NAD+
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These products are for laboratory research only and not intended for medical use. They are not FDA-approved to diagnose, treat, cure, or prevent any disease. By purchasing, you certify they will be used solely for research and not for human or animal consumption.
Research Summary
26 PubMed CitationsOverview NAD+ (Nicotinamide Adenine Dinucleotide) is a coenzyme present in every living cell, serving a dual function as an electron transporter in redox reactions (glycolysis, TCA cycle → ATP production) and a critical substrate for non-redox signaling enzymes including sirtuins (SIRT1–7), PARPs, CD38/CD157, and SARM1.[1][2] Mammalian cells synthesize NAD+ through three primary pathways: De Novo Synthesis: From L-tryptophan via the kynurenine pathway Preiss-Handler Pathway: From nicotinic acid (vitamin B3) Salvage Pathway (dominant): Recycling nicotinamide (NAM) via NAMPT → NMN → NAD+ (rate-limiting enzyme: NAMPT) NAD+ levels in human tissues decline 10–65% with age, driven by reduced NAMPT activity and increased consumption by CD38/PARPs during chronic inflammation. This decline is now considered a hallmark of aging.[1][3] NAD+ was originally discovered in 1906 by Arthur Harden and William John Young during fermentation studies, with its structure elucidated by Hans von Euler-Chelpin (1929) and its hydride transfer function identified by Otto Heinrich Warburg...
NAD+ — Research Data at a Glance
| Property | Value |
|---|---|
| PubMed Citations Referenced | 26 |
| Contributing Researchers | 3 |
| Storage Conditions | Store NMN/NAD+ powder at −20°C; protect from light and moisture. |
| Purity Standard | ≥99% (HPLC verified, 3rd-party COA) |
| Research Use Only | Not for human consumption. RUO only. |
Compare NAD+ with Other Peptides
Overview
Overview
NAD+ (Nicotinamide Adenine Dinucleotide) is a coenzyme present in every living cell, serving a dual function as an electron transporter in redox reactions (glycolysis, TCA cycle → ATP production) and a critical substrate for non-redox signaling enzymes including sirtuins (SIRT1–7), PARPs, CD38/CD157, and SARM1.[1][2]
Mammalian cells synthesize NAD+ through three primary pathways:
- De Novo Synthesis: From L-tryptophan via the kynurenine pathway
- Preiss-Handler Pathway: From nicotinic acid (vitamin B3)
- Salvage Pathway (dominant): Recycling nicotinamide (NAM) via NAMPT → NMN → NAD+ (rate-limiting enzyme: NAMPT)
NAD+ levels in human tissues decline 10–65% with age, driven by reduced NAMPT activity and increased consumption by CD38/PARPs during chronic inflammation. This decline is now considered a hallmark of aging.[1][3]
NAD+ was originally discovered in 1906 by Arthur Harden and William John Young during fermentation studies, with its structure elucidated by Hans von Euler-Chelpin (1929) and its hydride transfer function identified by Otto Heinrich Warburg (1936).[2]
Mechanism of Action
Mechanism of Action
1. Sirtuin Activation (SIRT1–7)
Sirtuins are NAD+-dependent protein deacylases (class III histone deacetylases). They bind NAD+ and an acetylated target protein, cleaving the glycosidic bond to release nicotinamide (NAM) and generate O-acetyl-ADP-ribose. Km range: 94–888 µM.[6]
- SIRT1 Pathway: Deacetylates PGC-1α → mitochondrial biogenesis; FOXO → stress resistance; also deacetylates LKB1 → activates AMPK → positive feedback loop increasing NAD+ and fatty acid oxidation[6]
