NAD+

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Cat Number

CIA53849

CAS Number

53-84-9

For research use only. We do not supply to patients.

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CAS Number

53-84-9

EINECS

200-184-4

Storage

Store at -20℃

Synonyms

β-Nicotinamide adenine dinucleotide hydrate; β-DPN; β-NAD; Coenzyme 1; Cozymase; DPN; Diphosphopyridine nucleotide; NAD; Nadide

Molecular Formula

C21H27N7O14P2

Molecular Weight

663.43

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

Appearance

Powder

General Description

NAD+ was first reported in 1906 as a component of yeast extract that can enhance the fermentation rate. Later on, NAD+ was discovered as an essential carrier for hydrogen transfer for redox reaction. As a redox carrier, NAD+ receives hydride from metabolism such as glycolysis, TCA cycle and fatty acid oxidation (FAO) to generate NADH. In addition to being a critical coenzyme for energy metabolism, the critical role of NAD+ has grown to be a co-substrate for various enzymes such as sirtuins, PARPs, CD157, CD73, CD38 and SARM1.

Mechanism of Action

NAD+ is a central coenzyme in glycolysis, tricarboxylic acid cycle, and oxidative phosphorylation. With aging, a reduction in NAD+ levels causes mitochondrial dysfunction and inadequate energy production. Supplementation with NAD+ precursors (NMN, NR) increases intracellular NAD+ levels, restores mitochondrial function and corrects age-related disorders in energy metabolism (reduced muscle endurance, cell viability).

Application

NAD+ supplementation is emerging as a possible therapeutic avenue in a variety of diseases. In particular, rare diseases with premature aging or DNA repair defects such as Werner syndrome, Cockayne syndrome, ataxia-telangiectasia, and xeroderma pigmentosum group A could be potentially treated with NAD+ supplementation. It could lead to a variety of benefits by bolstering DNA repair capacity, improving mitochondrial function (e.g., mitophagy), or modulating metabolic pathways. Examples of these benefits include increasing NAD+ levels in patients with rare DNA repair disorders, improving arterial stiffness, promoting wound healing, improving kidney function, improving ataxia scores, increasing immunoglobulin levels, and improving motor coordination and eye movements. NAD+ has also been shown to have beneficial effects in areas including neurodegenerative diseases (such as Alzheimer's disease and Parkinson's disease), vision, hearing, and inflammation.

Epidemiological and experimental evidence suggests that aging and chronic systemic low-grade inflammation ("inflammaging") are the main contributors to cardiovascular and cerebrovascular diseases. Only recently did Researchers establish a causal link between the age-dependent reduction in NAD+ and persistent low-grade inflammation. The key finding of this study was that senescent cells cause the expansion of M1-like mouse macrophages that overexpress CD38, a key NAD+consuming enzyme in mammals. Thus, the increased CD38 expression further aggravates the age-dependent reduction in NAD+, especially in metabolically active tissues such as the liver and adipose tissue. In addition, CD38 is highly expressed in endothelial cells, human macrophages and monocytes in inflammatory conditions, and in blood samples from older adults. Therefore, a combination of interventions that decrease NAD+ consumption, increase NAD+ biosynthesis, or both, are putatively an approach to prevent age-related inflammation.

Fig. 1 Elevating cellular NAD+ activates various vasoprotective mechanisms. (Abdellatif M, et al. 2022)

References

Abdellatif M, et al. NAD+ and vascular dysfunction: from mechanisms to therapeutic opportunities. Journal of Lipid and Atherosclerosis. 2022, 11(2): 111.

Ischemia-reperfusion (IR) injury is a complication of kidney transplantation associated with mitochondrial dysfunction and NAD+ depletion. To address this issue, a new NAD+-loaded nanoparticle was developed for direct intracellular delivery. In mice, nanoparticles were delivered by either direct injection into the renal artery or by systemic intravenous (IV) administration following 30 minutes of ischemia. A single dose of the NAD+-loaded nanoparticles was found to be superior to free NAD+ and saline controls. The treatment significantly reduced blood creatinine levels and attenuated histological tubular damage. These effects were found to be similar regardless of the delivery method. These data show that NAD+-loaded nanoparticles are a promising approach to reducing IR injury. The ability to restore cellular energy metabolism in this way may improve the use of marginal organs and decrease the incidence of delayed graft function.

Fig. 2 Nanoparticle characterization. (Verhoven B, et al. 2026)

References

Verhoven B, et al. Attenuating ischemia and reperfusion injury using NAD+-loaded nanoparticles in mouse kidneys. Transplantation Direct. 2026, 12(1): e1890.

Does NAD+ need to be protected from direct sunlight while kept in the warehouse?

Yes, NAD+ is light-sensitive and must be stored in amber containers or opaque packaging.

How are the shipping costs calculated for heavy NAD+ bulk orders shipped?

Shipping costs for bulk NAD+ are calculated based on total weight, volume, and destination.

When will I receive the tracking number for my NAD+ shipment after payment?

Tracking details for your NAD+ order are emailed within 24 hours of package dispatch.

Is a certificate of analysis (COA) included with every batch of NAD+ sent out?

Every NAD+ shipment includes a batch-specific COA to verify purity and physical properties.