Product Overview

NAD+ (Nicotinamide Adenine Dinucleotide, INCI: Nicotinamide Adenine Dinucleotide, β-NAD, Coenzyme I, CAS 53-84-9, C₂₁H₂₇N₇O₁₄P₂, MW 663.43 g/mol) is the master coenzyme of cellular life — essential for over 500 enzymatic reactions spanning energy metabolism, genomic maintenance, and epigenetic regulation. NAD+ operates through four interconnected biochemical systems: (1) Redox coenzyme — the NAD+/NADH couple is the central electron carrier of catabolism. In glycolysis, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) reduces NAD+ to NADH. In the Krebs cycle, three dehydrogenases (isocitrate, α-ketoglutarate, and malate dehydrogenase) each reduce NAD+ to NADH. Fatty acid β-oxidation generates NADH at the 3-hydroxyacyl-CoA dehydrogenase step. The resulting NADH pool donates electrons to Complex I (NADH:ubiquinone oxidoreductase) of the mitochondrial electron transport chain (ETC), driving the proton-motive force that powers ATP synthase — yielding approximately 2.5 ATP per NADH oxidized. The NAD+/NADH ratio (typically 3–10 in the cytoplasm, ~7 in mitochondria) is the key metabolic rheostat sensed by AMPK, SIRT1, and the circadian clock. (2) Sirtuin co-substrate — NAD+ is the obligate and rate-limiting substrate for all seven mammalian sirtuins (SIRT1-7). Sirtuins are NAD+-dependent lysine deacetylases (class III HDACs) that catalyze the reaction: acetyl-lysine + NAD+ → deacetylated-lysine + nicotinamide + 2′-O-acetyl-ADP-ribose. SIRT1 deacetylates PGC-1α (mitochondrial biogenesis), p53 (apoptosis suppression), FOXO (stress resistance), NF-κB (inflammation), and histones H3/H4 (epigenetic silencing). SIRT3 is the primary mitochondrial deacetylase regulating fatty acid oxidation, ketogenesis, and ETC complex activity. SIRT6 is a chromatin-bound deacetylase critical for telomere maintenance, BER DNA repair, and TNF-α suppression. NAD+ availability is the rate-limiting factor for all sirtuin activity — when NAD+ declines, sirtuins are silenced. (3) PARP substrate — DNA repair. PARP1 (and PARP2) are nuclear enzymes that detect single-strand DNA breaks and consume NAD+ to synthesize poly(ADP-ribose) (PAR) chains at damage sites, recruiting XRCC1, DNA ligase III, and DNA polymerase β for base excision repair (BER). PARP1 is the dominant NAD+ consumer in the nucleus — under severe genotoxic stress, PARP1 hyperactivation can deplete cellular NAD+ by over 80%, triggering energetic collapse and necrotic cell death (the parthanatos pathway). (4) CD38/CD157 — NAD+ glycohydrolases. CD38 is a type II transmembrane NADase that hydrolyzes NAD+ to produce cADPR (cyclic ADP-ribose), ADPR, and NAADP — calcium-mobilizing second messengers. CD38 expression increases with age across multiple tissues (spleen, liver, adipose, brain, skeletal muscle), driven by the senescence-associated secretory phenotype (SASP), and is now recognized as the primary enzymatic driver of age-related NAD+ decline. Why NAD+ declines with age: NAD+ levels drop approximately 50% between ages 20 and 50, driven by a convergence of factors: (a) CD38 upregulation from accumulating senescent cells and chronic low-grade inflammation (inflammaging), (b) PARP1 hyperactivation from lifelong DNA damage accumulation (oxidative lesions, strand breaks, telomere attrition), (c) decreased NAMPT expression — the rate-limiting enzyme of the NAD+ salvage pathway that recycles nicotinamide back to NAD+, and (d) reduced de novo NAD+ synthesis from tryptophan through the kynurenine pathway. UPOR Biotech’s NAD+ is produced via fermentation using optimized yeast (Saccharomyces cerevisiae) and bacterial (Escherichia coli) biosynthesis strains under cGMP-controlled conditions. The fermentation process utilizes the natural NAD+ biosynthetic pathway: nicotinic acid (niacin) is converted through the Preiss-Handler pathway (nicotinic acid → nicotinic acid mononucleotide → nicotinic acid adenine dinucleotide → NAD+) in yeast, while E. coli strains utilize the deamidated salvage pathway. After fermentation, NAD+ is extracted, purified via ion-exchange and reverse-phase chromatography, lyophilized, and analyzed by HPLC for purity (≥98% or ≥99%) and NAD+/NADH ratio. This biofermentation process yields β-NAD+ that is structurally identical to endogenous human NAD+ — including the critical β-configuration of the nicotinamide-ribose glycosidic bond essential for enzymatic recognition.