- SIRT3 Pathway: Mitochondrial localization; deacetylates MnSOD → enhanced antioxidant defense; activates OXPHOS enzymes[6]
2. PARP1/2 DNA Repair
PARP1 detects DNA strand breaks → consumes NAD+ to build poly(ADP-ribose) chains → recruits repair enzymes (XRCC1). Km 20–97 µM — higher affinity than sirtuins, can outcompete for NAD+ during DNA damage. Excessive activation → NAD+/ATP depletion → parthanatos (cell death).[6][7]
3. CD38/CD157 Hydrolysis
CD38 is the major regulator of tissue NAD+ levels (Km ~15–25 µM). It hydrolyzes NAD+ into NAM and ADP-ribose, and cyclizes NAD+ into cADPR → Ca²⁺ mobilization from intracellular stores. CD38 expression increases with aging, directly driving NAD+ decline.[1][8]
4. SARM1 Axonal NADase
SARM1 contains a TIR domain with intrinsic NADase activity. Activated by nerve injury → rapid axonal NAD+ depletion → local metabolic collapse and calcium influx → Wallerian degeneration.[7]
5. Extracellular Signaling
Extracellular NAD+ acts at P2X7 purinergic receptors on T-regulatory cells → ART2-P2X7 pathway → immune modulation.[6]
Precursor Entry Mechanisms
| Precursor | Cellular Entry | Notes |
|---|---|---|
| NAD+ (direct) | Cannot passively cross plasma membrane | Exception: Connexin 43 in heart muscle |
| NR | Equilibrative nucleoside transporters (ENTs) | Best oral bioavailability; GRAS status |
| NMN | Dephosphorylated → NR by CD73 extracellularly | Slc12a8 transporter in small intestine |
| NAM | Passive diffusion | Feedback-inhibits sirtuins/PARPs at high doses |
Research Applications
Research Applications
NAD+ research spans aging biology, metabolic disease, neurodegeneration, and cardiovascular health with 15+ clinical trials and extensive preclinical data:
- Aging and Longevity — Declining NAD+ is a hallmark of aging; supplementation mimics caloric restriction, rejuvenates stem cells, extends healthspan in mice.[3][9]
- Metabolic Disorders — NMN increased muscle insulin sensitivity 25% in prediabetic women (Yoshino 2021, Science); NR prevented diet-induced obesity 40% in mice.[10][11]
- Neurodegenerative Diseases — Alzheimer's (NMN → restored spatial memory), Parkinson's (NADPARK: NR → increased cerebral NAD+, MRS-confirmed), ALS (NR + pterostilbene → improved function).[12][13]
- Cardiovascular Health — Heart failure, cardiomyopathy, ischemia-reperfusion; NMN restores capillary density/endurance 80% in aged mice (SIRT1-dependent vascular rejuvenation).[14]
- DNA Repair / Cancer — NAD+ is sole PARP substrate; complex dual role in genomic stability vs tumor metabolism.[7]
- Immune Modulation — CD38 on macrophages drives M1/M2 polarization; CD38 inhibitors (78c, apigenin) reverse age-related NAD+ decline.[8]
- Acute Organ Injury — NMN protects against cisplatin-induced AKI (SIRT1-dependent); intranasal NAD+ reduces brain infarct volume post-ischemia.[15]
- Ophthalmology — Photoreceptor survival, retinal degeneration, glaucoma.[2]
- Muscle Performance — Dose-dependent VO₂ improvement in amateur runners (NMN 600/1200 mg); grip strength in elderly.[16]
- Fertility — NMN restores oocyte quality, improves ovulation, rescues fertility in aged female mice.[2]
Biochemical Characteristics
| Property | Value |
|---|---|
| Molecular Formula | C₂₁H₂₇N₇O₁₄P₂ |
| Molecular Weight | 663.43 g/mol |
| CAS Number | 53-84-9 |
| PubChem CID | 5893 |
| Structure | Dinucleotide: adenosine 5′-phosphate + ribosylnicotinamide 5′-phosphate joined by pyrophosphate linkage |
| Classification | Coenzyme (NOT a peptide/protein) |
