NAD+ for Research in Canada

What NAD+ is

NAD+ (nicotinamide adenine dinucleotide, oxidised form; PubChem title “nadide”) is a coenzyme found in all living cells. It carries electrons in oxidation–reduction reactions, which puts it at the centre of energy metabolism, and it is also consumed as a substrate by non-redox enzymes, notably the sirtuins, CD38 and the poly(ADP-ribose) polymerases (PARPs)^{[1, 2]}. Unlike almost everything else in this catalogue, NAD+ is not a peptide: it is a dinucleotide, two nucleotides joined through a diphosphate bridge (PubChem CID 5892). The 1000mg vial listed here is research-grade material sold for laboratory research only.

Key facts

• Identity: C₂₁H₂₇N₇O₁₄P₂, 663.4 g/mol (PubChem CID 5892); CAS 53-84-9; ChEMBL1234613 (NADIDE, 663.43 g/mol).
• Two jobs: redox coenzyme, and substrate that is used up by sirtuins, PARP-1 and CD38; cells replace it mainly through the NAMPT salvage pathway^[4].
• Fast turnover: in some tissues NAD has a half-life on the order of minutes^[3].
• Evidence base: cell and mouse work on metabolism and ageing, human tissue measurements, and very limited human data on NAD+ itself given by infusion^{[7, 5, 15]}.
• Batch documentation on this site: no batch-specific COA for NAD+ 1000MG is posted in the COA library at the time of writing.

Why researchers study it

NAD+ research used to be the domain of enzymology, because NAD(H) and NADP(H) were seen mainly as co-factors in redox reactions such as mitochondrial electron transport. That picture has widened: NAD pathway metabolites are now linked to signalling, post-translational modification, epigenetic change and RNA capping, and the non-redox reactions steadily break the molecule down, which makes NAD metabolism unusually dynamic^[3]. Reviews connect NAD+ with DNA repair, chromatin remodelling, cellular senescence and immune-cell function^[1], and with the question of whether its concentration changes during ageing^[2].

Identity

What has been studied, by model

Human tissue and imaging

In pelvic skin samples from 49 people (newborns and patients aged 15–77 having unrelated surgery), NAD+ levels correlated negatively with age in both sexes, while PARP activity rose with age in men and tracked inversely with NAD+; the authors proposed that PARP activation by accumulated DNA damage drives NAD+ breakdown^[5]. Methods to measure NAD in the living brain have also been developed: a ³¹P magnetic resonance spectroscopy assay quantified cerebral NAD concentration and NAD+/NADH redox state at a clinical field strength of 4 T^[14]. A 2021 review, however, found the evidence for an across-the-board age-related decline “very limited and often restricted to a single tissue or cell type”, especially in humans^[6].

Mouse studies

Isotope-tracing work in aged mice found only a modest tissue NAD+ fall (median about 30%) with synthesis unimpaired; turnover of the smaller pool was faster, pointing to greater consumption rather than reduced production^[7]. One consuming enzyme is CD38: its expression and activity rose with age in mice, and it was required for the age-related NAD decline and mitochondrial dysfunction, partly through SIRT3^[8]. In ageing mouse muscle, falling NAD+ was linked to a “pseudohypoxic” state that disrupted nuclear–mitochondrial communication, and raising NAD+ restored mitochondrial function in a SIRT1-dependent way^[9]. Much of the intervention work uses precursors rather than NAD+ itself — for example nicotinamide mononucleotide (NMN) in high-fat-diet and aged mice^[10] — and a 2018 review of the in-vivo evidence covers those precursor molecules^[11].

Extracellular NAD+ in cells and mice

How NAD+ added from outside reaches cells is still debated. In HeLa cells, excess extracellular NAD+ triggered a SIRT1-dependent “reset” that brought intracellular levels back to normal by cutting uptake of its breakdown products, reducing CD73, the SLC12A8 transporter and nicotinamide riboside kinase^[12]. In mouse hypothalamic cells, by contrast, extracellular NAD was imported through connexin 43 independently of CD73, and in mice NAD given centrally or peripherally raised hypothalamic NAD and changed fasting-induced feeding^[13].

Study summary

Human data on NAD+ itself

Most human NAD research gives precursors by mouth, not NAD+. A 2026 systematic review found that oral nicotinamide riboside and NMN raised NAD-related markers and were generally well tolerated, but that effects on functional and metabolic outcomes were heterogeneous and often null, and it identified no eligible outcome trials of intravenous or intramuscular NAD+ itself^[16]. A retrospective review of records from a commercial infusion setting compared intravenous NAD+ with intravenous nicotinamide riboside: people receiving NAD+ reported moderate to severe gastrointestinal symptoms, increased heart rate and chest pressure during infusions, which lengthened infusion times, and all symptoms resolved once infusions ended^[15]. This page gives no dosing or administration information, and nothing here is a claim of benefit in people.

