NAD+

Also identified as Nicotinamide adenine dinucleotide

Dinucleotide coenzyme

Molecular weight: 663.4
Molecular formula: C21H27N7O14P2
CAS: 53-84-9
Published studies reviewed: 3

FOR RESEARCH USE ONLY. NOT FOR HUMAN OR VETERINARY USE. NOT FOR HUMAN CONSUMPTION.

Compounds described on this site are supplied solely for laboratory research. They are not offered for human or veterinary use or for clinical use, and they are not intended to diagnose, mitigate, cure or prevent any disease.

NAD+ (nicotinamide adenine dinucleotide) is the dinucleotide coenzyme present in every cell; its precursors nicotinamide riboside and nicotinamide mononucleotide, and its reduced form NADH, are different substances and are excluded. Three publications are reviewed: a cell-culture study of NAD+ uptake, a small randomised pilot that traced NAD+ and its metabolites in plasma and urine, and a retrospective tolerability record review by employees of the wellness chain that kept the records. None of the human records measured a clinical outcome.

At a glance

Also identified as: Nicotinamide adenine dinucleotide
Class: Dinucleotide coenzyme
Target or mechanism: The human publications recorded here do not characterise a molecular target.
Evidence types represented: in vitro, human
Published studies reviewed: 3
Last reviewed: 2026-09-26

Overview

NAD+ is a coenzyme present in every cell, central to the redox reactions of metabolism.

⚠️ Much of the human literature that circulates under this name studied nicotinamide riboside or nicotinamide mononucleotide — precursors the body converts to NAD+, and different compounds. A trial of a precursor is not a trial of this molecule, and no such trial is recorded on this page as though it were. The same applies to NADH, the reduced form, which is also a different substance from the one described here.

Two human publications are recorded, and they are very different in kind. The first is a pilot study in which 11 volunteers were randomised to NAD+ or to saline, with plasma and urine sampled repeatedly and analysed by mass spectrometry — a study of where the molecule goes once given, not of whether anything improves. The second is a retrospective review of medical records from a commercial wellness chain, written by that chain's employees, comparing tolerability between people who received NAD+ and people who received a precursor.

A laboratory study in cultured cells is also recorded: intracellular NAD+ rose when NAD+ was added to the medium, which its authors read as uptake of the intact molecule.

None of the human records is a trial of a clinical outcome, and nothing on this page establishes one.

Mechanism under investigation

The human publications recorded here do not characterise a molecular target. In the laboratory study, silencing or inhibiting the NAD-dependent enzyme SIRT1 abolished one of the effects of added NAD+ on cultured cells. The pilot study measured concentrations of NAD+ and of four of its metabolites in plasma and urine during and after it was given, and its authors describe the resulting profile as consistent with NAD+ glycohydrolase and NAD+ pyrophosphatase activity.

Scope of the published work

Areas investigated

Plasma and urine NAD+ metabolome
Tolerability
Liver function markers
Uptake by cultured cells

Models used

Randomised pilot study in healthy volunteers
Retrospective record review
Cell lines and primary cell cultures

Every human figure on this page was recorded in a controlled study, under supervision, using material prepared for that study, in a population selected by its entry criteria. It is not the research material PepGenex supplies and no result here transfers to it.

Limitations

Evidence represented on this page: in vitro and human. No animal research is represented. The page reviews 3 published studies, and each figure is reported for the study that published it; results are not pooled across studies.

Common questions

What is NAD+?

NAD+ is a coenzyme present in every cell, central to the redox reactions of metabolism.

How does NAD+ work, according to the published research?

Intracellular NAD content increased when cell lines or primary cultures were exposed to NAD in the medium. NAD precursors did not reproduce the effect and were not found in the medium containing NAD, which the authors read as evidence that the dinucleotide was taken up intact. (Pittelli et al., 2011, PMID 21917911)

What has published research on NAD+ found, and what are its limits?

This page records 3 publications, reporting laboratory (in vitro) work in 1, human work in 2. Each is listed with its identifier under References.

Human studies represented: Reyna et al., 2026, PMID 41704678; Grant et al., 2019, PMID 31572171.

Evidence represented on this page: in vitro and human.

No animal research is represented.

