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NAD+


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NAD+

HPLC Certified

CAS #:

53-84-9

Formula:

C21H27N7O14P2

M.W.:

663.4

PURITY

≥99%

RUO

(Research use only)

SKU: AZ-NAD-500 / AZ-NAD-1000

Specs: Amount: 500mg / 1000mg | Format: Lyophilized Powder | Container: 10mL Vial | Storage: 2-8°C | Type: Coenzyme / Nucleotide, Non-Peptide | Research Alias: Nicotinamide Adenine Dinucleotide / NAD | Research Category: Coenzyme Research

NAD+


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NAD+

CAS #:

53-84-9

Formula:

C21H27N7O14P2

M.W.:

663.4

PURITY

≥99%

RUO

Research use only

Specs: Amount: 500mg / 1000mg | Format: Lyophilized Powder | Container: 10mL Vial | Storage: 2-8°C | Type: Coenzyme / Nucleotide, Non-Peptide | Research Alias: Nicotinamide Adenine Dinucleotide / NAD | Research Category: Coenzyme Research

What Is NAD+?

NAD+ (nicotinamide adenine dinucleotide) is a dinucleotide coenzyme found in every living cell, where it functions as a central carrier of electrons in metabolic redox reactions. The molecule cycles between an oxidized state (NAD+) and a reduced state (NADH), shuttling electrons through the pathways that convert nutrients into usable cellular energy. Beyond electron transfer, NAD+ serves as a direct substrate for two major enzyme families studied extensively in cellular biology: sirtuins, which regulate gene expression and mitochondrial activity through protein deacetylation, and poly(ADP-ribose) polymerases (PARPs), which consume NAD+ to repair damaged DNA. This dual role as both an energy carrier and an enzyme substrate has made NAD+ one of the most studied molecules in cellular metabolism research, with applications spanning mitochondrial biology, genomic stability, and models of cellular aging. At Azoth, NAD+ research material is manufactured to a high purity standard and supplied exclusively for laboratory and analytical research applications.

Molecular Profile

CAS Number: 53-84-9 Molecular Formula: C21H27N7O14P2 Molecular Weight: 663.43 g/mol PubChem CID: 925 Synonyms: beta-NAD, Diphosphopyridine Nucleotide (DPN), Coenzyme I

How Does NAD+ Work? Several Mechanisms Explored

Redox Cycling and Cellular Energy Metabolism NAD+ functions as the primary electron acceptor in glycolysis, the citric acid cycle, and oxidative phosphorylation. As it accepts electrons from these pathways, NAD+ is converted to NADH, which then donates those electrons to the electron transport chain to drive ATP synthesis. This redox cycle places NAD+ at the center of cellular energy production, and the NAD+/NADH ratio is widely used in research models as a marker of mitochondrial and metabolic status. Sirtuin Activation and Mitochondrial Signaling NAD+ is an obligate cosubstrate for the sirtuin family of enzymes (SIRT1 through SIRT7), which use it to remove acetyl groups from histones and other regulatory proteins. In aged mouse models, a decline in nuclear NAD+ was linked to a pseudohypoxic state that disrupted communication between the nucleus and mitochondria, reducing expression of mitochondrially encoded oxidative phosphorylation subunits. Raising NAD+ levels in these animals restored mitochondrial gene expression in a SIRT1-dependent manner. PARP-Mediated DNA Repair Poly(ADP-ribose) polymerases, particularly PARP1, consume NAD+ as a substrate when repairing single- and double-strand DNA breaks. Because sirtuins and PARPs draw from the same intracellular NAD+ pool, research has examined how NAD+ availability shapes the balance between DNA repair capacity and mitochondrial function, with reduced NAD+ pools associated with increased PARylation in disease models. NAD+ Salvage Pathway and NAMPT Intracellular NAD+ levels are maintained through the salvage pathway, in which nicotinamide phosphoribosyltransferase (NAMPT) converts nicotinamide back into NAD+ precursors. Research models have shown that NAMPT activity and NAD+ salvage capacity decline with age and in models of neuromuscular dysfunction, making the salvage pathway a focus of ongoing preclinical investigation.

Buy NAD+ Research Compound for These Research Applications

Mitochondrial Function and Cellular Energy Metabolism Research Mitochondrial decline is a frequently studied feature in aging and metabolic disease models. Research in aged mice linked falling nuclear NAD+ levels to a pseudohypoxic state that disrupted nuclear-mitochondrial communication and reduced expression of oxidative phosphorylation subunits. Restoring NAD+ levels in these animals reestablished mitochondrial gene expression in a SIRT1-dependent manner, making NAD+ a frequently used tool in mitochondrial function research models.

DNA Repair and Genomic Stability Research Because NAD+ is consumed directly by PARP enzymes during DNA repair, researchers use NAD+ and its precursors in cell and animal models to study how NAD+ availability affects genomic stability under oxidative stress or DNA repair deficiency. Reviews of NAD+-dependent enzyme activity have outlined how sirtuins and PARPs compete for the same NAD+ pool, a balance that remains central to ongoing research into cellular stress responses.