| Redox States | NAD+ (oxidized) ↔ NADH (reduced, accepts hydride ion) |
| Synonyms | Coenzyme I, diphosphopyridine nucleotide, oxidized nicotinamide adenine dinucleotide |
| Key Precursors | NMN (CID: 14180), NR (Niagen®), NAM, NA, L-Tryptophan |
| Rate-Limiting Enzyme | NAMPT (nicotinamide phosphoribosyltransferase) — Salvage pathway |
| Plasma Half-Life | ~1–2h cytoplasm/nucleus; ~8h mitochondria |
Identifiers
| Purity Standard | |
|---|---|
| Identity Confirmation | |
| Endotoxin | |
| Quality Control |
Preclinical Research Summary
Preclinical Research Summary
Key Preclinical Studies
| Study | Model | Key Findings | Ref |
|---|---|---|---|
| Mills et al. (2016) | C57BL/6N mice — NMN 100–300 mg/kg/day oral × 12 mo | Suppressed weight gain ~10% (p<0.001); increased energy expenditure; improved insulin sensitivity; no obvious toxicity | [17] |
| Das et al. (2018) | Elderly C57BL/6 mice — NMN 500 mg/kg/day oral × 28d | Capillary density restored to young-mouse levels; endurance improved 80% via SIRT1-dependent vascular rejuvenation | [14] |
| Hou et al. (2018) | 3xTgAD Alzheimer's mice — NMN 100 mg/kg SC × 28d–3mo | Decreased Aβ oligomers; restored spatial memory in water maze tasks | [2] |
| Zhang et al. (2016) | Aged C57BL/6 mice — NR 400 mg/kg/day oral × ~6mo | Extended median lifespan 5% (p<0.05); enhanced muscle stem cell function; increased grip strength | [9] |
| Cantó et al. (2012) | HFD mice — NR 400 mg/kg/day oral × 8–12 wk | Prevented weight gain (40% less than controls); increased thermogenesis | [11] |
| Ying/Won (2007/2012) | Rat ischemia — NAD+ 10–20 mg/kg intranasal × 2h post-injury | Reduced infarct volume (p<0.01); bypasses BBB; profound neuroprotection | [15] |
| Tarragó et al. (2018) | Aged mice (32 mo) — 78c (CD38 inhibitor) oral | Increased NAD+ in liver/muscle/heart; improved glucose tolerance | [8] |
Human Clinical Data: NMN Trials
| Trial | Population | Dose/Route | Key Results | Ref |
|---|---|---|---|---|
| Christen et al. (2025) | n=65 healthy adults | 1000 mg NMN vs NR vs NAM × 14d | NMN and NR: NAD+ ↑~2-fold; NAM did NOT increase; gut bacteria convert NMN/NR → NA → NAD+ | [4] |
| Yoshino et al. (2021) | n=25 prediabetic women | 250 mg NMN oral × 10 wk | Muscle insulin sensitivity ↑25% (AKT/mTOR phosphorylation); no AEs | [10] |
| Igarashi et al. (2022) | n=42 men ≥65y | 250 mg NMN oral × 12 wk | Improved gait speed, left grip strength; hearing improved; safe | [18] |
| Liao et al. (2021) | n=48 amateur runners | 300/600/1200 mg NMN × 6 wk | Dose-dependent VO₂ improvement (VT1, VT2) at 600/1200 mg | [16] |
| Yi et al. (2023) | n=80 adults 40–65y | 300/600/900 mg NMN × 60d | NAD+ ↑3–6-fold; 6MWT ↑~1.5-fold (600/900 mg); biological age unchanged vs ↑ in placebo | [19] |
| Pencina et al. (2023) | n=32 overweight 55–80y | MIB-626 1000–2000 mg × 14–28d | NAD+ metabolites ↑200-fold; body weight and diastolic BP decreased | [20] |
Human Clinical Data: NR Trials
| Trial | Population | Dose/Route | Key Results | Ref |
|---|---|---|---|---|
| Trammell et al. (2016) | n=12 healthy adults | 100–1000 mg NR single dose | Dose-dependent NAD+ ↑; 1000 mg → 2.7-fold increase | [5] |
| Martens et al. (2018) | n=24 ages 55–79 | 1000 mg NR oral × 6 wk | PBMC NAD+ ↑~60%; trend toward reduced SBP + aortic stiffness | [21] |
| Brakedal et al. (2022) — NADPARK | n=30 Parkinson's | 1000 mg NR oral × 30d | Increased cerebral NAD+ (MRS-confirmed); mild motor improvement | [12] |
| Wang et al. (2022) | n=30 HFrEF | 2000 mg NR oral × 12 wk | Blood NAD+ doubled; NLRP3 reduced; no cardiac functional improvement | [22] |