The page reviews 3 published studies, and each figure is reported for the study that published it; results are not pooled across studies.

Is NAD+ approved by the U.S. FDA?

This page cites no FDA approval record for NAD+; PepGenex Science states a U.S. regulatory status only where a sourced record exists.

PepGenex research materials are not FDA approved and are not for human or veterinary use.

What risks have published studies of NAD+ reported?

2 published human studies on this page report adverse events or safety measurements. Each is listed with its publication in the adverse-events section of this page.

Trial events do not establish a complete safety profile.

What adverse events have been reported in published studies of NAD+?

Adverse events and safety measurements as reported by the published human studies on this page. Each entry is attributed to its publication.

Reyna et al., 2026, PMID 41704678

Design and population: A retrospective review of electronic medical records of clients of a commercial wellness chain, who had received either NAD+ or nicotinamide riboside, with 30 days of follow-up. Nicotinamide riboside is a different compound and its group is a comparator here, not evidence about NAD+. The recorded outcomes were reported symptoms, total time taken to give the compound, blood pressure, resting heart rate and the biomarkers ALT, AST, hsCRP, BUN/creatinine and TSH, with HbA1c, fasting glucose, HDL-C, LDL-C and triglycerides as exploratory measures. There was no randomisation and no placebo group. Six clients had received NAD+ and eight had received nicotinamide riboside. From the full text; the abstract prints no group sizes.
Events reported: Tolerability differed between the two groups. Those who received NAD+ reported moderate to severe gastrointestinal symptoms, increased heart rate and chest pressure while it was being given; those who received nicotinamide riboside reported minor tongue, jaw and arm tingling and mild cramping. All reported symptoms resolved once it had been given in full.

Grant et al., 2019, PMID 31572171

Design and population: Participants were randomised to a test group, which received NAD+ in normal saline, or to a control group, which received normal saline alone. Plasma was sampled at baseline and at 30, 60, 120, 360 and 480 minutes from the start of the exposure period, and urine at baseline, 30 minutes, 2, 6 and 8 hours; NAD+ and its metabolites were measured by liquid chromatography with tandem mass spectrometry. Participants ate an identical niacin-reduced diet the day before and fasted through the study, and were not permitted products containing NAD+, nicotinamide riboside or nicotinamide for 14 days beforehand. From the full text. Eleven male participants aged 30 to 55 took part — 8 in the NAD+ group and 3 in the saline control group — each with a body mass index below 30, not diabetic, smoking less than one cigarette and drinking less than two standard alcoholic drinks a day. From the full text.
Events reported: No adverse events were observed during the 6-hour exposure period in either the saline or the NAD+ group. Between baseline and 8 hours the NAD+ group showed significant decreases in the liver enzymes GGT (1.3 units/L), LD (57 units/L) and AST (3.6 units/L), and a significant increase of 2.75 µmol/L in plasma bilirubin (each p ≤ 0.05, Wilcoxon signed ranks); the authors state that none of the changes was considered clinically significant, and that no liver-function marker changed significantly in the saline group, while noting that the small sample may reduce the sensitivity of that comparison. From the full text.

Trial events do not establish a complete safety profile.

Published research

Grouped by the kind of study. Select one to narrow what is shown below.

Laboratory (in vitro)(1)

Laboratory (in vitro)

Pharmacological effects of exogenous NAD on mitochondrial bioenergetics, DNA repair, and apoptosis.

Pittelli M, Felici R, Pitozzi V, Giovannelli L, Bigagli E, Cialdai F, Romano G, Moroni F, Chiarugi A, Molecular Pharmacology, 2011;80(6):1136-1146

published

Intracellular NAD content increased when cell lines or primary cultures were exposed to NAD in the medium. NAD precursors did not reproduce the effect and were not found in the medium containing NAD, which the authors read as evidence that the dinucleotide was taken up intact.
In the mitochondria of cells exposed to NAD, NAD and NADH content, oxygen consumption and ATP production were increased, while DNA repair — an NAD-dependent process — was unaltered. Exposure to NAD reduced apoptosis triggered by staurosporine, C2-ceramide or N-methyl-N'-nitro-N-nitrosoguanidine; blocking or silencing the NAD-dependent enzyme SIRT1 abolished the reduction against staurosporine only.

