NAD+ 500MG
NAD⁺ (nicotinamide adenine dinucleotide) is an essential cellular coenzyme involved in redox metabolism and energy production across all living systems. It functions as a critical electron carrier by cycling between its oxidized (NAD⁺) and reduced (NADH) states, enabling mitochondrial oxidative phosphorylation and glycolytic energy transfer in experimental models. Beyond its metabolic role, NAD⁺ serves as a required substrate for sirtuins and poly(ADP-ribose) polymerases (PARPs), enzymes involved in DNA repair, gene expression regulation, and cellular stress responses. Preclinical research utilizes NAD⁺ to investigate mitochondrial homeostasis, muscle metabolism, neuroprotection, and molecular mechanisms associated with aging and cellular resilience.
For research use only. Not for human consumption.
References:
Cantó C et al., Cell Metab, 2015 22(1):31–53
Verdin E, Science, 2015 350(6265):1208–1213
Yoshino J et al., Cell Metab, 2018 27(3):529–547
Original price was: $90.00.$60.00Current price is: $60.00.
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Overview
Nicotinamide adenine dinucleotide (NAD⁺) is a pyridine nucleotide cofactor present in oxidized (NAD⁺) and reduced (NADH) states. In biochemical and cellular research, NAD⁺ is primarily examined as an electron carrier participating in redox-associated reactions and as a substrate for multiple enzyme classes. Published literature describes NAD⁺ as a molecule involved in intracellular metabolic networks and, in specific experimental contexts, extracellular signaling measurements.
All information below is presented strictly within a non-clinical, preclinical research framework. No therapeutic, diagnostic, or medical claims are stated or implied.
Biochemical Characteristics
Molecular Formula: C21H27N7O14P2
Molecular Weight: 663.43 g/mol
PubChem CID: 925
CAS Number: 53-84-9
NAD⁺ functions as a redox-active cofactor capable of accepting and donating electrons in enzymatic reactions. In experimental systems, NAD⁺ availability is commonly treated as a measurable variable associated with metabolic flux, enzyme activity assays, and intracellular signaling readouts. NAD⁺ is also evaluated as a substrate for enzymes involved in post-translational modification processes, including ADP-ribosylation.
Research Applications
In laboratory research, NAD⁺ is used as a reference compound or experimental variable in:
- Redox biochemistry and mitochondrial metabolism assays
- Enzyme activity measurements involving sirtuins, PARPs, and dehydrogenases
- Transcriptomic and metabolomic profiling studies reporting NAD⁺-associated expression patterns
- Cellular stress and aging-associated model systems
- Extracellular signaling experiments measuring nucleotide release and receptor-linked responses
All applications are limited to controlled in vitro or animal-model research environments.
Pathway / Mechanistic Context
Across the referenced literature, NAD⁺ is discussed in relation to multiple pathway-annotated datasets. These discussions are framed as reported measurements, observed associations, or differential expression trends rather than direct functional outcomes. Frequently referenced pathway contexts include:
- Redox metabolism and mitochondrial electron transport chain–associated readouts
- Sirtuin-annotated gene and protein activity measurements
- PARP-linked DNA damage response datasets
- PGC-1α–associated transcriptional profiles
- Inflammation-related signaling components evaluated through cytokine or gene-expression endpoints
Preclinical Research Summary
Mitochondrial and Metabolic Models
Animal and cell-based studies describe associations between NAD⁺ availability and measured mitochondrial parameters, including oxidative phosphorylation markers and redox state indicators. These findings are reported as dataset-level observations derived from preclinical models.
Gene Expression and Aging-Associated Datasets
Transcriptomic analyses in aging-related models report differential expression patterns among nuclear and mitochondrial gene sets in experimental conditions involving altered NAD⁺ levels. Interpretation is limited to reported expression profiles rather than direct claims of functional restoration.
Neurodegeneration-Oriented Models
In mouse models of neurodegenerative disease, published studies report associations between NAD⁺ exposure and measured neuronal survival markers, oxidative stress indicators, and mitochondrial readouts. These observations are presented as preclinical correlations within disease-model systems.