| Wu et al. (2025) | Older adults with MCI | 1000 mg NR oral × 8 wk | Reduced plasma pTau217 by 7% (vs 18% ↑ placebo) — Alzheimer's biomarker | [13] |
| de la Rubia et al. (2019) | n=32 ALS | 1200 mg NR + pterostilbene × 16 wk | Improved ALSFRS, pulmonary function, muscle strength vs placebo | [23] |
Direct IV NAD+ Data
| Trial | Population | Dose/Route | Key Results | Ref |
|---|---|---|---|---|
| Grant et al. (2019) | n=11 healthy men | 750 mg IV NAD+ × 6h | Plasma NAD+ ↑~400%; PBMC intracellular NAD+ did NOT increase → questions IV efficacy for intracellular levels | [24] |
Safety Summary
| Parameter | Finding |
|---|---|
| NR Safety | Safe up to 2000 mg/day × 12 weeks — GRAS status; no serious AEs |
| NMN Safety | Safe up to 1250 mg/day × 4 weeks confirmed; no serious AEs at 250 mg × 12 weeks |
| Common AEs | Mild: nausea, flushing, GI discomfort, headache (oral); injection site reactions, lightheadedness (IV) |
| Theoretical Risks | Tumorigenesis (not observed in long-term animal studies); SARM1 axonal degeneration; methylation depletion from excess NAM |
| Contraindications | Active cancer (theoretical), pregnancy/breastfeeding, serious liver/kidney conditions |
The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: in glass) are performed outside of the body. These products are not medicines or drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law.
For Laboratory Research Only. Not for human use, medical use, diagnostic use, or veterinary use.
ALL ARTICLES AND PRODUCT INFORMATION PROVIDED ON THIS WEBSITE ARE FOR INFORMATIONAL AND EDUCATIONAL PURPOSES ONLY.
Authors & Attribution
✍️ Article Author
Prof. David A. Sinclair
David A. Sinclair, PhD, is Professor of Genetics at Harvard Medical School and Co-Director of the Paul F. Glenn Center for the Biological Mechanisms of Aging. Prof. Sinclair's laboratory established that NAD+ levels decline with age and that this decline compromises the activity of sirtuins (SIRT1), enzymes critical for DNA repair and longevity. His work has focused on developing 'NAD-boosting' molecules (NMN) to restore metabolic function and extend healthspan. He authored seminal reviews: 'Slowing ageing by design: the rise of NAD+ and sirtuin-activating compounds' (2016) and 'Therapeutic potential of NAD-boosting molecules' (2018). David A. Sinclair is being referenced as one of the leading scientists involved in NAD+ research. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →🎓 Scientific Journal Author
Dr. Shin-ichiro Imai
Shin-ichiro Imai, MD, PhD, is at Washington University School of Medicine. Dr. Imai formulated the 'NAD World' conceptual framework (now NAD World 3.0), positioning NAD+ metabolism as a systemic regulatory network connecting metabolism, biological rhythm, and aging. He has extensively studied NAMPT as the rate-limiting salvage enzyme and positioned NMN as a critical signaling molecule for maintaining biological robustness. Key publications include the NMN diabetes mouse study (2011, Cell Metabolism), 'NAD+ and sirtuins in aging and disease' (2014), and 'NAD World 3.0' (2025). Shin-ichiro Imai is being referenced as one of the leading scientists involved in NAD+ research. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →Dr. Shin-ichiro Imai is being referenced as one of the leading scientists involved in the research and development of NAD+. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide.