As a leading NAD+ manufacturer and bulk supplier, UPOR Biotech provides high-purity NAD+ powder for B2B nutraceutical brands, longevity supplement companies, NAD+ IV therapy clinics, cosmetic formulators, contract manufacturers, and private-label distributors worldwide. The global NAD+ and NAD+ precursor supplement market has experienced explosive growth — projected to exceed USD 1.2 billion by 2030 — driven by the convergence of longevity science, biohacking culture, and a growing base of clinical evidence supporting NAD+ repletion strategies. NAD+ IV therapy has emerged as one of the fastest-growing segments in the wellness and integrative medicine space: high-dose NAD+ infusion protocols (100–750 mg per session, typically delivered over 2–6 hours) are used for addiction recovery, chronic fatigue, neurodegenerative support, athletic performance optimization, and anti-aging maintenance. Direct NAD+ (as opposed to precursors NMN or NR) remains the gold standard for intravenous administration because it bypasses gastrointestinal absorption, hepatic first-pass metabolism, and the rate-limiting enzymatic conversion steps required by precursors. OEM and private label NAD+ formulations available — capsules, powders, liposomal NAD+, IV infusion lyophilized vials, and cosmetic anti-aging serums. Flexible MOQ starting at 1 kg. Free sample available for qualified B2B buyers. Every shipment includes full documentation: COA, MSDS, HPLC chromatogram, NMR (research grade), and stability data.

NAD+ vs NMN vs NR — Which NAD+ Precursor Delivers the Best Bioavailability and Cellular Uptake?

The NAD+ precursor landscape presents three distinct strategies for elevating cellular NAD+ — each with fundamentally different pharmacokinetics, molecular weight, transport mechanisms, and clinical evidence profiles. Direct NAD+ (Nicotinamide Adenine Dinucleotide, MW 663.43 g/mol) is the fully assembled coenzyme with two phosphate groups and the complete dinucleotide structure. While historically assumed to have limited cell permeability due to its size and charge, NAD+ is efficiently salvaged extracellularly: ecto-enzymes CD73 (ecto-5′-nucleotidase) and CD38 sequentially degrade NAD+ to nicotinamide riboside (NR) at the plasma membrane, which is then transported into cells via equilibrative nucleoside transporters (ENT1/ENT2) and reconverted to NAD+ intracellularly through the NRK → NMNAT pathway. NAD+ IV therapy bypasses all bioavailability barriers, delivering NAD+ directly to the bloodstream — this is the only route achieving acute supraphysiologic NAD+ levels. NMN (Nicotinamide Mononucleotide, MW 334.22 g/mol) is the direct one-step precursor to NAD+ — NMNAT enzymes simply add the adenylate moiety from ATP to form NAD+. NMN’s key advantage is the discovery of the Slc12a8 transporter (2019, mouse model) that facilitates direct NMN uptake in the small intestine and potentially some tissues, though human expression and functional significance remain under investigation. NMN raises tissue NAD+ within 15–30 minutes in murine models; human RCTs (2021–2024) demonstrate safety and NAD+ elevation at oral doses of 250–900 mg/day. NR (Nicotinamide Riboside, MW 255.25 g/mol) is the smallest precursor — a riboside without phosphate groups — crossing cell membranes via ENTs and requiring two enzymatic steps (NRK → NMNAT) to form NAD+. NR holds the longest human safety track record (clinical trials since 2016, including the first long-term chronic dosing studies at 300–1000 mg/day). Which is best? The answer depends entirely on the delivery route and therapeutic goal: For IV infusion — direct NAD+ is the only option delivering the complete coenzyme to plasma. For oral supplementation — NMN and NR each show robust human evidence, with NMN offering the shorter biosynthetic path and NR offering the longer safety record. For parenteral and sublingual formulations — NAD+ and NMN are both viable. For cost-sensitive formulations — NR (lowest MW, simplest synthesis) typically offers lowest cost per gram. UPOR Biotech supplies high-purity NAD+ as the foundational molecule for all three strategies — direct NAD+ formulations, NMN/NR product quality control standard, and as the analytical reference material for NAD+ metabolomics research.