Inflammation-Related Measurements
Several studies reference NAD⁺-linked datasets involving NAMPT, cytokine measurements, and inflammatory signaling components. Reported outcomes are based on gene-expression profiles, enzyme activity measurements, or pathway-level annotations.
Collectively, the literature positions NAD⁺ as a biochemical variable used to explore metabolism-, aging-, and stress-related mechanisms in non-clinical research systems.
Form & Analytical Testing
This product is supplied as a research-grade compound intended for laboratory use. Analytical characterization may include chromatographic purity assessment and mass-based identity confirmation. Lot-specific specifications should be verified using the accompanying certificate of analysis when provided.
Referenced Citations
- “NAD+ Science 101 – What Is NAD+ & Why It’s Important,” Elysium Health. [Online]. Available: https://www.elysiumhealth.com/en-us/knowledge/science-101/everything-you-need-to-know-about-nicotinamide-adenine-dinucleotide-nad. [Accessed: 25-Jul-2019].
- “Nicotinamide Riboside: Benefits, Side Effects and Dosage,” Healthline. [Online]. Available: https://www.healthline.com/nutrition/nicotinamide-riboside. [Accessed: 25-Jul-2019].
- R. T. Matthews, L. Yang, S. Browne, M. Baik, and M. F. Beal, “Coenzyme Q10 administration increases brain mitochondrial concentrations and exerts neuroprotective effects,” Proc. Natl. Acad. Sci. U. S. A., vol. 95, no. 15, pp. 8892–8897, Jul. 1998. [PMC]
- “What You Need to Know About Resveratrol Supplements,” WebMD. [Online]. Available: https://www.webmd.com/heart-disease/resveratrol-supplements. [Accessed: 25-Jul-2019].
- N. Sun, R. J. Youle, and T. Finkel, “The Mitochondrial Basis of Aging,” Mol. Cell, vol. 61, no. 5, pp. 654–666, Mar. 2016. [PMC]
- D. Stipp, “Beyond Resveratrol: The Anti-Aging NAD Fad,” Scientific American Blog Network. [Online]. Available: https://blogs.scientificamerican.com/guest-blog/beyond-resveratrol-the-anti-aging-nad-fad/. [Accessed: 08-Jul-2019].
- A. P. Gomes et al., “Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging,” Cell, vol. 155, no. 7, pp. 1624–1638, Dec. 2013. [PMC]
- S. Imai and L. Guarente, “NAD+ and sirtuins in aging and disease,” Trends Cell Biol., vol. 24, no. 8, pp. 464–471, Aug. 2014. [PubMed]
- A. R. Mendelsohn and J. W. Larrick, “Partial reversal of skeletal muscle aging by restoration of normal NAD+ levels,” Rejuvenation Res., vol. 17, no. 1, pp. 62–69, Feb. 2014. [PubMed]
- C. Kang, E. Chung, G. Diffee, and L. L. Ji, “Exercise training attenuates aging-associated mitochondrial dysfunction in rat skeletal muscle: role of PGC-1α,” Exp. Gerontol., vol. 48, no. 11, pp. 1343–1350, Nov. 2013. [PubMed]
- S. Ringholm et al., “Effect of lifelong resveratrol supplementation and exercise training on skeletal muscle oxidative capacity in aging mice; impact of PGC-1α,” Exp. Gerontol., vol. 48, no. 11, pp. 1311–1318, Nov. 2013. [PubMed]
- A. Lloret and M. F. Beal, “PGC-1α, Sirtuins and PARPs in Huntington’s Disease and Other Neurodegenerative Conditions: NAD+ to Rule Them All,” Neurochem. Res., May 2019. [PubMed]
- C. Shan et al., “Protective effects of β- nicotinamide adenine dinucleotide against motor deficits and dopaminergic neuronal damage in a mouse model of Parkinson’s disease,” Prog. Neuropsychopharmacol. Biol. Psychiatry, vol. 94, p. 109670, Jun. 2019. [PubMed]
- D. C. Maddison and F. Giorgini, “The kynurenine pathway and neurodegenerative disease,” Semin. Cell Dev. Biol., vol. 40, pp. 134–141, Apr. 2015. [PubMed]
- A. Garten, S. Schuster, M. Penke, T. Gorski, T. de Giorgis, and W. Kiess, “Physiological and pathophysiological roles of NAMPT and NAD metabolism,” Nat. Rev. Endocrinol., vol. 11, no. 9, pp. 535–546, Sep. 2015. [PubMed]
- S. Yamaguchi and J. Yoshino, “Adipose Tissue NAD+ Biology in Obesity and Insulin Resistance: From Mechanism to Therapy,” BioEssays News Rev. Mol. Cell. Dev. Biol., vol. 39, no. 5, May 2017. [PMC]
- J. E. Humiston, “Nicotinamide Adenine Dinucleotide,” p. 68. [FDA]
ALL ARTICLES AND PRODUCT INFORMATION PROVIDED ON THIS WEBSITE ARE FOR INFORMATIONAL AND EDUCATIONAL PURPOSES ONLY.