🔬 Contributing Researcher
Dr. Charles Brenner
Charles Brenner, PhD, holds the Alfred E. Mann Family Foundation Chair in Diabetes and Cancer Metabolism at City of Hope National Medical Center and serves as Chief Scientific Advisor at Niagen Bioscience. In 2004, Dr. Brenner discovered the nicotinamide riboside kinase (NRK) pathway, establishing NR as a vitamin precursor to NAD+. He led the first clinical trial establishing NR safety and oral bioavailability in humans (2016, Nature Communications). His foundational work includes 'Discoveries of nicotinamide riboside as a nutrient and conserved NRK genes' (2004) and 'Nicotinic acid, nicotinamide, and nicotinamide riboside: a molecular evaluation of NAD+ precursor vitamins in human nutrition' (2008). Charles Brenner is being referenced as one of the leading scientists involved in NAD+ research. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →Dr. Charles Brenner is being referenced as one of the leading scientists involved in the research and development of NAD+. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide.
Referenced Citations
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.
DOIRajman L, Chwalek K, Sinclair DA. Therapeutic potential of NAD-boosting molecules: the in vivo evidence. Cell Metabolism. 2018;27(3):529-547.
DOIVerdin E. NAD+ in aging, metabolism, and neurodegeneration. Science. 2015;350(6265):1208-1213.
DOIChristen S, Redeuil K, Goulet L, et al. The differential impact of three different NAD+ boosters on circulatory NAD and microbial metabolism in humans. Nature Metabolism. 2025 Jan 15 [Epub].
DOITrammell SAJ, Schmidt MS, Weidemann BJ, et al. Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. Nature Communications. 2016;7(1):12948.
DOIImai S, Guarente L. NAD+ and sirtuins in aging and disease. Trends in Cell Biology. 2014;24(8):464-471.
DOIEssuman K, Summers DW, Sasaki Y, Mao X, DiAntonio A, Milbrandt J. The SARM1 Toll/interleukin-1 receptor domain possesses intrinsic NAD+ cleavage activity that promotes pathological axonal degeneration. Neuron. 2017;93(6):1334-1343.e5.
DOITarragó MG, Chini CCS, Kanamori KS, et al. A potent and specific CD38 inhibitor ameliorates age-related metabolic dysfunction by reversing tissue NAD+ decline. Cell Metabolism. 2018;27(5):1081-1095.e10.
DOIZhang H, Ryu D, Wu Y, et al. NAD+ repletion improves mitochondrial and stem cell function and enhances life span in mice. Science. 2016;352(6292):1436-1443.
DOIYoshino M, Yoshino J, Kayser BD, et al. Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. Science. 2021;372(6547):1224-1229.
DOICantó C, Houtkooper RH, Pirinen E, et al. The NAD+ precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat diet-induced obesity. Cell Metabolism. 2012;15(6):838-847.
DOIBrakedal B, Dölle C, Riber F, et al. The NADPARK study: a randomized phase I trial of nicotinamide riboside supplementation in Parkinson's disease. Cell Metabolism. 2022;34(3):396-407.e6.
DOIWu J, et al. Nicotinamide riboside reduces pTau217 in older adults with mild cognitive impairment. Alzheimer's & Dementia: TRCI. 2025.
PubMedDas A, Huang GX, Bonkowski MS, et al. Impairment of an endothelial NAD+-H₂S signaling network is a reversible cause of vascular aging. Cell. 2018;173(1):74-89.e20.
DOIGuan Y, Wang SR, Huang XZ, et al. Nicotinamide mononucleotide, an NAD+ precursor, rescues age-associated susceptibility to AKI in a sirtuin 1-dependent manner. Journal of the American Society of Nephrology. 2017;28(8):2337-2352.
