NAD+

NAD+

$275.00

Nicotinamide adenine dinucleotide (NAD+) is a coenzyme that plays a vital role in cellular energy production and metabolic regulation. As a central molecule in redox reactions, NAD+ is essential for converting nutrients into energy via mitochondrial oxidative phosphorylation. It also serves as a substrate for enzymes involved in DNA repair, cell signaling, and aging-related processes, making it a crucial focus in modern biochemical research.

In research environments, NAD+ is often utilized in studies investigating cellular respiration, sirtuin activation, and neurobiological functions. It has also been explored for its role in metabolic health, stress response, and mitochondrial biogenesis. The compound’s levels are known to decline with age in many organisms, leading to increased interest in its supplementation and regeneration pathways in experimental models.

This 500mg NAD+ formulation is presented in high-purity, research-grade quality, suitable for various in vitro and in vivo non-clinical applications. It is a valuable component in studies involving energy metabolism, oxidative stress, and age-related cellular decline.

0% 1 - 4 $275.00
10% 5 - 9 $247.50
20% 10 + $220.00
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Description

Nicotinamide adenine dinucleotide (NAD+) is a coenzyme found in all living cells and plays a fundamental role in energy metabolism, redox reactions, and cellular signaling. Comprising a nicotinamide ring and an adenine dinucleotide, NAD+ alternates between oxidized (NAD+) and reduced (NADH) forms to facilitate electron transfer in key metabolic pathways, including glycolysis, the citric acid cycle, and oxidative phosphorylation.

NAD+ is a critical molecule in mitochondrial function, acting as a carrier for electrons during ATP production. In addition to its core role in bioenergetics, NAD+ serves as a substrate for several enzymatic reactions. It is consumed by sirtuins, a family of NAD+-dependent deacetylases involved in gene expression, mitochondrial biogenesis, and stress resistance. NAD+ is also a substrate for poly(ADP-ribose) polymerases (PARPs), enzymes that participate in DNA repair and genomic stability.

Research into NAD+ has expanded significantly in recent years due to its involvement in cellular aging and age-related decline. Experimental studies in animal models have shown that restoring NAD+ levels may support improved mitochondrial function, metabolic flexibility, and cellular resilience under oxidative stress conditions.

Another area of interest is the compound’s potential role in neuroprotection. NAD+ has been studied in non-clinical models for its involvement in neuronal survival, synaptic plasticity, and regulation of calcium signaling. These properties have made NAD+ a molecule of growing interest in the fields of neuroscience, metabolism, and longevity research.

This high-purity 500mg NAD+ product is designed for use in laboratory studies where large-scale or long-term application is necessary. It is ideal for researchers exploring energy metabolism, mitochondrial function, NAD+-consuming enzymes, and age-associated cellular decline.

This compound does not affect hormone levels, is not classified as a drug or dietary supplement, and is not intended for therapeutic use. It is provided exclusively for scientific, investigational, and non-clinical use in appropriately controlled laboratory environments.

Not for human or animal consumption. Research use only.

Product Data:

  • Chemical Name: Nicotinamide adenine dinucleotide
  • CAS Number: 53-84-9
  • Molecular Formula: C21H27N7O14P2
  • Molecular Weight: 663.43 g/mol

 

Research

NAD+ has become a focal point in biological and biochemical research due to its central role in essential cellular processes. It is deeply involved in oxidation-reduction reactions, energy production, and the regulation of several critical enzymes that control cell survival and repair mechanisms.

One of the most prominent research areas involving NAD+ is cellular aging. In various models, age-related decline in NAD+ levels has been correlated with decreased mitochondrial efficiency, increased oxidative damage, and impaired DNA repair capacity. This decline is often accompanied by the overactivation of PARP enzymes in response to DNA damage, which consumes NAD+ and contributes to energy depletion. Studies have shown that maintaining or restoring NAD+ levels may support mitochondrial homeostasis and enhance cellular resilience against stress.

NAD+ is also vital for activating sirtuins, a class of NAD+-dependent enzymes that regulate inflammation, metabolism, and circadian rhythm. Research has demonstrated that enhanced sirtuin activity through increased NAD+ availability may promote beneficial metabolic changes, including improved glucose utilization and fatty acid oxidation, in experimental models.

In neuroscience, NAD+ is studied for its role in brain cell energy metabolism, synaptic function, and neuroprotection. Experimental models of neurodegenerative diseases have explored NAD+ precursors and supplements as tools to mitigate neural decline, often focusing on the preservation of mitochondrial function and regulation of neuroinflammatory processes.

Furthermore, recent studies have examined NAD+ involvement in immunometabolism, the field that investigates the interplay between cellular energy status and immune response. NAD+ is believed to influence macrophage function and T-cell activation, making it a target of interest in immunological and inflammatory research models.

The compound has also been explored in metabolic disorder research, particularly in experimental systems modeling insulin resistance and obesity. Increasing intracellular NAD+ concentrations has shown promising effects on improving metabolic markers in non-clinical settings.

Ongoing investigations are evaluating synthetic and natural NAD+ precursors such as NMN (nicotinamide mononucleotide) and NR (nicotinamide riboside), but direct NAD+ supplementation remains a key focus in controlled studies where enzymatic degradation or transport limitations are managed.

Overall, NAD+ continues to offer significant insight into cellular health, stress adaptation, metabolic regulation, and age-associated decline in laboratory settings. As more is learned about its mechanisms and interactions, the compound serves as a cornerstone for experiments aiming to decode the biology of energy and longevity.

This product is intended for research use only. Not for human or animal use.

References:

  1. “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].
  2. “Nicotinamide Riboside: Benefits, Side Effects and Dosage,” Healthline. [Online]. Available: https://www.healthline.com/nutrition/nicotinamide-riboside. [Accessed: 25-Jul-2019].
  3. 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]
  4. “What You Need to Know About Resveratrol Supplements,” WebMD. [Online]. Available: https://www.webmd.com/heart-disease/resveratrol-supplements. [Accessed: 25-Jul-2019].
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  6. 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].
  7. 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]
  8. 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]
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  10. 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]
  11. 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]
  12. 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]
  13. 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]
  14. D. C. Maddison and F. Giorgini, “The kynurenine pathway and neurodegenerative disease,” Semin. Cell Dev. Biol., vol. 40, pp. 134–141, Apr. 2015. [PubMed]
  15. 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]
  16. 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]
  17. J. E. Humiston, “Nicotinamide Adenine Dinucleotide,” p. 68. [FDA]

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