Price per pack (10 vials). Discount applies to this compound only – no mix and match.
| 500mg | ||
|---|---|---|
| Quantity | Price per Pack | Savings |
| 1 pack | $350 per pack | |
| 2 packs | $298 per pack | 15% off |
| 3 packs | $253 per pack | 28% off |
| 5 packs | $228 per pack | 35% off |
| 10 packs | $205 per pack | 41% off |
| 25 packs | $184 per pack | 47% off |
Nicotinamide Adenine Dinucleotide (NAD+) is a coenzyme present in every living cell, functioning as the central electron carrier in oxidative metabolism and as a required substrate for a class of regulatory enzymes — sirtuins and PARPs — that govern DNA repair, gene silencing, and mitochondrial biogenesis. Interest in NAD+ as a research target intensified following work by David Sinclair at Harvard and Johan Auwerx at EPFL, whose publications between 2013 and 2016 demonstrated that age-associated NAD+ decline in mammals produces measurable deterioration in sirtuin-dependent processes, and that NAD+ restoration via precursors (NMN, NR) or direct supplementation partially reversed these deficits in aged rodents. Direct NAD+ research — particularly via intravenous delivery to bypass low oral bioavailability — allows investigators to study the immediate biochemical effects of NAD+ repletion without the metabolic conversion steps required by precursor approaches.
NAD+ operates in two distinct modes. In its redox role, it accepts electrons from metabolic intermediates (becoming NADH), driving ATP production in the electron transport chain. In its signaling role, NAD+ is consumed — not recycled — as a substrate by sirtuins (SIRT1, SIRT3, SIRT6), PARP enzymes, and CD38, meaning cellular NAD+ availability directly gates the activity of these regulatory proteins. SIRT1 and SIRT6 deacetylate histones and transcription factors involved in aging, inflammation, and circadian regulation; SIRT3 governs mitochondrial protein acetylation; PARP-1 drives DNA strand break repair. Declining NAD+ with age thus produces a compound deficit across all three systems simultaneously — a mechanistic rationale that has made NAD+ restoration one of the more intensively studied interventions in aging biology.
| Mechanism | Effect |
|---|---|
| SIRT1/SIRT6 co-substrate | Histone deacetylation; epigenetic regulation of aging-associated gene expression |
| SIRT3 co-substrate (mitochondrial) | Mitochondrial protein deacetylation; oxidative phosphorylation regulation |
| PARP-1 substrate → DNA repair | Poly-ADP ribosylation at DNA damage sites; strand break repair initiation |
| Redox cycling (NAD+/NADH) | Electron transport chain fueling; ATP production efficiency |
| CD38 substrate consumption | Calcium signaling modulation; immune cell activation — CD38 activity increases with inflammation and age |
| Mitochondrial biogenesis (SIRT1 → PGC-1α deacetylation) | Increased mitochondrial mass and oxidative capacity in muscle and neuronal models |
NAD+ is used in studies examining:
| Format | Lyophilized powder |
| Purity | ≥99% |
| Aliases | Nicotinamide adenine dinucleotide, NAD, β-NAD+, coenzyme I |
| Available sizes | 500mg |
| Solubility | Water-soluble; typically reconstituted in sterile water or saline for IV research use |
| Storage | 2–8°C, protect from light; oxidation-sensitive — minimize air exposure after opening |
| Use | Research purposes only — not for human use |
Oral bioavailability of exogenous NAD+ is limited due to degradation in the gut prior to absorption; published clinical research has primarily used IV infusion for direct repletion studies. Dose ranges below reflect IV administration frameworks seen in the literature.
NAD+ is commonly paired in research settings with:
Every batch is ≥99% purity. If you independently test your compound and the results don’t match — send us the COA and we’ll issue store credit, no questions asked.