Neurodegenerative Disease Models NAD+ and its precursor molecules have been investigated across multiple animal models of neurodegenerative disease. In a DNA repair-deficient mouse model of Alzheimer’s disease, supplementation with an NAD+ precursor was associated with reduced DNA damage markers, decreased neuroinflammation, and normalized tau pathology in hippocampal tissue. Separately, in Drosophila models of Parkinson’s disease linked to PINK1 mutations, dietary supplementation with an NAD+ precursor rescued mitochondrial defects and protected dopaminergic neurons from degeneration.

Skeletal Muscle and Metabolic Pathway Research In mouse and invertebrate models of muscular dystrophy, NAD+ levels declined alongside increased PARP activity and reduced NAMPT expression. Restoring NAD+ in these models was associated with increased mitochondrial content, higher expression of muscle structural proteins, and reduced markers of inflammation and fibrosis, providing a framework for ongoing research into NAD+’s role in skeletal muscle pathways.

Research Summary: What the Preclinical Science Shows

The body of preclinical research on NAD+ spans mitochondrial biology, genomics, and neuroscience, with most findings derived from cell culture and animal models. A note on terminology: because NAD+ itself has limited cell membrane permeability, many of the studies summarized below raised intracellular NAD+ levels using its precursor molecules, nicotinamide riboside (NR), nicotinamide mononucleotide (NMN), or nicotinamide (NAM), all of which are converted to NAD+ through the salvage pathway. Below is a summary of key preclinical research areas.

Research AreaModelKey Findings
Mitochondrial Function and Nuclear-Mitochondrial CommunicationAged mouse modelsRestoring NAD+ levels reestablished mitochondrial gene expression and reversed pseudohypoxic signaling in a SIRT1-dependent manner.
Sirtuin and PARP Pathway ActivityIn vitro and animal modelsNAD+ availability directly regulates sirtuin deacetylase activity and PARP-mediated DNA repair capacity.
Alzheimer’s Disease ModelsDNA repair-deficient mouse modelsNAD+ precursor supplementation reduced DNA damage, neuroinflammation, and tau pathology markers in hippocampal tissue.
Parkinson’s Disease ModelsDrosophila PINK1 modelsNAD+ precursor supplementation rescued mitochondrial defects and protected dopaminergic neurons from degeneration.
Muscular Dystrophy and Skeletal Musclemdx mouse modelsNAD+ repletion increased mitochondrial content and structural protein expression, and reduced fibrosis markers.
NAD+ Salvage Pathway (NAMPT)Cell and animal modelsNAMPT-mediated NAD+ salvage capacity declines in models of aging and neuromuscular dysfunction.

Clinical research into NAD+ precursors has expanded in recent years. A Phase I clinical trial (NCT03816020) registered on ClinicalTrials.gov evaluated nicotinamide riboside, an NAD+ precursor, in individuals with early-stage Parkinson’s disease, with follow-on Phase II and III trials currently in progress. Larger, well-controlled trials are necessary before any conclusions about clinical outcomes can be drawn.

Why Researchers Choose NAD+ from Azoth

Scientific rigor and product consistency are essential in laboratory research. Azoth provides NAD+ manufactured to strict purity specifications, backed by third-party certificate of analysis documentation for each batch.

  • Verified 99%+ purity via HPLC testing
  • USA-manufactured under strict quality protocols
  • Third-party tested for identity, purity, and stability
  • Lyophilized powder format for maximum shelf stability
  • Certificate of Analysis available for every batch

Whether your focus is cellular energy metabolism, DNA repair pathways, or mitochondrial function research in animal models, Azoth provides the compound quality your laboratory research demands.

Storage and Handling

NAD+ is supplied in lyophilized (freeze-dried) powder form. Store at 2-8°C in a cool, dry environment away from direct light and moisture. After reconstitution with bacteriostatic water, keep refrigerated and use in accordance with your laboratory research protocol. Stability is maintained for up to 24 months when stored correctly in lyophilized form.

Legal Disclaimer

NAD+ sold by Azoth is intended for laboratory and in vitro research use only. It is not approved by the Food and Drug Administration (FDA) for human consumption, medical use, diagnostic procedures, or veterinary use. This product has not been evaluated by the FDA and is not intended to diagnose, treat, cure, or prevent any disease or medical condition. Bodily introduction of any kind into humans or animals is strictly prohibited by law. All purchasers must be licensed researchers or qualified laboratory professionals. By purchasing this product, you acknowledge that you are aware of the applicable regulations in your jurisdiction and that you will use this compound exclusively within a qualified research environment.

