Clinical Reference
What is NAD+?
NAD+ — nicotinamide adenine dinucleotide — is a coenzyme present in every living cell, and one of the most heavily studied molecules in metabolic biology. This page is a working reference for practitioners evaluating it: what the molecule does, how cells maintain it, and where the injectable form differs from oral precursors.
The molecule
NAD+ is a dinucleotide: two nucleotides joined through a pair of bridging phosphate groups. One carries an adenine base, the other a nicotinamide base. Its formula is C₂₁H₂₇N₇O₁₄P₂, molecular weight 663.43 g/mol, CAS registry number 53-84-9.
NAD+ is a coenzyme, not a peptide. This comes up constantly, because NAD+ is routinely stocked alongside peptide compounds by the same suppliers. Structurally the two are unrelated: peptides are chains of amino acids linked by peptide bonds. NAD+ contains no amino acids and no peptide bonds at all.
The redox couple: NAD+ and NADH
The plus sign is not decoration. It denotes the oxidized form, which carries a positive charge on its nicotinamide ring and is the form that accepts electrons. When it accepts a hydride ion it becomes NADH, the reduced form. Cells cycle between the two continuously.
This makes NAD+ the principal electron acceptor in catabolism. It collects electrons in glycolysis, in the citric acid cycle, and in fatty acid oxidation, then delivers them to complex I of the electron transport chain, where the resulting proton gradient drives ATP synthesis. Without an adequate oxidized NAD+ pool, those pathways stall regardless of how much substrate is available.
The ratio of NAD+ to NADH is itself a signal. It reports the cell's oxidative state and acts as an input to several regulatory enzymes, which is why the ratio is often more informative in the literature than the absolute concentration of either form.
What consumes NAD+
NAD+ is not only a shuttle. A second class of enzymes consumes it as a substrate, cleaving it and releasing nicotinamide. These reactions are why the pool must be actively replenished.
| Family | Role | Relevance |
|---|---|---|
| Sirtuins (SIRT1–7) | NAD+-dependent deacetylases acting on histones and metabolic enzymes | Directly couple the NAD+ pool to transcriptional and metabolic regulation |
| PARPs | Poly-ADP-ribose polymerases, activated by DNA strand breaks | Heavy DNA damage drives large PARP activation and rapid NAD+ depletion |
| CD38 / CD157 | NAD+ glycohydrolases on immune and other cell surfaces | CD38 expression rises with age in several models and is a major consumer |
| SARM1 | NAD+ hydrolase implicated in axon degeneration signalling | An active area of neurological research |
The salvage pathway
Most NAD+ in mammalian tissue is not synthesised from scratch. It is recycled. The nicotinamide released by the consuming enzymes above is captured by NAMPT (nicotinamide phosphoribosyltransferase) and converted to NMN, which NMNAT enzymes then convert back to NAD+. NAMPT is the rate-limiting step in that loop.
Two other routes exist: de novo synthesis from tryptophan by way of the kynurenine pathway, and the Preiss–Handler pathway from nicotinic acid. Both contribute far less in most tissues than salvage does.
Age-related decline
Tissue NAD+ concentrations fall measurably with age across multiple mammalian models. The decline appears to be driven from both directions: reduced salvage capacity, and increased consumption — notably rising CD38 expression and a higher chronic PARP load from accumulated DNA damage. That observation is the origin of most current NAD+ research interest.
What that observation does not establish, and what the literature has not settled, is whether raising the pool by exogenous administration produces a defined clinical outcome. Practitioners should read the primary literature directly rather than the summaries that circulate around it.
Injectable NAD+ versus oral precursors
These are different interventions and are frequently conflated.
Injectable NAD+ delivers the intact coenzyme parenterally — subcutaneously or by intravenous infusion — bypassing first-pass metabolism. Supplied as a lyophilized powder, it is reconstituted immediately before administration.
Oral precursors — NMN and NR — are not NAD+. They are upstream compounds that must be transported into cells and converted through the salvage pathway. Their pharmacokinetics, tissue distribution, and regulatory classification all differ from the injectable form. We cover that comparison in detail on the NAD+ vs NMN vs NR page.
Handling and stability
Lyophilized NAD+ is stored at −20 °C and protected from light. Reconstitution is performed with bacteriostatic water or another appropriate solution, directed gently down the vial wall rather than injected onto the powder directly, which can degrade it. Once reconstituted, material is held at 2–8 °C. NAD+ in solution is meaningfully less stable than in the lyophilized state, which is why it is supplied dry.
Regulatory notice
NAD+ is not an FDA-approved drug product. Nothing on this page is medical advice, and nothing here should be read as a claim that NAD+ diagnoses, treats, cures or prevents any disease. Mitova Bioscience supplies licensed physicians, clinics and healthcare practices only, for use within the scope of their license and applicable state and federal law. Dose, route and patient suitability are determinations for the treating practitioner alone.
Common questions
Is NAD+ a peptide?
No. NAD+ is a dinucleotide coenzyme. Peptides are chains of amino acids joined by peptide bonds; NAD+ contains neither amino acids nor peptide bonds. The confusion is purely a product of the two being sold side by side.
What is the difference between NAD and NAD+?
Same molecule, different oxidation state. "NAD" is the general name. The plus sign specifies the oxidized, electron-accepting form; the reduced form is NADH. Writing "NAD+" is a statement about which half of the redox couple is meant.
What does NAD+ actually do in the body?
Two distinct jobs. As a redox cofactor it carries electrons from catabolic pathways to the electron transport chain, enabling ATP production. As a substrate it is consumed by sirtuins, PARPs, CD38 and SARM1 in signalling and DNA-repair reactions. The second role is why the pool depletes and must be continuously regenerated.
Why is NAD+ supplied as a lyophilized powder?
Stability. NAD+ degrades appreciably faster in solution than in the dry lyophilized state. Shipping it dry and reconstituting at the point of use preserves the assayed purity through transit and storage.
Does Mitova Bioscience provide dosing protocols?
No. We supply verified raw material with lot-matched analytical documentation. Dose, route, frequency and patient suitability are clinical determinations that rest entirely with the treating licensed practitioner.