What is NAD+? The coenzyme behind ageing research, explained

Where does NAD+ come from?

Nicotinamide adenine dinucleotide is a coenzyme made by every living cell. It consists of two nucleotides joined through their phosphate groups: one carries the base adenine, the other carries nicotinamide, a form of vitamin B3. Its oxidised form is written NAD+ and its reduced form NADH. The calculated molecular weight of NAD+ is about 663 g/mol.

Cells build NAD+ through several routes: from the amino acid tryptophan, from nicotinic acid, and through a salvage pathway that recycles nicotinamide. Precursors such as nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) enter this salvage pathway. A 2021 review in Nature Reviews Molecular Cell Biology describes how this balance of synthesis, recycling and consumption sets the NAD+ level in each tissue.

How is it described at the molecular level?

NAD+ has two broad roles. In redox reactions it accepts electrons and becomes NADH, which is central to glycolysis, the citric acid cycle and the delivery of electrons to the mitochondrial respiratory chain. In signalling it is consumed as a substrate by three groups of enzymes: sirtuins, which remove acetyl groups from proteins; poly(ADP-ribose) polymerases (PARPs), which take part in DNA repair; and CD38 and related enzymes, which break NAD+ down.

Reviews link NAD+ to metabolic pathways, DNA repair, chromatin remodelling, cellular senescence and immune function. They also describe a gradual decline in tissue NAD+ with age across several organisms, including rodents and humans. In mice, a 2016 study found that CD38 expression and activity rose with age and that CD38 was required for the age-related NAD decline and the accompanying mitochondrial dysfunction, in part through the sirtuin SIRT3. The same study identified CD38 as the main enzyme breaking down NMN in vivo.

What has been observed in published research?

• Animal models: a 2018 review in Cell Metabolism summarised studies in which restoring NAD+ levels in old or diseased animals improved metabolic and other measures and extended lifespan in some models.
• Systematic evidence: a 2026 PRISMA-guided review identified 80 rodent studies and 33 human intervention studies from 2010 to 2025. Rodent studies frequently reported metabolic, mitochondrial and inflammatory improvements, though effects varied by model.
• NR in older adults (human trial): in a randomised, double-blind, placebo-controlled crossover trial, six weeks of oral NR was well tolerated and raised NAD+ metabolism in healthy middle-aged and older adults.
• NMN in prediabetes (human trial): in a 10 week randomised, placebo-controlled trial in postmenopausal women with prediabetes, insulin-stimulated glucose disposal and muscle insulin signalling increased after NMN but not after placebo.
• NAD+ infusion (human pilot): during a six hour intravenous infusion, plasma NAD+ and its metabolites did not change for the first two hours. The authors concluded that NAD+ was rapidly removed from plasma, and they found NAD+ and methylnicotinamide in urine.
• NAD+ versus NR infusion (human, retrospective): a 2026 review of records from a commercial setting found that NAD+ infusions caused moderate to severe gastrointestinal symptoms, faster heart rate and chest pressure, and took on average 97 minutes against 37 minutes for NR.

What the evidence does not establish

Most human evidence concerns the oral precursors NR and NMN, not NAD+ itself. Those trials consistently showed that NAD+ related metabolites rose, but the 2026 systematic review found that effects on function, metabolism and blood vessels were heterogeneous and often null. Raising a biomarker is not the same as changing an outcome.

For NAD+ given directly, the human record is a single pilot pharmacokinetic study and one retrospective review without a control group. The systematic review found no eligible outcome trials of intravenous or intramuscular NAD+ and called for larger randomised studies. Animal findings on lifespan cannot be applied to people.

How does NAD+ compare with related compounds?

The closest relatives of NAD+ are its precursors. Nicotinamide riboside and nicotinamide mononucleotide are smaller molecules that cells convert into NAD+, and they account for most of the randomised human trials in this field. Nicotinamide itself, a form of vitamin B3, is both a precursor and a product of NAD+ breakdown. The 2016 CD38 study is relevant here because it identified CD38 as the main enzyme breaking down NMN in mice, which affects how much of a precursor reaches the cell.

In ageing research NAD+ is often discussed next to peptides such as MOTS-c, SS-31 and Epithalon. These act through different targets: MOTS-c through AMPK and nuclear genes, SS-31 through cardiolipin in the mitochondrial membrane and Epithalon through reported effects on telomerase. NAD+ connects to these themes through sirtuins and energy metabolism, but no published study has compared NAD+ directly with any of these peptides.

Which formats does Vitality Peps supply?

Vitality Peps supplies NAD+ as a 1000 mg lyophilised vial and as a 500 mg prepared pen format for laboratory research, each documented by a batch certificate of analysis. Bacteriostatic water is listed separately for reconstituting the vial.

How is it handled in the laboratory?

NAD+ is sensitive to moisture, heat and light, so the lyophilised powder is stored cold and dry in its sealed vial. Before use it is brought to room temperature and reconstituted with bacteriostatic water, and the working concentration is calculated from the actual mass on the batch certificate. Reconstituted solution is refrigerated, labelled and dated. The pen format contains a prepared solution: it is kept refrigerated and dated on opening.

Research use only

NAD+ supplied by Vitality Peps is for in vitro laboratory research only. Not a medicine, not a supplement, not for human or veterinary consumption. Nothing above is instructions for use.