Technical Specifications

PropertySpecification
Product NameNAD+ (Nicotinamide Adenine Dinucleotide) Powder — Nutraceutical/Cosmetic Grade (≥98% HPLC) / Research Grade (≥99%)
INCI NameNicotinamide Adenine Dinucleotide
Common Name / SynonymsNAD+; NADH (reduced form); β-NAD; β-Nicotinamide Adenine Dinucleotide; Coenzyme I; Diphosphopyridine Nucleotide (DPN); Nicotinamide Adenine Dinucleotide Oxidized; NAD; β-DPN; Diphosphopyridine Nucleotide Oxidized
CAS Number53-84-9 (NAD+ free acid); 20111-18-6 (NADH disodium salt); 64417-72-7 (NAD+ sodium salt)
Molecular FormulaC₂₁H₂₇N₇O₁₄P₂ (free acid)
Molecular Weight663.43 g/mol (free acid); 709.41 g/mol (disodium salt)
SourceFermentation-derived (Saccharomyces cerevisiae yeast / Escherichia coli bacterial biosynthesis) — bioidentical to endogenous human β-NAD+. The β-configuration of the nicotinamide-ribose glycosidic bond is preserved, which is the naturally occurring and enzymatically active anomer.
Key Advantage / MechanismMaster coenzyme of cellular metabolism: redox coenzyme (NAD+/NADH couple — glycolysis, Krebs cycle, fatty acid β-oxidation → ETC Complex I electron donor → 2.5 ATP per NADH), obligate sirtuin co-substrate (SIRT1-7 deacetylase activity — longevity, mitochondrial biogenesis, inflammation regulation), sole PARP substrate (PARP1/PARP2 — DNA damage detection and base excision repair), CD38/CD157 consumer enzyme target (age-related NAD+ decline driver). NAD+ levels decline ~50% by age 50.
AppearanceWhite to off-white lyophilized powder; hygroscopic
Assay (Nutraceutical/Cosmetic Grade)≥98.0% (HPLC, anhydrous basis, λ = 259 nm)
Assay (Research Grade)≥99.0% (HPLC, anhydrous basis, λ = 259 nm)
IdentificationHPLC retention time matches NAD+ reference standard (Sigma-Aldrich N7004 or equivalent USP RS); UV λmax = 259 nm (ε = 17.8 × 10³ M⁻¹cm⁻¹ at pH 7.0); A₂₅₀/A₂₆₀ ratio: 0.80–0.84; A₂₈₀/A₂₆₀ ratio: 0.20–0.24 (indicating ≤5% NADH/adenylate impurity)
NAD+/NADH Ratio (Oxidized Form)≥95% NAD+ (oxidized); NADH ≤5% (enzymatic assay, absorbance at 340 nm after ethanol/alcohol dehydrogenase reduction)