What the evidence does not show

• No randomised outcome trial of NAD+ itself, by any route, was identified in the 2026 systematic review^[16].
• Mouse findings on ageing and metabolism mostly involve precursors such as NMN, genetic models or CD38 inhibition, not NAD+ powder^{[10, 8, 11]}.
• Whether extracellular NAD+ enters cells intact, or is first broken down, depends on the cell type and remains debated^{[12, 13]}.
• The claim that NAD+ falls with age in every tissue is not established^[6].
• No study of any SPO batch exists, and no batch COA is posted yet.

Handling and storage

NAD+ 1000MG is supplied as lyophilized powder in a sealed vial. Keep it frozen at −20 °C, dry and protected from light, and avoid repeated freeze–thaw cycles. Solvents such as bacteriostatic water are listed separately, and preparation methods are set by the researcher.

References

1. Covarrubias AJ, Perrone R, Grozio A et al. (2021). NAD+ metabolism and its roles in cellular processes during ageing. Nature reviews. Molecular cell biology 22(2):119-141. doi:10.1038/s41580-020-00313-x. PMID 33353981
2. Verdin E (2015). NAD⁺ in aging, metabolism, and neurodegeneration. Science (New York, N.Y.) 350(6265):1208-13. doi:10.1126/science.aac4854. PMID 26785480
3. Chini CCS, Zeidler JD, Kashyap S et al. (2021). Evolving concepts in NAD+ metabolism. Cell metabolism 33(6):1076-1087. doi:10.1016/j.cmet.2021.04.003. PMID 33930322
4. Ji LL, Yeo D (2022). Maintenance of NAD+ Homeostasis in Skeletal Muscle during Aging and Exercise. Cells 11(4). doi:10.3390/cells11040710. PMID 35203360
5. Massudi H, Grant R, Braidy N et al. (2012). Age-associated changes in oxidative stress and NAD+ metabolism in human tissue. PloS one 7(7):e42357. doi:10.1371/journal.pone.0042357. PMID 22848760
6. Peluso A, Damgaard MV, Mori MAS et al. (2021). Age-Dependent Decline of NAD+-Universal Truth or Confounded Consensus? Nutrients 14(1). doi:10.3390/nu14010101. PMID 35010977
7. McReynolds MR, Chellappa K, Chiles E et al. (2021). NAD+ flux is maintained in aged mice despite lower tissue concentrations. Cell systems 12(12):1160-1172.e4. doi:10.1016/j.cels.2021.09.001. PMID 34559996
8. Camacho-Pereira J, Tarragó MG, Chini CCS et al. (2016). CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism. Cell metabolism 23(6):1127-1139. doi:10.1016/j.cmet.2016.05.006. PMID 27304511
9. Gomes AP, Price NL, Ling AJ et al. (2013). Declining NAD(+) induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging. Cell 155(7):1624-38. doi:10.1016/j.cell.2013.11.037. PMID 24360282
10. Yoshino J, Mills KF, Yoon MJ et al. (2011). Nicotinamide mononucleotide, a key NAD(+) intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell metabolism 14(4):528-36. doi:10.1016/j.cmet.2011.08.014. PMID 21982712
11. Rajman L, Chwalek K, Sinclair DA (2018). Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence. Cell metabolism 27(3):529-547. doi:10.1016/j.cmet.2018.02.011. PMID 29514064
12. Buonvicino D, Ranieri G, Pittelli M et al. (2021). SIRT1-dependent restoration of NAD+ homeostasis after increased extracellular NAD+ exposure. The Journal of biological chemistry 297(1):100855. doi:10.1016/j.jbc.2021.100855. PMID 34097876
13. Roh E, Park JW, Kang GM et al. (2018). Exogenous nicotinamide adenine dinucleotide regulates energy metabolism via hypothalamic connexin 43. Metabolism: clinical and experimental 88:51-60. doi:10.1016/j.metabol.2018.08.005. PMID 30179604
14. Lu M, Zhu XH, Chen W (2016). In vivo (31) P MRS assessment of intracellular NAD metabolites and NAD(+) /NADH redox state in human brain at 4 T. NMR in biomedicine 29(7):1010-7. doi:10.1002/nbm.3559. PMID 27257783
15. Reyna K, Heinzen G, Patel N et al. (2026). Intravenous infusion of nicotinamide adenine dinucleotide (NAD+) versus nicotinamide riboside (NR): a retrospective tolerability pilot study in a real-world setting. Frontiers in aging 7:1652582. doi:10.3389/fragi.2026.1652582. PMID 41704678
16. Gallagher C, Emmanuel OO (2026). NAD⁺ supplementation for anti-aging and wellness: A PRISMA-guided systematic review of preclinical and clinical evidence. Ageing research reviews 116:103057. doi:10.1016/j.arr.2026.103057. PMID 41655607