RUO Disclaimer
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.
| Properties | |
|---|---|
| Molecular Formula | C21H28N7O14P2+ |
| Molecular Weight | 664.4 |
| Monoisotopic Mass | 664.11694759 |
| Polar Area | 318 |
| Complexity | 1130 |
| XLogP | -5.9 |
| Hydrogen Bond Acceptor Count | 18 |
| Rotatable Bond Count | 11 |
| PubChem LCSS | Nadide (JAN/USAN/INN) Laboratory Chemical Safety Summary |
| Identifiers | |
|---|---|
| CID | 5893 |
| InChI | InChI=1S/C21H27N7O14P2/c22-17-12-19(25-7-24-17)28(8-26-12)21-16(32)14(30)11(41-21)6-39-44(36,37)42-43(34,35)38-5-10-13(29)15(31)20(40-10)27-3-1-2-9(4-27)18(23)33/h1-4,7-8,10-11,13-16,20-21,29-32H,5-6H2,(H5-,22,23,24,25,33,34,35,36,37)/p+1/t10-,11-,13-,14-,15-,16-,20-,21-/m1/s1 |
| InChIKey | BAWFJGJZGIEFAR-NNYOXOHSSA-O |
| Isometric SMILES | C1=CC(=C[N+](=C1)[C@H]2[C@@H]([C@@H]([C@H](O2)COP(=O)(O)OP(=O)(O)OC[C@@H]3[C@H]([C@H]([C@@H](O3)N4C=NC5=C(N=CN=C54)N)O)O)O)O)C(=O)N |
| Canonical SMILES | C1=CC(=C[N+](=C1)C2C(C(C(O2)COP(=O)(O)OP(=O)(O)OCC3C(C(C(O3)N4C=NC5=C(N=CN=C54)N)O)O)O)O)C(=O)N |
| IUPAC Name | [[(2R,3S,4R,5R)-5-(6-aminopurin-9-yl)-3,4-dihydroxyoxolan-2-yl]methoxy-hydroxyphosphoryl] [(2R,3S,4R,5R)-5-(3-carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxyoxolan-2-yl]methyl hydrogen phosphate |
Storage Instructions:
All of our products are manufactured using the Lyophilization (Freeze Drying) process, which ensures that our products remain 100% stable for shipping for up to 3-4 months.
Once the peptides are reconstituted (mixed with bacteriostatic water), they must be stored in the fridge to maintain stability. After reconstitution, the peptides will remain stable for up to 30 days.
Lyophilization is a unique dehydration process, also known as cryodesiccation, where the peptides are frozen and then subjected to low pressure. This causes the water in the peptide vial to sublimate directly from solid to gas, leaving behind a stable, crystalline white structure known as lyophilized peptide. The puffy white powder can be stored at room temperature until you’re ready to reconstitute it with bacteriostatic water.
Once peptides have been received, it is imperative that they are kept cold and away from light. If the peptides will be used immediately, or in the next several days, weeks or months, short-term refrigeration under 4C (39F) is generally acceptable. Lyophilized peptides are usually stable at room temperatures for several weeks or more, so if they will be utilized within weeks or months such storage is typically adequate.
However, for longer term storage (several months to years) it is more preferable to store peptides in a freezer at -80C (-112F). When storing peptides for months or even years, freezing is optimal in order to preserve the peptide’s stability.
For further information on proper storage techniques, click the link below:
Peptide Storage