pH (1% Aqueous Solution)2.0 – 4.0 (free acid form); 5.5 – 7.5 (sodium salt form, available on request)
SolubilityFreely soluble in water (≥100 mg/mL at 25°C); soluble in saline (0.9% NaCl), PBS buffer (pH 7.4), and cell culture media; slightly soluble in ethanol; practically insoluble in acetone, chloroform, and diethyl ether
Water Content (Karl Fischer)≤5.0% (w/w)
Heavy Metals (Total)≤10 ppm (as Pb)
Elemental ImpuritiesPb ≤2 ppm; As ≤1 ppm; Hg ≤1 ppm; Cd ≤1 ppm; Ni ≤5 ppm; Cr ≤5 ppm (USP <232> / ICH Q3D compliant)
Microbial LimitsTAMC ≤100 CFU/g; TYMC ≤10 CFU/g (USP <61> / EP <2.6.12>); Pathogens (E. coli, Salmonella, S. aureus, P. aeruginosa) — Absent in 10 g (USP <62> / EP <2.6.13>)
Residual SolventsUSP <467> / EP <5.4> / ICH Q3C Class 3 compliant; Methanol ≤3000 ppm; Ethanol ≤5000 ppm; Acetone ≤5000 ppm
Endotoxin (Research Grade)≤0.5 EU/mg (LAL kinetic chromogenic method, USP <85>); ≤0.1 EU/mg available for cell therapy and clinical trial material
Recommended Usage (Nutraceutical)100 – 500 mg/day oral (capsule/powder/liposomal); 100 – 750 mg/session IV infusion (clinician-administered); 0.1 – 1.0% topical (cosmetic anti-aging formulations). NAD+ precursor equivalent dosing for NAD+ boosters.
Grade / StandardsNutraceutical/Cosmetic Grade (≥98% HPLC); Research Grade (≥99% HPLC, endotoxin-tested, suitable for cell culture and in vitro/in vivo studies)
CertificationsISO 9001:2015, ISO 22000, HACCP, FDA Facility Registration, HALAL, KOSHER, Non-GMO, BSE/TSE-Free
Packaging1 kg / 5 kg / 10 kg vacuum-sealed aluminum foil bags with PE liner and desiccant pouch; 25 kg fiber drums with double PE liner and vacuum sealing. Argon-flushed headspace available for oxidation-sensitive applications.
Storage-20°C to -80°C (long-term, ≥24 months, recommended); 2–8°C (short-term, ≤30 days). Tightly sealed in original container with desiccant; protect from light (NAD+ is photolabile) and moisture (hygroscopic). Avoid freeze-thaw cycles.
Shelf Life2 years from date of manufacture under recommended storage conditions (-20°C, desiccated, protected from light)

