$195.00
Core cellular coenzyme for redox, DNA repair and sirtuin/PARP signaling. Potential benefits of augmenting NAD+ pools include supporting metabolic health, stress resistance and aspects of healthy aging. Human supplementation studies show mixed, mostly short‑term biochemical gains; clinical outcome benefits remain uncertain.
Description
NAD+ (nicotinamide adenine dinucleotide, oxidized form) is a ubiquitous redox coenzyme present in all living cells. Beyond its classical role as an electron carrier in energy metabolism (glycolysis, TCA cycle, oxidative phosphorylation), NAD+ serves as an essential co‑substrate for NAD‑dependent enzymes including sirtuins, poly(ADP‑ribose) polymerases (PARPs), and CD38/CD157 ecto‑enzymes. Cellular NAD+ pools influence DNA repair, chromatin state, mitochondrial function, stress responses, circadian regulation, immune signaling, and aging biology.
Chemical Structure / Identifiers
| Property | Detail |
| Preferred Name | β‑Nicotinamide adenine dinucleotide (oxidized form); NAD+ |
| Synonyms | Diphosphopyridine nucleotide (DPN); Coenzyme I; Nadide |
| Molecular Formula (anhydrous) | C21H27N7O14P2 |
| Molecular Weight (anhydrous) | ≈ 663.43 g/mol |
| CAS Number | 53‑84‑9 |
| PubChem CID | 925 (β‑NAD); 5892/5893 (Nadide entries) |
Primary Research Focus
• Cellular energy and redox: electron carrier in dehydrogenase reactions; central to ATP production.
• Sirtuin biology: co‑substrate for class III histone deacetylases regulating metabolism, stress resistance, and longevity pathways.
• DNA repair/chromatin: PARP‑dependent ADP‑ribosylation uses NAD+ to coordinate DNA damage responses and chromatin remodeling.
• Immune and inflammatory signaling: CD38‑mediated NAD+ turnover modulates calcium signaling and immune cell function.
• Aging and metabolic health: NAD+ declines with age; NAD+ augmentation via precursors (e.g., NR, NMN) is under investigation for cardiometabolic and neuroprotective effects.
Safety / Limitations
• Research Use Only in this context; NAD+ biology is well established, but many supplementation claims remain under active study.
• Evidence for NAD+ augmentation in humans is mixed and often short‑term; long‑term efficacy and safety data are limited and context‑dependent.
• Some interventions (e.g., high‑dose precursors) can alter methyl‑donor balance or interact with existing conditions/medications; clinical oversight is advised in experimental contexts.
Key Publications / References
PubChem Compound Summary: β‑Nicotinamide adenine dinucleotide (CID 925). https://pubchem.ncbi.nlm.nih.gov/compound/925
Katsyuba & Auwerx (2020). NAD+ homeostasis in health and disease. Nat Rev Mol Cell Biol. https://europepmc.org/article/med/32694684
Covarrubias et al. (2021). NAD+ metabolism in cellular processes during aging. Nat Rev Mol Cell Biol. https://pmc.ncbi.nlm.nih.gov/articles/PMC7963035/
Kane & Sinclair (2018). Sirtuins and NAD+ in development and treatment of cardiovascular/metabolic disease. Front Pharmacol. https://pmc.ncbi.nlm.nih.gov/articles/PMC6206880/
Conlon (2021). The role of NAD+ in regenerative medicine. Rejuvenation Res. https://pmc.ncbi.nlm.nih.gov/articles/PMC9512238/
Cantó et al. (2009). AMPK regulates energy expenditure by modulating NAD+ metabolism. PNAS. https://europepmc.org/article/med/19262508
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