No. It is a coenzyme present in every cell — the electron carrier in energy metabolism and the substrate for sirtuins and PARP enzymes. It is the one item in this catalogue that is not a peptide or a steroid.

Does the NAD+ research apply to NAD+ itself?

Mostly not. The intact molecule is poorly taken up by cells, so almost all human research uses precursors that cells can import and convert. Reading a precursor trial as evidence about NAD+ skips the exact step the field exists to work around.

What have the precursor trials shown?

That oral nicotinamide riboside is bioavailable and raises the blood NAD+ metabolome dose-dependently — a robust pharmacokinetic result. Trials measuring clinical outcomes rather than biomarkers have been inconsistent.

Do NAD+ levels really fall with age?

That observation is well supported. Whether the fall causes ageing, or results from it, or merely accompanies it, is the assumption the field rests on and has not been established.

Is NAD+ approved as a medicine?

No. It is supplied here as a laboratory reagent for in-vitro research and not for human or veterinary use.

Research guides

NAD+, NR and NMN: what the research says

Almost all human NAD+ evidence is about oral precursors, not NAD+ itself, because cells take up the intact molecule poorly. The two are not interchangeable.

Available in the catalogue

Supplied as research material. Sizes and pricing are on the product page. Availability is not a statement about what a compound does.

NAD+
Longevity & Cellular

NAD+ is the odd item in this catalogue: not a peptide, not a molecule designed for a target, but a coenzyme present in every cell. That changes what the evidence question even is — nobody doubts NAD+ does something, because without it metabolism stops. The question is entirely about whether supplying more of it from outside changes anything.

What the molecule is

Nicotinamide adenine dinucleotide: the electron carrier in the reactions that release energy from nutrients, and the required substrate for sirtuins and PARP enzymes involved in DNA repair and gene regulation. Cellular levels fall with age, which is the observation the entire research field is built on.

The uptake problem, which is the whole story

The intact molecule is poorly taken up by cells. That single pharmacological fact is why almost all human research uses precursors — nicotinamide riboside and nicotinamide mononucleotide — that cells can import and convert. A study of a precursor is a study of that precursor, and reading it as evidence about NAD+ itself skips exactly the step the field exists to work around.

It is the most common error made about this compound, and it is made by people summarising the research in good faith, because the papers are all filed under NAD+ metabolism.

What the precursor trials found

The foundational human work established that oral nicotinamide riboside is bioavailable and raises the blood NAD+ metabolome dose-dependently. That is a pharmacokinetic result and a genuine one: the precursor gets in and levels go up.

What has been harder is showing that raising levels produces a clinical benefit. A randomised trial in peripheral artery disease and a phase 2 trial in amnestic mild cognitive impairment have been published, and systematic reviews of nicotinamide mononucleotide have pooled the trials on safety and metabolic outcomes. The pattern across this literature is consistent bioavailability and inconsistent clinical effect.

Raising a biomarker is not the same as improving an outcome. That distinction is the single most useful thing to hold onto when reading anything about this compound, because the biomarker result is robust and the outcome results are not.

What studies reported

Each entry states what a study examined and the model it used. Nothing below describes an outcome for a person.

Everything below is drawn from published research, and each entry names the model the study used. Approval status varies by compound and by country, and nothing described here is supplied as a medicine or for use in a person.

Trammell et al. (2016)Nature Communications · 7:12948
Reported that single oral doses of the precursor produced dose-dependent increases in the blood NAD+ metabolome, establishing oral bioavailability; a separate single-participant pilot in the same paper reported a rise of up to 2.7-fold.
mouse and human, oral nicotinamide riboside Source
McDermott et al. (2024)Nature Communications · 15(1):5046
The NICE randomised clinical trial of nicotinamide riboside in peripheral artery disease, reporting on its prespecified endpoints.
human, randomised clinical trial Source
Martens et al. (2026)Alzheimer's & Dementia · 22(7):e71605
A randomised controlled pilot study of nicotinamide riboside supplementation in older adults with amnestic mild cognitive impairment.
human, phase 2 randomised controlled pilot Source
Yang et al. (2026)Nutrients · 18(14)
Pooled the randomised evidence on oral nicotinamide mononucleotide supplementation in adults, examining safety and metabolism-related outcomes.
human, systematic review and meta-analysis Source

Adverse and null findings reported

No dedicated safety study has been published for this compound. That is not a finding that none exists — it means the question has not been asked in print, and the gaps below say so.

What the research does not establish

An absence cannot be cited, so these are stated plainly. They are the part of the picture that silence would otherwise hide.

The `adverse` list is empty of dedicated safety publications, but the pooled analyses cited above report on safety within their own populations. That is not the same as a characterised safety profile for administering NAD+ itself, which has not been published.
Almost the entire human literature concerns oral precursors — nicotinamide riboside and nicotinamide mononucleotide — because the intact molecule is poorly taken up by cells. None of it is direct evidence about NAD+ as supplied.
Bioavailability of precursors is well established. Clinical benefit is not: the trials that have measured outcomes rather than biomarkers have produced inconsistent results.
The observation that NAD+ levels fall with age is robust. That the fall is a cause of ageing rather than a consequence or a correlate is an assumption the field is built on and has not established.
Sirtuins and PARP enzymes are implicated in DNA repair and gene regulation, and what sustained elevation of their substrate does over years has not been studied in humans.
It is supplied here as a laboratory reagent. Nothing about the precursor supplement literature transfers to material used in that way.

Common questions

Is NAD+ a peptide?: No. It is a coenzyme present in every cell — the electron carrier in energy metabolism and the substrate for sirtuins and PARP enzymes. It is the one item in this catalogue that is not a peptide or a steroid.
Does the NAD+ research apply to NAD+ itself?: Mostly not. The intact molecule is poorly taken up by cells, so almost all human research uses precursors that cells can import and convert. Reading a precursor trial as evidence about NAD+ skips the exact step the field exists to work around.
What have the precursor trials shown?: That oral nicotinamide riboside is bioavailable and raises the blood NAD+ metabolome dose-dependently — a robust pharmacokinetic result. Trials measuring clinical outcomes rather than biomarkers have been inconsistent.
Do NAD+ levels really fall with age?: That observation is well supported. Whether the fall causes ageing, or results from it, or merely accompanies it, is the assumption the field rests on and has not been established.
Is NAD+ approved as a medicine?: No. It is supplied here as a laboratory reagent for in-vitro research and not for human or veterinary use.

Compounds covered

The reference page for each compound this article discusses.

NAD+

MOTS-c: what the research says
A peptide encoded in mitochondrial rather than nuclear DNA, whose discovery mattered more than the molecule. The founding mouse work, and the ten years since.
SS-31 (elamipretide): what the research says
One of very few compounds here to reach phase 3. The MMPOWER-3 trial missed its primary endpoints, and that result is the most useful thing it has.
How to store research peptides
Lyophilised peptides at -20°C, reconstituted at 2–8°C, ambient in transit. Why the dry cake tolerates shipping, and what actually degrades a vial.

About this article

Everything reported here comes from published research, and each finding names the model the study used — cell culture, rat, or human. Findings in one model do not transfer to another, most of the work described is preclinical, and none of it is a claim that a compound is safe or effective for any purpose. Nothing on this page describes doses, routes of administration, or use in a person.

Approval status varies by compound and by country. A few of the substances described are the active ingredient of medicines authorised in the EU; most have no marketing authorisation anywhere and have never been assessed by a regulator. Neither is supplied as a medicine here. All material supplied by ASSAY is sold for in-vitro laboratory research only, and is not a drug, food, cosmetic or medical device, and not for human or veterinary use.

All guides