All information below describes the compound's chemical identity, laboratory handling, and the published research literature. It describes molecular targets and results in laboratory and animal models only — not effects in humans — and is not evidence of any human benefit.
What Is NAD+?
NAD+ (Nicotinamide Adenine Dinucleotide) is a dinucleotide coenzyme found in all living cells. Structurally, it comprises a nicotinamide nucleotide joined to an adenine nucleotide through a phosphate bridge; it is not a peptide and carries no amino acid sequence. The molecule exists in two interconverting forms — NAD+ (oxidized) and NADH (reduced) — that cycle as electron carriers in redox reactions central to cellular metabolism. It was first described by Harden and Young in the early twentieth century and is a naturally occurring coenzyme rather than a synthetic analogue.
It is supplied as a reference compound for in vitro and animal research use only. The sections below summarize its chemical identity, laboratory handling, the molecular targets and model systems examined in the published literature, and the primary references — without describing outcomes, efficacy, or effects in humans.
Research Targets & Pathways
Published preclinical literature has examined NAD+ in relation to several molecular systems. These are pathway associations reported in laboratory and animal models; refer to the cited studies for methods and findings.
- Sirtuin deacetylases (SIRT1) — examined in relation to NAD+-dependent deacetylation activity in metabolic and aging models.
- AMPK–mTOR–SIRT3 axis — examined in relation to mitochondrial bioenergetic signaling.
- PARP1 — examined in relation to NAD+ consumption during the DNA-damage response.
- SARM1 NADase — examined in relation to NAD+ hydrolysis and axonal-degeneration signaling.
- CD38 — examined as an NAD+-consuming enzyme in NAD+ turnover studies.
- NAMPT / salvage pathway — examined in relation to NAD+ biosynthesis.
- PGC-1α — examined in relation to mitochondrial-biogenesis signaling.
- FOXO3 / PI3K–Akt signaling — examined in redox-homeostasis and myogenic-differentiation assay systems.
Model Systems Studied
NAD+ and its precursors have been used as test compounds across a range of published preclinical model systems, primarily in rodents, invertebrate models, and in vitro cell assays. Refer to the cited literature for study designs, endpoints, and findings.
- Rodent aging — aged-mouse muscle and tissue models; high-fat-diet mouse models.
- Invertebrate longevity — C. elegans aging models.
- Neurological — neuronal cell models and a Cockayne-syndrome neurodegeneration model.
- Skeletal muscle — C2C12 myoblast differentiation assays.
- In vitro — A549 lung-carcinoma cells, mouse embryonic fibroblasts, and human peripheral blood mononuclear cells (PBMCs).
Note: much of the published in vivo NAD+ evidence derives from precursor (NMN/NR) supplementation studies rather than direct NAD+ administration; NAD+ precursor research remains an active field, and several cell- and animal-model findings await full clinical replication.
Molecular & Technical Profile
C21H27N7O14P2 | MW 663.43 g/mol | CAS 53-84-9 | Type: dinucleotide coenzyme (non-peptide)
Storage, Reconstitution & Working Concentrations
Storage, reconstitution, and working-concentration values are general laboratory guidance for in vitro and animal research; always confirm against the lot-specific Certificate of Analysis.
Current Research Status
As of the time of this writing, NAD+ has not been approved by the U.S. Food and Drug Administration (FDA) for any human therapeutic use. The available evidence base is primarily preclinical, derived from cell-based and rodent models, with much of the in vivo data generated using NAD+ precursor molecules (NMN and NR). While early human pharmacokinetic studies of these precursors have measured changes in the blood NAD+ metabolome, translation to defined human clinical contexts has not been established through controlled clinical trials. Ongoing research continues to characterize the coenzyme's mechanistic profile and identify which experimental findings may have translational relevance.
Research FAQ
Is NAD+ approved for human use?
No. NAD+ has not been approved by the FDA for any human therapeutic use. The evidence base is preclinical (cell-based and rodent models), and the compound is supplied for laboratory research use only — not for human consumption.
What is NAD+'s molecular formula?
A dinucleotide coenzyme — molecular formula C21H27N7O14P2, MW 663.43 g/mol, CAS 53-84-9. It is not a peptide and has no amino acid sequence; it comprises a nicotinamide nucleotide joined to an adenine nucleotide through a phosphate bridge.
How is NAD+ stored and reconstituted?
Store lyophilized at −20°C, protected from light and moisture. Reconstitute in sterile nuclease-free water or PBS (pH 7.0–7.4); store the reconstituted solution at 2–8°C for up to ~28 days, limit freeze–thaw cycles, and avoid alkaline conditions above pH 9.
What targets and model systems has NAD+ been studied in?
Preclinical work has examined NAD+ in relation to sirtuin deacetylases (SIRT1, SIRT3), PARP1, the SARM1 NADase, CD38, and NAMPT biosynthesis, across aged rodents, C. elegans, and in vitro assays in C2C12 myoblasts, neuronal cells, and human PBMCs. Much of the in vivo evidence derives from precursor (NMN/NR) supplementation studies.
Selected References
- Verdin E. (2015). NAD+ in aging, metabolism, and neurodegeneration. Science, 350(6265):1208–1213.
- Rajman L, Chwalek K, Sinclair DA. (2018). Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence. Cell Metabolism, 27(3):529–547.
- Mills KF, et al. (2016). Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice. Cell Metabolism, 24(6):795–806.
- Elhassan YS, et al. (2019). Nicotinamide Riboside Augments the Aged Human Skeletal Muscle NAD+ Metabolome and Induces Transcriptomic and Anti-inflammatory Signatures. Cell Reports, 28(7):1717–1728.
- Hou Y, et al. (2021). NAD+ supplementation reduces neuroinflammation and cell senescence in a transgenic mouse model of Alzheimer's disease via cGAS–STING. PNAS, 118(37):e2011226118.