Nicotinamide adenine dinucleotide (NAD⁺) is a ubiquitous pyridine nucleotide coenzyme used in laboratory systems to study cellular redox balance, bioenergetics, and metabolic network behavior. In experimental settings, NAD⁺ is commonly evaluated through its reversible cycling with NADH, providing a measurable handle on electron-transfer reactions that support glycolytic and mitochondrial readouts.

Beyond classical redox chemistry, NAD⁺ is also treated as an enzymatic substrate for multiple NAD⁺-consuming enzyme families (including sirtuins and PARPs) that connect nucleotide availability to signaling, DNA-damage response measurements, and transcription-linked datasets in non-clinical models.

Note: This product is supplied as a lyophilized powder and should be reconstituted with bacteriostatic water for appropriate research handling.

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For laboratory research only. Not for human consumption, medical, or veterinary use.

Molecular formula: C21H27N7O14P2

Molecular weight: 663.43 g/mol

CAS number: 53-84-9

PubChem: CID 925

In research workflows, NAD⁺ is frequently handled as a redox-active cofactor for dehydrogenase-coupled assays and as a limiting reagent or tracked pool for NAD⁺-dependent enzyme activity measurements.

NAD⁺ is routinely incorporated into redox biochemistry assays to quantify or couple oxidation–reduction reactions (for example, dehydrogenase-driven readouts that report on NAD⁺/NADH turnover).

NAD⁺ is also used in NAD⁺-dependent enzyme systems where consumption of NAD⁺ (or formation of reaction products) is measured as a proxy for activity in sirtuin, PARP, and related signaling-linked enzyme assays.

In cellular and animal-model research, NAD⁺ status is often profiled alongside transcriptomic, proteomic, and metabolomic outputs to contextualize pathway shifts tied to mitochondrial function, stress-response programs, and aging-associated datasets.

NAD⁺ sits at the intersection of bioenergetic flux and signaling-linked NAD⁺ consumption, so research discussions commonly frame it as both an electron carrier for metabolic reactions and a substrate pool competed over by multiple enzyme families.

Within aging and stress-oriented literature, reported declines in NAD⁺ levels (across multiple model systems) are often interpreted alongside measures of DNA-damage signaling, chromatin regulation, and immune or inflammatory readouts, with emphasis on mechanistic links rather than clinical claims.

Because NAD⁺ pools are compartmentalized and dynamically replenished, it is also frequently discussed in the context of biosynthetic routes and turnover pathways that shape measurable NAD⁺ availability in different subcellular locations.

Mitochondrial and metabolic model systems frequently report relationships between NAD⁺ availability and measured oxidative phosphorylation or redox-state endpoints, treating NAD⁺ as a quantitative variable that shifts alongside metabolic program changes.

In aging-oriented datasets, published work commonly links altered NAD⁺ levels to downstream signatures in gene expression, DNA repair–associated pathways, and NAD⁺-consuming enzyme activity, describing associations observed under controlled experimental conditions.

Rodent studies have also evaluated exogenous NAD⁺ exposure using non-clinical paradigms, reporting changes in measured tissue NAD⁺ metrics and injury-associated endpoints in models of acute neurologic insult; these findings are presented within preclinical frameworks and do not establish clinical utility.

Covarrubias AJ, Perrone R, Grozio A, Verdin E. NAD⁺ metabolism and its roles in cellular processes during ageing. Nature Reviews Molecular Cell Biology. 2021;22(2):119–141. doi:10.1038/s41580-020-00313-x.

Cantó C, Menzies KJ, Auwerx J. NAD⁺ metabolism and the control of energy homeostasis: a balancing act between mitochondria and the nucleus. Cell Metabolism. 2015;22(1):31–53. doi:10.1016/j.cmet.2015.05.023.

Ying W, Wei G, Wang D, Wang Q, Tang X, Shi J, Zhang P, Lu H. Intranasal administration with NAD⁺ profoundly decreases brain injury in a rat model of transient focal ischemia. Frontiers in Bioscience. 2007;12:2728–2734. doi:10.2741/2267.

Verdin E. NAD⁺ in aging, metabolism, and neurodegeneration. Science. 2015;350(6265):1208–1213. doi:10.1126/science.aac4854.

Imai S, Guarente L. NAD⁺ and sirtuins in aging and disease. Trends in Cell Biology. 2014;24(8):464–471.

Nikiforov A, Dölle C, Niere M, Ziegler M. The human NAD metabolome: functions, metabolism and compartmentalization. Critical Reviews in Biochemistry and Molecular Biology. 2015.

Won SJ, et al. Prevention of traumatic brain injury-induced neuron death by intranasal delivery of nicotinamide adenine dinucleotide. Journal of Neurotrauma. (Full text in PMC).

beta-Nicotinamide adenine dinucleotide (NAD⁺) chemical record. PubChem.

To protect experimental integrity, store peptides cold, dry, and shielded from light to minimize oxidation, contamination, and degradation. For near-term use, keep unopened material refrigerated at ≤4 °C (≤39 °F) and limit time at room temperature during handling. Lyophilized (dry) peptides can tolerate short periods at room temperature, but refrigeration is preferred for best stability and longevity. For longer-term storage, keep unmixed material frozen—−18 °C (0 °F) is acceptable, while −80 °C (−112 °F) is optimal for multi-month to multi-year preservation. Avoid frost-free freezers and repeated freeze–thaw cycles, which can accelerate breakdown. If reconstituted (in solution), use sterile buffer (ideally pH 5–6 when feasible), split into aliquots, and freeze (preferably −80 °C (−112 °F)) to reduce handling-related degradation.

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