DOILiao B, Zhao Y, Wang D, Zhang X, Hao X, Hu M. Nicotinamide mononucleotide supplementation enhances aerobic capacity in amateur runners. Journal of the International Society of Sports Nutrition. 2021;18(1):54.
DOIMills KF, Yoshida S, Stein LR, et al. Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in mice. Cell Metabolism. 2016;24(6):795-806.
DOIIgarashi M, Nakagawa-Nagahama Y, Miura M, et al. Chronic nicotinamide mononucleotide supplementation elevates blood nicotinamide adenine dinucleotide levels and alters muscle function in healthy older men. npj Aging. 2022;8(1):5.
DOIYi L, Maier AB, Tao R, et al. The efficacy and safety of β-nicotinamide mononucleotide supplementation in healthy middle-aged adults. GeroScience. 2023;45(1):29-43.
DOIPencina KM, Lavu S, Dos Santos M, et al. MIB-626, an oral formulation of a microcrystalline unique polymorph of β-nicotinamide mononucleotide, increases circulating NMN and NAD+ in a randomized clinical trial. Journal of Clinical Endocrinology & Metabolism. 2023;108(4):862-871.
DOIMartens CR, Denman BA, Mazzo MR, et al. Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults. Nature Communications. 2018;9(1):1286.
DOIWang DD, et al. Nicotinamide riboside in heart failure with reduced ejection fraction. JACC: Basic to Translational Science. 2022.
PubMedde la Rubia JE, Drehmer E, Platero JL, et al. Efficacy and tolerability of EH301 for amyotrophic lateral sclerosis: a randomized, double-blind, placebo-controlled human pilot study. Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration. 2019;20(1-2):115-122.
DOIGrant R, Berg J, Mestayer R, et al. A pilot study investigating changes in the human plasma and urine NAD+ metabolome during a 6 hour intravenous infusion of NAD+. Frontiers in Aging Neuroscience. 2019;11:257.
DOIYoshino J, Mills KF, Yoon MJ, Imai S. Nicotinamide mononucleotide, a key NAD+ intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell Metabolism. 2011;14(4):528-536.
DOIPoljsak B, Kovač V, Špalj S, Milisav I. The central role of the NAD+ molecule in the development of aging and the prevention of chronic age-related diseases. International Journal of Molecular Sciences. 2023;24(3):2959.
DOIRUO Disclaimer
For Research Use Only (RUO). This product is intended solely for in-vitro research and laboratory experimentation. It is not a drug, food, cosmetic, or medical device and has not been approved by the FDA for any human or veterinary use. It must not be used for therapeutic, diagnostic, or any other non-research purpose. Pure US Peptide does not condone or encourage the use of this product for anything other than strictly defined research applications. Users assume full responsibility for compliance with all applicable regulations and guidelines.
Certificate of Analysis (COA)
Every batch is strictly tested by accredited third-party laboratories (ISO 17025) to ensure 99%+ purity.
Latest Lab Report
Storage & Handling
Summary
Store NMN/NAD+ powder at −20°C; protect from light and moisture. NAD+ in water stable at 4°C for 30 days. NMN stable in drinking water 7–10 days at RT.
Recommended Laboratory Storage Conditions
Lyophilized Powder: Store at −20°C for long-term stability. White to slightly yellow crystalline powder. Protect from light and moisture in dark, airtight containers.
Reconstituted Solution: NAD+ in water is relatively stable at 4°C for up to 30 days. NMN stable in drinking water for 7–10 days at room temperature.
Forms Available: Lyophilized powder, oral capsules/sublingual tablets (NMN, NR), injectable sterile solutions (SC/IM/IV), intranasal sprays, liposomal formulations.
Salt Forms: NR often stabilized as Nicotinamide Riboside Chloride (Niagen®).
Handling: Standard laboratory safety precautions (gloves, goggles). No CYP450 metabolism for direct NAD+.
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