NAD+ 1,000mg
$175.00
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Compound Identity
COMPOUND NAME
Nicotinamide adenine dinucleotide (NAD+)
SYNONYMS
?-Nicotinamide adenine dinucleotide, NAD, Diphosphopyridine nucleotide, Coenzyme I, Nadide
MOLECULAR FORMULA
C21H27N7O14P2
MOLECULAR WEIGHT
~663.43 g/mol
STRUCTURE
Synthetic coenzyme
PEPTIDE SEQUENCE
N/A; not a peptide
CHEMICAL STRUCTURE

Molecular Formula: C21H27N7O14P2
Source: PubChem
Mechanism of Action
NAD+ functions as an essential electron carrier by cycling between oxidized (NAD+) and reduced (NADH) forms in cellular metabolism, accepting and donating electrons during glycolysis, the TCA cycle, and oxidative phosphorylation to support ATP production. Beyond its redox coenzyme activity, NAD+ serves as a substrate for sirtuins, poly(ADP-ribose) polymerases (PARPs), and other signaling enzymes that consume NAD+ during the processes of DNA repair, deacetylation, and cellular stress response. These enzymatic reactions profoundly influence energy homeostasis, repair capacity, cellular stress resistance, and gene expression
Biological Activity
NAD+ is indispensable for over 400 cellular reactions, supports mitochondrial function, and modulates antioxidant defenses. Its levels directly impact metabolic health, aging processes, DNA repair, and cellular resilience to stress1,2. NAD+ depletion, as seen in aging and certain diseases, is linked to mitochondrial dysfunction, impaired oxidative metabolism, and decreased repair capacity3,4.
Storage
- Store at -20°C or below, protected from light and moisture.
Drug Categories
Coenzymes, Redox agents, Energy metabolism intermediates
Additional Notes
Summary Table
Disclaimer
For Research Use Only. Not intended for human or veterinary use. This compound is supplied solely for laboratory and R&D purposes.
Detailed Product Description
Nicotinamide adenine dinucleotide (NAD+) is an essential molecule found in all living cells, acting at the crossroads of energy metabolism and cellular signaling. As a coenzyme, NAD+ participates in redox reactions critical for ATP production by shuttling electrons during glycolysis, the TCA cycle, and oxidative phosphorylation. Besides its cofactor role, NAD+ is also a substrate for NAD+-consuming enzymes such as sirtuins (regulators of gene expression and longevity pathways) and PARPs, which mediate DNA repair and cellular stress responses. Declines in NAD+ levels are associated with aging, metabolic dysfunction, and neurodegeneration, making NAD+ replenishment and boosting strategies of growing scientific and clinical interest. Unlike synthetic peptides or hormones, NAD+ is a naturally occurring nucleotide-derived molecule, and its manipulation can influence cell vitality, resilience, and repair capacity1,2,3.
Research Highlights
Cellular NAD+ depletion with age or disease may impair energy metabolism and increase vulnerability to stress3,4.
NAD+ supplementation and precursor therapy (e.
g., NR, NMN) potentially restore NAD+ pools and improve cellular function3.
Widely used in metabolism, aging, and neurobiology research; not for therapeutic or veterinary use unless otherwise specified.
Nicotinamide adenine dinucleotide (NAD+) serves as a central metabolic cofactor and essential substrate for a number of intracellular enzymes that regulate critical biological processes. Its mechanism of action is primarily mediated by its role as a substrate for NAD+-dependent enzymes such as the sirtuin family (SIRT1-7), poly(ADP-ribose) polymerases (PARPs), and certain ectoenzymes like CD38 and CD157. Sirtuins utilize NAD+ to catalyze deacetylation and ADP-ribosylation reactions, thereby modulating gene expression, metabolism, and stress resistance in a manner tightly linked to cellular NAD+ availability. PARPs, on the other hand, respond to DNA damage by using NAD+ to generate ADP-ribose polymers, which are essential for DNA repair and maintaining genome stability; overactivation of PARPs, such as during extensive genotoxic stress, can result in significant NAD+ depletion and subsequent compromise of cellular energy homeostasis. CD38 and CD157 act as multifunctional ectoenzymes that metabolize NAD+ to produce signaling molecules like ADP-ribose and cyclic ADP-ribose, which are involved in calcium signaling and immune regulation. In neurons, the enzyme SARM1 is rapidly activated under conditions of metabolic stress or axonal injury, triggering swift NAD+ cleavage and initiating axonal degeneration. Collectively, NAD+ exerts its effects not through traditional receptor binding but through its indispensable role as a co-substrate and regulator of these enzymatic systems, which sense and respond to fluctuations in NAD+ levels to coordinate cellular metabolism, survival, DNA repair, signaling, and cell fate decisions1-4.
Pharmacokinetic Profile
Route of Administration
Intravenous
Dosing Frequency
Once daily
- Route of Administration: Intravenous, Oral
- Dosing Frequency: Once daily
- Half-Life: The precise plasma half-life of exogenously administered NAD+ in humans is not well characterized in the literature. However, available human studies indicate that NAD+ is rapidly cleared from the plasma for at least the first two hours of infusion, reflecting immediate tissue uptake and/or metabolism.
Formulation & Handling
- Lyophilized powder, reconstituted in sterile saline.
- Store lyophilized powder at –20?°C; Reconstituted solution cannot be stored.
Clinical Trial Activity
References
Quality & Purity
This product is synthesized via solid-phase peptide synthesis (SPPS) and tested to ≥99% purity by HPLC with identity confirmed by mass spectrometry. A Certificate of Analysis (COA) is available for every batch. Learn about our full quality and testing process →
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