NAD+

Overview

Nicotinamide Adenine Dinucleotide (NAD+) is a pyridine dinucleotide coenzyme essential for electron transfer reactions across cellular metabolism. As a research reference compound, NAD+ has been studied extensively in preclinical models for its roles in mitochondrial function, sirtuin pathway activation, PARP-mediated DNA damage response, and redox biology (Belenky et al., 2007 — PMID: 17350155).

History

NAD+ was first described in the early 20th century as a cofactor in cellular respiration. Research into NAD+ biology expanded dramatically in the 2000s with the characterization of sirtuins as NAD+-dependent deacetylases. More recent research has focused on age-related NAD+ decline, its implications for mitochondrial function, and the investigation of NAD+ precursors and direct NAD+ supplementation in preclinical models (Canto et al., 2015).

Structure & Molecular Data

CAS Number	53-84-9
Molecular Formula	C₂₁H₂₇N₇O₁₄P₂
Molecular Weight	663.43 g/mol
Amino Acid Count / Structure	N/A — coenzyme/dinucleotide
PubChem CID	5893
Sequence	Nicotinamide-adenine-dinucleotide (not a peptide)
Appearance	Lyophilized white-to-off-white powder
Storage	Store at -20°C. Protect from light and moisture.
Solubility	Soluble in sterile water

 

Compound Class & Mechanism

NAD+ functions as a coenzyme in hundreds of enzymatic reactions across cellular metabolism, accepting and donating electrons between oxidized (NAD+) and reduced (NADH) states. In preclinical research, NAD+ availability has been associated with regulation of glycolysis, the TCA cycle, oxidative phosphorylation, and fatty acid oxidation pathways.

Beyond its role in electron transfer, NAD+ serves as a substrate for sirtuins (SIRT1-7), poly-ADP-ribose polymerases (PARPs), and CD38, all of which consume NAD+ in their enzymatic activities. Research has documented these non-redox NAD+ consumption pathways as key determinants of cellular aging, DNA damage response, and metabolic signaling in preclinical models (Verdin, 2015 — PMID: 26785477).

Research Findings

NAD+ has been investigated across preclinical models spanning mitochondrial function, aging research, DNA damage response, and metabolic biology. Published research has documented findings in the following domains:

Key Research Areas

• Mitochondrial Research: NAD+ availability and mitochondrial biogenesis in preclinical models
• Sirtuin Pathway: SIRT1-7 enzymatic activity and NAD+ substrate dynamics
• DNA Damage Response: PARP-mediated DNA repair and NAD+ consumption research
• Aging Research: age-related NAD+ decline in controlled research models

Collectively, NAD+ occupies a central position in modern metabolic research, with research interest spanning mitochondrial biology, aging research, and stress response pathways. Its role as a substrate for multiple enzyme families makes it a foundational research reference compound (Rajman et al., 2018).

Research Context

Researchers study NAD+ to investigate mitochondrial function, sirtuin pathway dynamics, and age-related metabolic decline in preclinical models. The compound’s central role in cellular metabolism makes it foundational to a wide range of research domains including oncology, cardiovascular research, neurodegeneration models, and basic bioenergetics.

References

Belenky P. et al. (2007). NAD+ metabolism in health and disease. Trends in Biochemical Sciences. PMID: 17350155

Verdin E. (2015). NAD+ in aging, metabolism, and neurodegeneration. Science. PMID: 26785477

Canto C., Menzies KJ., Auwerx J. (2015). NAD+ metabolism and the control of energy homeostasis. Cell Metabolism.

Rajman L., Chwalek K., Sinclair DA. (2018). Therapeutic potential of NAD-boosting molecules. Cell Metabolism.

Yoshino J. et al. (2011). Nicotinamide mononucleotide, a key NAD(+) intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell Metabolism.

Mills KF. et al. (2016). Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in mice. Cell Metabolism.

 

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