceptor, NAD+ is reduced to NADH in glycolysis, the tricarboxylic acid pathway, and fatty acid oxidation, with NADH reoxidized by mitochondrial complex I to drive oxidative phosphorylation. Separately, NAD+ is cleaved as a substrate by sirtuin deacylases, poly(ADP-ribose) polymerases involved in DNA repair, and the CD38/CD157 glycohydrolases, releasing nicotinamide. Cellular pools are maintained primarily through the salvage pathway, in which nicotinamide phosphoribosyltransferase (NAMPT) is rate-limiting, with additional de novo synthesis from tryptophan and the Preiss-Handler pathway from nicotinic acid. Compartmentalized pools in the nucleus, cytosol, and mitochondria are maintained semi-independently.
Key research findings
- 01
Rodent and human tissue studies have characterized age-associated declines in NAD+ levels across multiple organs.
- 02
Mouse studies have linked tissue NAD+ decline to increased CD38 expression, including on inflammatory macrophages activated by senescent cells.
- 03
Preclinical models have characterized the effects of supplying precursors such as nicotinamide riboside and nicotinamide mononucleotide on tissue NAD+ content and sirtuin-dependent signaling.
- 04
Early-phase clinical studies have characterized the pharmacokinetics of NAD+ precursors and their effects on blood NAD+ metabolite levels in healthy participants.
Published references
NAD(+) metabolism and its roles in cellular processes during ageing
NAD⁺ in aging, metabolism, and neurodegeneration
The information above is derived from published preclinical and clinical research. It is provided for educational purposes only and does not constitute medical advice, diagnosis, or treatment recommendations.