Key Benefits — NAD+ (Nicotinamide Adenine Dinucleotide)

Master Coenzyme of Cellular Energy — Glycolysis, Krebs Cycle & Oxidative Phosphorylation

NAD+ is the central electron carrier of catabolism: accepts hydride from glycolysis (GAPDH), Krebs cycle (3 dehydrogenases), and β-oxidation to form NADH. NADH donates electrons to ETC Complex I, driving the proton gradient that produces ~2.5 ATP per NADH. The NAD+/NADH ratio is the master metabolic rheostat.

Cellular Energy

Sirtuin Activation & Longevity — SIRT1-7 Co-Substrate for Healthspan Extension

NAD+ is the obligate and rate-limiting co-substrate for all seven mammalian sirtuins. SIRT1 deacetylates PGC-1α (mitochondrial biogenesis), p53, FOXO, NF-κB, and histones. SIRT3 regulates mitochondrial fatty acid oxidation. SIRT6 maintains telomeres and DNA repair. NAD+ decline directly silences sirtuin activity — repletion restores it.

Sirtuin Activation

DNA Repair & Genomic Stability — PARP1/PARP2 Sole Substrate

PARP1 is the dominant nuclear NAD+ consumer — it detects single-strand breaks and consumes NAD+ to synthesize poly(ADP-ribose) chains that recruit BER repair machinery (XRCC1, DNA ligase III, Pol β). Without adequate NAD+, DNA damage accumulates, driving mutation load, cellular senescence, and the aging phenotype.

DNA Repair

Fermentation-Derived Bioidentical β-NAD+ — ≥98% Nutraceutical/Cosmetic & ≥99% Research Grade

Produced via yeast (S. cerevisiae) and bacterial (E. coli) biosynthesis under cGMP conditions. Purified by ion-exchange and RP-HPLC, lyophilized, and fully characterized. Bioidentical to endogenous human NAD+ — correct β-configuration at the nicotinamide-ribose glycosidic bond. Available in nutraceutical/cosmetic and research grades.

Fermentation-Derived

Applications

NAD+ IV Therapy & Intravenous Nutrient Infusions

High-dose NAD+ infusion protocols (100–750 mg/session, 2–6 hour delivery) for addiction recovery, chronic fatigue, neurodegeneration, athletic performance, and anti-aging maintenance. Direct NAD+ bypasses GI absorption, hepatic first-pass metabolism, and precursor conversion bottlenecks — the gold standard for acute NAD+ repletion. OEM lyophilized IV vial manufacturing available.

Anti-Aging & Longevity Dietary Supplements — Capsules, Powders & Liposomal NAD+

NAD+ at 100–500 mg/day in oral supplement formats: capsules, powdered drink mixes, sublingual tablets, and liposomal NAD+ for enhanced bioavailability. The fastest-growing segment of the longevity nutraceutical market (projected >USD 1.2B by 2030). Custom OEM formulations available with flexible MOQ starting at 1 kg.

Premium Cosmeceutical Anti-Aging Skincare — NAD+ Topical Serums & Creams

NAD+ at 0.1–1.0% in anti-aging serums, creams, and masks. Topical NAD+ supports keratinocyte and fibroblast sirtuin activity, mitochondrial function, and DNA repair in UV-exposed skin. Emerging niche in premium cosmeceutical anti-aging — positioned as the intracellular energy coenzyme for skin rejuvenation. INCI: Nicotinamide Adenine Dinucleotide.

Sports Nutrition & Performance Recovery Formulations

NAD+ supports mitochondrial ATP production, muscle recovery via PARP-mediated repair of exercise-induced DNA damage, and SIRT1/SIRT3-regulated oxidative metabolism. Positioned for elite athletes, biohackers, and active aging consumers. NAD+ combined with CoQ10 and creatine for comprehensive mitochondrial performance support.

Cellular Health & Mitochondrial Function Nutraceuticals

NAD+ as the core ingredient in mitochondrial health formulations targeting metabolic syndrome, age-related energetic decline, and circadian rhythm optimization. The NAD+-SIRT1-CLOCK:BMAL1 feedback loop links cellular metabolism to circadian gene expression — NAD+ supplementation supports healthy sleep-wake cycles disrupted by aging.

Research & Academic Studies — Sirtuin Biology, PARP, CD38 & NAD+ Metabolomics

Research-grade NAD+ (≥99% HPLC, endotoxin-tested ≤0.5 EU/mg) for in vitro cell culture studies, in vivo animal models, enzymatic assays (sirtuin, PARP, CD38 activity), and NAD+ metabolomics LC-MS/MS analytical reference standards. Custom specifications available for GMP clinical trial material. Bulk academic pricing.