#Research FindingsJournalDataSource Link
1Cantó C, Menzies KJ, Auwerx J. “NAD+ Metabolism and the Control of Energy Homeostasis: A Balancing Act between Mitochondria and the Nucleus.”Cell Metab.2015; 22(1):31-53.https://pubmed.ncbi.nlm.nih.gov/26118927/
2Gomes AP, et al. “Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging.”Cell2013; 155(7):1624-1638.https://pmc.ncbi.nlm.nih.gov/articles/PMC4076149/
3Imai S, Guarente L. “NAD+ and Sirtuins in Aging and Disease.”Trends Cell Biol.2014; 24(8):464-471.https://pmc.ncbi.nlm.nih.gov/articles/PMC4112140/
4Ryu D, et al. “NAD+ Repletion Improves Muscle Function in Muscular Dystrophy and Counters Global PARylation.”Sci. Transl. Med.2016; 8(361):361ra139.https://pubmed.ncbi.nlm.nih.gov/27798264/
5Hou Y, et al. “NAD+ Supplementation Normalizes Key Alzheimer’s Features and DNA Damage Responses in a New AD Mouse Model with Introduced DNA Repair Deficiency.”PNAS2018; 115(8):E1876-E1885.https://pubmed.ncbi.nlm.nih.gov/29432159/
6Lehmann S, Loh SHY, Martins LM. “Enhancing NAD+ Salvage Metabolism Is Neuroprotective in a PINK1 Model of Parkinson’s Disease.”Biol. Open2017; 6(2):141-147.https://pmc.ncbi.nlm.nih.gov/articles/PMC5312101/
7ClinicalTrials.gov. “The NADPARK Study: Nicotinamide Riboside Supplementation in Parkinson’s Disease (NCT03816020).”ClinicalTrials.govRegistered.https://clinicaltrials.gov/study/NCT03816020

What Is NAD+?

NAD+ (nicotinamide adenine dinucleotide) is a dinucleotide coenzyme found in every living cell, where it functions as a central carrier of electrons in metabolic redox reactions. The molecule cycles between an oxidized state (NAD+) and a reduced state (NADH), shuttling electrons through the pathways that convert nutrients into usable cellular energy. Beyond electron transfer, NAD+ serves as a direct substrate for two major enzyme families studied extensively in cellular biology: sirtuins, which regulate gene expression and mitochondrial activity through protein deacetylation, and poly(ADP-ribose) polymerases (PARPs), which consume NAD+ to repair damaged DNA. This dual role as both an energy carrier and an enzyme substrate has made NAD+ one of the most studied molecules in cellular metabolism research, with applications spanning mitochondrial biology, genomic stability, and models of cellular aging. At Azoth, NAD+ research material is manufactured to a high purity standard and supplied exclusively for laboratory and analytical research applications.

Molecular Profile

CAS Number: 53-84-9 Molecular Formula: C21H27N7O14P2 Molecular Weight: 663.43 g/mol PubChem CID: 925 Synonyms: beta-NAD, Diphosphopyridine Nucleotide (DPN), Coenzyme I

How Does NAD+ Work? Several Mechanisms Explored

Redox Cycling and Cellular Energy Metabolism NAD+ functions as the primary electron acceptor in glycolysis, the citric acid cycle, and oxidative phosphorylation. As it accepts electrons from these pathways, NAD+ is converted to NADH, which then donates those electrons to the electron transport chain to drive ATP synthesis. This redox cycle places NAD+ at the center of cellular energy production, and the NAD+/NADH ratio is widely used in research models as a marker of mitochondrial and metabolic status.

Sirtuin Activation and Mitochondrial Signaling NAD+ is an obligate cosubstrate for the sirtuin family of enzymes (SIRT1 through SIRT7), which use it to remove acetyl groups from histones and other regulatory proteins. In aged mouse models, a decline in nuclear NAD+ was linked to a pseudohypoxic state that disrupted communication between the nucleus and mitochondria, reducing expression of mitochondrially encoded oxidative phosphorylation subunits. Raising NAD+ levels in these animals restored mitochondrial gene expression in a SIRT1-dependent manner.

PARP-Mediated DNA Repair Poly(ADP-ribose) polymerases, particularly PARP1, consume NAD+ as a substrate when repairing single- and double-strand DNA breaks. Because sirtuins and PARPs draw from the same intracellular NAD+ pool, research has examined how NAD+ availability shapes the balance between DNA repair capacity and mitochondrial function, with reduced NAD+ pools associated with increased PARylation in disease models.

NAD+ Salvage Pathway and NAMPT Intracellular NAD+ levels are maintained through the salvage pathway, in which nicotinamide phosphoribosyltransferase (NAMPT) converts nicotinamide back into NAD+ precursors. Research models have shown that NAMPT activity and NAD+ salvage capacity decline with age and in models of neuromuscular dysfunction, making the salvage pathway a focus of ongoing preclinical investigation.

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RESEARCH USE ONLY. All AZOTH products are intended solely for laboratory research, analytical, and scientific use. Products are not for human consumption, human use, veterinary use, diagnostic use, therapeutic use, or administration of any kind. AZOTH is not a compounding pharmacy or outsourcing facility. Statements on this site have not been evaluated by the FDA. Products are not intended to diagnose, treat, cure, or prevent any disease.

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