NAD+
500mg | $129.00pH buffered
NAD+ is the molecule that connects energy production to cellular maintenance. It carries electrons through the respiratory chain for ATP synthesis, and the same supply is consumed by enzymes that adjust gene expression, coordinate circadian timing, and execute DNA repair.
This shared dependence makes NAD+ central to research on aging, metabolic resilience, and how tissues maintain function under sustained demand.
Made in USA•Purity: 99% HPLC
- ATP ProductionCarries electrons from nutrient breakdown to the mitochondrial respiratory chain, where they drive ATP synthesis. This cycling is continuous—NAD+ is recycled, not consumed.
- Metabolic and Circadian AdaptationConsumed by sirtuin enzymes when they adjust gene expression for stress responses, metabolic flexibility, and circadian timing. Unlike electron transport, this is irreversible—the molecule is cleaved.
- DNA Damage ResponseConsumed by PARP enzymes during DNA strand break detection and repair. Sustained damage from oxidative stress or inflammation keeps PARPs active and draws heavily on NAD+ supply.
- Why Availability DeclinesCD38—an enzyme on immune and endothelial cells—degrades NAD+ during inflammatory signaling. Its expression rises with age and inflammation, making it the dominant driver of tissue NAD+ decline.
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For in-vitro laboratory research use only. Not for human consumption.
Research Status:Randomized Controlled Trials
High-quality RCTs for oral precursors (NR/NMN) demonstrating NAD+ elevation in blood and tissue; clinical trials for injectable NAD+ pharmacokinetics ongoing (NCT06919328)
For laboratory research use only.
NAD+ connects energy production to cellular maintenance. The molecule carries electrons through the mitochondrial respiratory chain to generate ATP, and the same supply is consumed—irreversibly—by enzymes that coordinate stress responses, adjust metabolic timing, and repair DNA damage. Because oxidative metabolism and adaptive maintenance draw from the same source, NAD+ availability determines how much sustained work a cell can perform while still responding to changing conditions.
Precursor Trials in Humans
Nicotinamide riboside (NR) has the deepest controlled trial base. Three weeks of supplementation raised skeletal muscle NAD+ metabolites in older adults, with shifts in anti-inflammatory gene expression (Elhassan et al., 2019). Longer supplementation—8 to 12 weeks—elevated circulating NAD+ 40–60% with good tolerability (Martens et al., 2018). The NADPARK trial confirmed brain penetration: Parkinson's patients showed increased cerebral NAD+ on phosphorus MRS after oral NR (Brakedal et al., 2022).
Nicotinamide mononucleotide (NMN) increased muscle insulin sensitivity in prediabetic women over 10 weeks (Yoshino et al., 2021). Head-to-head comparisons with NR show comparable NAD+ elevation, though tissue distribution may differ.
Functional endpoints have been mixed. Cardiovascular markers show the most consistent effect: 6–8 weeks of NR modestly reduced systolic blood pressure and improved arterial compliance in older adults. Exercise tolerance, cognitive performance, and six-minute walk have shown directional improvement in some trials but not others.
Tissue-Level Studies
Rodent and human tissue studies have quantified the age-related decline. Skeletal muscle shows approximately 35% reduction in NAD+ salvage enzyme expression with age. Liver and adipose tissue NAD+ levels fall 30–50% from peak. CD38 knockout mice do not exhibit this decline, establishing the enzyme as the dominant driver (Camacho-Pereira et al., 2016).
Senescent cell accumulation appears to be the upstream trigger: damaged cells secrete inflammatory signals that expand CD38-positive macrophages in surrounding tissue, which then consume NAD+ from neighboring cells (Covarrubias et al., 2020).
Injectable Pharmacokinetics
A 2024 pilot compared intravenous NAD+ against intravenous NR at equivalent doses. IV NR raised whole-blood NAD+ approximately 21% within three hours—outperforming direct IV NAD+ infusion—with fewer infusion-related side effects and faster administration time. This suggests parenteral precursors may offer better kinetics than direct NAD+ delivery for acute elevation.