Frequently Asked Questions

NAD+ (Nicotinamide Adenine Dinucleotide, CAS 53-84-9, C₂₁H₂₇N₇O₁₄P₂, MW 663.43 g/mol) is the master coenzyme of cellular metabolism — essential for over 500 enzymatic reactions. NAD+ operates through four interconnected systems: (1) Redox coenzyme — NAD+ accepts hydride ions (H⁻) to form NADH in glycolysis (GAPDH), the Krebs cycle (three dehydrogenases), and fatty acid β-oxidation. NADH then donates electrons to Complex I of the mitochondrial ETC, driving ATP production (~2.5 ATP per NADH). The NAD+/NADH ratio is the master metabolic rheostat sensed by AMPK and sirtuins. (2) Sirtuin co-substrate (SIRT1-7) — NAD+ is the obligate co-substrate for all seven sirtuins, which deacetylate key proteins regulating longevity (PGC-1α, p53, FOXO, NF-κB, histones). Sirtuins consume NAD+ and release nicotinamide — NAD+ availability is rate-limiting for all sirtuin activity. (3) PARP substrate — PARP1 detects DNA single-strand breaks and consumes NAD+ to synthesize poly(ADP-ribose) chains that recruit DNA repair machinery (BER pathway). PARP1 is the dominant nuclear NAD+ consumer. (4) CD38/CD157 consumer enzymes — NAD+ glycohydrolases that hydrolyze NAD+ and increase with age, recognized as the primary driver of age-related NAD+ decline (~50% by age 50). UPOR Biotech produces NAD+ via fermentation (yeast/bacterial biosynthesis), yielding bioidentical β-NAD+ with the correct nicotinamide-ribose glycosidic bond configuration essential for enzymatic recognition. Available in nutraceutical/cosmetic grade (≥98% HPLC) and research grade (≥99% HPLC).

NAD+ supplementation delivers five clinically significant benefits: (1) Mitochondrial function restoration — NAD+ is the obligate electron acceptor for ETC Complex I; declining NAD+ impairs mitochondrial membrane potential and ATP output. NAD+ repletion restores oxidative phosphorylation and mitochondrial biogenesis via the SIRT1/PGC-1α axis. (2) Sirtuin activation (SIRT1-7) — NAD+ enables SIRT1-mediated deacetylation of p53 (genomic stability), FOXO (stress resistance), NF-κB (inflammation suppression), and PGC-1α (mitochondrial biogenesis). SIRT3 regulates mitochondrial fatty acid oxidation and ketogenesis. SIRT6 maintains telomere integrity and BER DNA repair. (3) DNA repair enhancement — adequate NAD+ ensures PARP1/PARP2-mediated base excision repair (BER) functions optimally, reducing mutation accumulation and genomic instability that characterize aging. (4) Circadian rhythm regulation — the NAD+-SIRT1-CLOCK:BMAL1 feedback loop couples cellular metabolism to circadian gene expression; declining NAD+ with age disrupts circadian-regulated sleep, metabolism, and hormone cycles. (5) Neuroprotection and cognitive health — NAD+ supports neuronal ATP demand (~20% of total body energy), maintains axonal integrity via the NMNAT/NAD+ Wallerian degeneration slow (WldS) pathway, and reduces neuroinflammation through SIRT1-mediated NF-κB suppression. Primary applications include anti-aging supplement formulations (capsule, powder, liposomal), NAD+ IV therapy protocols (100–750 mg/session), premium cosmeceutical skincare, sports nutrition, and cellular health research.

NAD+, NMN, and NR represent three distinct strategies for elevating cellular NAD+ — each with different pharmacokinetics, transport mechanisms, and evidence profiles. Direct NAD+ (MW 663.43 g/mol) — the fully assembled coenzyme. Extracellular NAD+ is salvaged via CD73-mediated degradation to NR at the cell surface, then transported via ENTs and reconverted intracellularly. NAD+ IV therapy is the only route achieving acute supraphysiologic NAD+ levels — bypassing all bioavailability barriers. NMN (Nicotinamide Mononucleotide, MW 334.22 g/mol) — the direct one-step precursor (NMNAT adds ATP’s adenylate to form NAD+). NMN enters cells via the Slc12a8 transporter (discovered 2019 in mice) and raises tissue NAD+ within 15–30 minutes. Human RCTs (2021–2024) confirm safety and NAD+ elevation at 250–900 mg/day oral. NR (Nicotinamide Riboside, MW 255.25 g/mol) — the smallest precursor, transported via ENTs and requiring two steps (NRK → NMNAT) to form NAD+. Longest human safety record (clinical trials since 2016) at 300–1000 mg/day. Which is best? For IV infusion — direct NAD+ only. For oral supplementation — NMN and NR both show robust human evidence (NMN: shorter biosynthetic path; NR: longer safety record). For parenteral/sublingual — NAD+ or NMN. For cost-sensitive formulations — NR (simplest synthesis). UPOR Biotech supplies high-purity NAD+ as the foundation for all three strategies — direct NAD+ formulations, NMN/NR quality control reference standard, and NAD+ metabolomics research material.

