NAD+

Nicotinamide adenine dinucleotide (NAD+) is a natural molecule found in every living cell that helps turn nutrients into energy and supports healthy cell function. Scientists study it closely for its potential role in slowing aspects of aging, improving DNA repair, supporting metabolism, and protecting cells from stress. Because it is deeply tied to how mitochondria—the “power plants” of cells—work, NAD+ is a key focus in research on energy, longevity, and overall cellular health. Structurally, NAD+ acts as a pivotal electron transporter involved in oxidation-reduction (redox) reactions, essential for energy production in mitochondria—the cellular powerhouses. In advanced scientific research, NAD+ is extensively studied for its role in mitochondrial function, aging processes, DNA repair mechanisms, cellular stress responses, and metabolic regulation.

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Description

Disclaimer: This is a research chemical only. It’s not a medication, and it’s not approved for human or animal use outside of authorized studies

Molecular Formula C₂₁H₂₇N₇O₁₄P₂
Molecular Weight likely a nucleotide derivative (~600–700 Da estimate)
PubChem CID 5892
CAS # 53‑84‑9

 

Nicotinamide adenine dinucleotide (NAD+) is a central metabolic coenzyme required for redox reactions, energy transduction, and cell signaling. At its core, NAD+ cycles between oxidized (NAD⁺) and reduced (NADH) states, acting as an essential electron carrier in glycolysis, the citric acid cycle, and oxidative phosphorylation—processes fundamental to ATP generation in mitochondria. Beyond its classical role in energy metabolism, NAD+ serves as a substrate for critical enzyme families including sirtuins, poly(ADP-ribose) polymerases (PARPs), and CD38/CD157 ectoenzymes. These pathways govern DNA repair, chromatin remodeling, calcium signaling, immune response, and stress adaptation.

Research interest in NAD+ has expanded dramatically due to its regulatory role in aging and age-related pathophysiology. Cellular NAD+ levels naturally decline with age, impairing mitochondrial function, reducing sirtuin activity, and increasing susceptibility to metabolic dysfunction and oxidative damage. Experimental models explore whether restoration of NAD+—via precursors, modulators, or enzymatic manipulation—can enhance mitochondrial biogenesis, improve insulin sensitivity, bolster neuroprotection, and attenuate inflammatory signaling cascades.

NAD+ is also studied as a signaling hub for adaptive responses under stress, including ischemia-reperfusion injury, genotoxic insult, and chronic inflammatory conditions. By linking energy status to genomic stability and stress resilience, NAD+ occupies a unique position at the intersection of metabolism, cellular repair, and longevity research. This makes it a focal point for laboratories investigating mitochondrial health, neurodegenerative disease pathways, immune regulation, and systemic aging models.

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