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Human study (phase not stated)(2)

Human study (phase not stated)n = 14

Intravenous infusion of nicotinamide adenine dinucleotide (NAD+) versus nicotinamide riboside (NR): a retrospective tolerability pilot study in a real-world setting.

Reyna K, Heinzen G, Patel N, Ritter M, Siojo A, Legere H, Pojednic R, Frontiers in Aging, 2026;7:1652582

published

A retrospective review of electronic medical records of clients of a commercial wellness chain, who had received either NAD+ or nicotinamide riboside, with 30 days of follow-up. Nicotinamide riboside is a different compound and its group is a comparator here, not evidence about NAD+. The recorded outcomes were reported symptoms, total time taken to give the compound, blood pressure, resting heart rate and the biomarkers ALT, AST, hsCRP, BUN/creatinine and TSH, with HbA1c, fasting glucose, HDL-C, LDL-C and triglycerides as exploratory measures. There was no randomisation and no placebo group.

Six clients had received NAD+ and eight had received nicotinamide riboside. From the full text; the abstract prints no group sizes.

Tolerability differed between the two groups. Those who received NAD+ reported moderate to severe gastrointestinal symptoms, increased heart rate and chest pressure while it was being given; those who received nicotinamide riboside reported minor tongue, jaw and arm tingling and mild cramping. All reported symptoms resolved once it had been given in full.
The average total time taken to give the compound over the four days was 97 minutes (SD 56.33) for the NAD+ group and 37 minutes (SD 13.08) for the nicotinamide riboside group, which the authors attribute to the more severe symptoms in the NAD+ group, clients being able to control their own rate. From the full text, where the Figure 1 legend prints 96 minutes for the same group and reports the difference at p < 0.05.
No significant changes were observed in ALT, AST, hsCRP, BUN/creatinine or TSH in either group. Alkaline phosphatase decreased significantly in the NAD+ group only, with values remaining within normal reference ranges, and the NAD+ group showed a significant reduction in HDL-C. Neither group showed a change in fasting glucose or LDL-C over the 30 days. The authors call these exploratory outcomes variable, and state that the retrospective design, the small sample, the absence of placebo or matched controls and the lack of standardised lifestyle controls mean they should be read with caution.

Context

Almost all of the human literature filed under this name studied something else: nicotinamide riboside, nicotinamide mononucleotide, niacin, nicotinamide, or NADH — the reduced form. Those are different molecules, and none of their results is recorded here. What is recorded is the small body of work in which NAD+ itself was given to people. Where a precursor appears below, it is the comparator group of a study that also gave NAD+, and it is named as the other compound.

Limitations

The second record is not a trial. It is a look back at the files of 14 clients of a commercial wellness chain, written by people employed by that chain, with no randomisation, no placebo and no standardisation of anything the clients did. Its tolerability observations are the part that carries weight — symptoms were recorded by nurses at the time — and its metabolic figures are exploratory, which is how the authors label them.

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Human study (phase not stated)n = 11

A Pilot Study Investigating Changes in the Human Plasma and Urine NAD+ Metabolome During a 6 Hour Intravenous Infusion of NAD+.

Grant R, Berg J, Mestayer R, Braidy N, Bennett J, Broom S, Watson J, Frontiers in Aging Neuroscience, 2019;11:257

published

Participants were randomised to a test group, which received NAD+ in normal saline, or to a control group, which received normal saline alone. Plasma was sampled at baseline and at 30, 60, 120, 360 and 480 minutes from the start of the exposure period, and urine at baseline, 30 minutes, 2, 6 and 8 hours; NAD+ and its metabolites were measured by liquid chromatography with tandem mass spectrometry. Participants ate an identical niacin-reduced diet the day before and fasted through the study, and were not permitted products containing NAD+, nicotinamide riboside or nicotinamide for 14 days beforehand. From the full text.

Eleven male participants aged 30 to 55 took part — 8 in the NAD+ group and 3 in the saline control group — each with a body mass index below 30, not diabetic, smoking less than one cigarette and drinking less than two standard alcoholic drinks a day. From the full text.

Plasma NAD+ concentration relative to baseline