NAD+, resveratrol, and CoQ10 target different — and complementary — nodes in the cellular aging network. NAD+ is the upstream master coenzyme: the obligate substrate for sirtuins (SIRT1-7), the sole substrate for PARPs (DNA repair), and the central electron carrier for mitochondrial ATP production. NAD+ repletion addresses the root cause of age-related sirtuin deactivation and energetic decline. Resveratrol is a sirtuin-activating compound (STAC) — it allosterically enhances SIRT1 deacetylase activity, but resveratrol cannot activate sirtuins without adequate NAD+ as co-substrate. Resveratrol has poor oral bioavailability (~20% absorption, ~1% systemic due to rapid sulfation/glucuronidation). CoQ10 (Ubiquinone, MW 863.34 g/mol) operates downstream of NAD+ — it shuttles electrons from ETC Complex I/II to Complex III within the inner mitochondrial membrane. CoQ10 does not influence sirtuin activity, PARP-mediated DNA repair, or the NAD+/NADH redox ratio. The optimal anti-aging stack: NAD+ (sirtuin/PARP/redox coenzyme) + CoQ10 (mitochondrial electron shuttle) + Resveratrol (SIRT1 allosteric activator) = comprehensive three-node coverage. NAD+ provides the fundamental coenzyme substrate, CoQ10 optimizes the downstream ETC step that NADH feeds into, and resveratrol amplifies the sirtuin signal that NAD+ enables. Without adequate NAD+, neither sirtuins nor mitochondrial respiration function optimally — making NAD+ the rate-limiting master molecule of cellular aging.

Every shipment includes: COA (HPLC purity ≥98.0% nutraceutical/cosmetic or ≥99.0% research grade, NAD+/NADH ratio, A₂₅₀/A₂₆₀ and A₂₈₀/A₂₆₀ ratios, full impurity profile, heavy metals ≤10 ppm with Pb ≤2 ppm / As ≤1 ppm / Hg ≤1 ppm / Cd ≤1 ppm / Ni ≤5 ppm / Cr ≤5 ppm, residual solvents per USP <467> / ICH Q3C, microbial panel per USP <61>/<62>, endotoxin ≤0.5 EU/mg for research grade), MSDS, HPLC Chromatogram (signed and dated, with UV λmax 259 nm confirmation and A₂₅₀/A₂₆₀ / A₂₈₀/A₂₆₀ ratios), NMR Spectrum (¹H and ³¹P, research grade), Bioidentity Statement (fermentation-derived, bioidentical to endogenous human β-NAD+), BSE/TSE-Free Statement, Non-GMO Statement, Allergen Statement, HALAL Certificate, KOSHER Certificate, ISO 22000 + HACCP, ISO 9001:2015, FDA Facility Registration, Stability Data (-20°C real-time 24-month and 25°C/60%RH accelerated 14-day), and Complete Lot Traceability from fermentation batch to finished lyophilized product. Free sample available for qualified B2B buyers. MOQ: 1 kg. All documents provided in English. Custom specifications (NAD+/NADH ratio, endotoxin limits, sterile processing) available for GMP manufacturing and clinical trial material upon request.