Intramuscular and subcutaneous NAD+ have clinical use based on pharmacokinetic logic (bypassing first-pass metabolism), but controlled pharmacokinetic data from these routes remain limited. Most published evidence is with oral precursors.
Duration of evidence. Most human data come from precursor trials lasting 8–12 weeks. Long-term outcome studies have not been completed. Blood NAD+ elevation may not reflect tissue-level changes in all compartments.
Cancer considerations. NAD+ fuels cellular metabolism broadly, including in malignant cells. Active cancer is typically considered a contraindication. One murine study raised concern about high-dose NR accelerating aggressive breast cancer metastasis, though this finding has not been replicated in humans. History of malignancy warrants oncology consultation.
Individual variability. Response to NAD+ precursors differs between individuals. Baseline depletion status, age, inflammatory burden, and genetic variation in metabolic enzymes (NAMPT, CD38 polymorphisms) likely influence both how much NAD+ rises and whether that elevation translates to functional change.
Injectable evidence gap. IV, IM, and SC NAD+ are used clinically based on mechanistic reasoning, not randomized efficacy data. The controlled trial base remains with oral precursors.
- Verdin E. "NAD+ in aging, metabolism, and neurodegeneration." Science. 2015;350(6265):1208-1213. PubMed
- Camacho-Pereira J et al. "CD38 dictates age-related NAD decline and mitochondrial dysfunction." Cell Metab. 2016;23(6):1127-1139. PMC
- Martens CR et al. "Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults." Nat Commun. 2018;9(1):1286. PubMed
- Elhassan YS et al. "Nicotinamide riboside augments the aged human skeletal muscle NAD+ metabolome." Cell Rep. 2019;28(7):1717-1728. PubMed
- Yoshino M et al. "Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women." Science. 2021;372(6547):1224-1229. PubMed
- Brakedal B et al. "The NADPARK study: nicotinamide riboside in Parkinson's disease." Cell Metab. 2022;34(3):396-407. PubMed
- Covarrubias AJ et al. "Senescent cells promote tissue NAD+ decline via CD38+ macrophages." Nat Metab. 2020;2(11):1265-1283. PubMed
For laboratory research use only.
| Molecular Formula | C21H27N7O14P2 |
|---|---|
| Molecular Weight | 663.43 g/mol |
| CAS Number | 53-84-9 |
| PubChem CID | 925 |
| Origin | A coenzyme present in all living cells that connects energy production to cellular maintenance. Carries electrons through the respiratory chain for ATP synthesis; consumed irreversibly by enzymes that coordinate stress adaptation, circadian timing, and DNA repair. |
This product ships as lyophilized (freeze-dried) powder. After reconstitution, the solution requires different storage conditions than the powder.
Reconstituted Solution
Refrigerate2–8°C (36–46°F)Up to 30 daysDo not freeze. Use within 30 days of mixing.
Lyophilized Powder
Refrigerated2–8°C (36–46°F)Weeks to months
Frozen−20°C (−4°F) or belowMonths to years
Oral NAD+ is hydrolyzed in digestion. Oral precursors (NR, NMN) require hepatic conversion and raise NAD+ gradually over weeks. Injectable NAD+ bypasses first-pass metabolism for more rapid elevation—relevant in research contexts examining acute pharmacokinetics.
Oral precursors have multiple RCTs demonstrating NAD+ elevation and acceptable tolerability. Injectable NAD+ (IV, IM, SC) has pharmacokinetic characterization but lacks the controlled efficacy trial evidence of oral routes. A 2024 pilot found IV NR outperformed IV NAD+ for acute NAD+ elevation.
Active cancer is typically considered a contraindication—NAD+ supports cellular metabolism broadly. One murine study raised concern about high-dose NR potentially accelerating aggressive breast cancer. History of malignancy warrants oncology consultation.
IV infusion produces rapid elevation but requires slow administration to minimize infusion-related effects. IM and SC injection release NAD+ gradually. Clinical use exists for all routes; controlled pharmacokinetic data is limited to IV comparisons.