NAD+

What makes NAD+ unusual as a research compound is its dual nature. In redox reactions — glycolysis, the citric acid cycle, oxidative phosphorylation — it functions as a recyclable coenzyme, accepting and donating electrons as NAD+ and NADH. But sirtuins, PARPs, and CD38 actually consume it. They break NAD+ apart to do their work, depleting the cellular pool. This creates a resource competition at the molecular level that sits at the center of aging and metabolic research.

The three-way competition

Sirtuins (SIRT1-7) are NAD+-dependent deacylases that regulate gene expression, DNA repair, and stress responses. PARPs consume NAD+ to build poly(ADP-ribose) chains during DNA damage repair. CD38 uses NAD+ for calcium signaling through cADPR synthesis. All three enzyme families draw from the same NAD+ pool, and published research shows that pool shrinks substantially with age across multiple tissue types (Covarrubias et al., Nature Reviews Molecular Cell Biology, 2021).

The implications are significant: when PARP activates during DNA damage, it can drain enough NAD+ to starve sirtuin-mediated regulatory functions. Wang et al. examined this dynamic specifically in the context of base excision repair after ischemic stress (Stroke, 2008; PubMed 18635843).

Specifications

Selected research

Mills et al. published one of the landmark studies in NAD+ precursor research — a 12-month NMN administration study in normal-aging mice that tracked body weight, energy metabolism, and a range of metabolic parameters over time (Cell Metabolism, 2016; PubMed 28068222). Zhang et al. examined the downstream consequences for mitochondrial and stem cell function (Cell, 2016). Imai et al. reviewed the broader NAD+ metabolism landscape comprehensively (Nat Rev Mol Cell Biol, 2024).

Research applications

• Sirtuin activity assays and NAD+-dependent deacylase research
• PARP activation and DNA damage repair studies
• Cellular bioenergetics and electron transport chain research
• Redox biochemistry — NAD+/NADH ratio quantification
• CD38 enzymatic regulation and cADPR signaling
• Mitochondrial function and oxidative phosphorylation

Quality and testing

Every Heritage Labs compound is manufactured to research-grade standards and shipped in protective packaging.

Storage

• Lyophilized: -20°C for long-term stability
• Reconstituted: 2-8°C
• Protection: Shield from light and moisture

References

1. Covarrubias AJ, et al. “NAD+ metabolism and its roles in cellular processes during ageing.” Nat Rev Mol Cell Biol. 2021;22(2):119-141.
2. Mills KF, et al. “Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in mice.” Cell Metabolism. 2016;24(6):795-806. PubMed 28068222
3. Zhang R, et al. “NAD+ repletion improves mitochondrial and stem cell function.” Cell. 2016;124(3):423-436.
4. Wang S, et al. “NAD+ repletion and base excision repair after ischemic stress.” Stroke. 2008;39(9):2587-2595. PubMed 18635843
5. Imai S, et al. “Roles of NAD+ metabolism in cellular signaling and disease.” Nat Rev Mol Cell Biol. 2024;25:452-467.
6. Rajman L, et al. “Therapeutic potential of NAD-boosting molecules.” Cell Metabolism. 2018;27(3):529-547.

For laboratory research use only. Not for human or veterinary use. Not a drug, food, or cosmetic.