In stockBestseller
- Batch verified
- Temperature controlled
- Discreet packaging
- Purity
- 99.5%
- Form
- Lyophilised powder
- Molecular weight
- 663.4 g/mol
- Storage
- -20°C, desiccated, protected from light
- Batch
- B-2408-113
For research use only · Not for human consumption
About this compound
−0.706
Correlation of tissue NAD+ with donor age
human skin · 49 donors · males, p = 0.001 (6)
+142%
Whole blood NAD+ at the highest oral dose
nicotinamide riboside 1,000 mg · day 14 · 140 adults (2)
~60%
NAD+ in blood mononuclear cells, against placebo
nicotinamide riboside 1,000 mg/day · 6 weeks · 30 adults (3)
2 h
Before infused NAD+ appeared in plasma at all
NAD+ 750 mg intravenous over 6 h · 11 men (5)
NAD+ is the one entry in this catalogue that is not a peptide. Nicotinamide adenine dinucleotide is a coenzyme — two nucleotides joined through a pair of phosphates — and unlike every other compound here it was not designed to act on anything. It is already present in the cell, at a concentration the cell itself maintains.
Covarrubias and colleagues describe two distinct roles for it. The first is redox: NAD+ accepts electrons and NADH releases them, which is what places the molecule at the centre of energy metabolism. Nothing is used up in that role — it cycles between the two states. The second role does use it up. Sirtuins, CD38 and the poly(ADP-ribose) polymerases are NAD+-dependent enzymes that take the molecule as a substrate rather than a catalyst, and what they cleave has to be rebuilt (1).
Most of that rebuilding runs through the salvage pathway, which recycles nicotinamide rather than assembling the molecule from scratch. Revollo and colleagues measured the kinetics of that pathway in mouse fibroblasts and reported nicotinamide phosphoribosyltransferase — NAMPT — to be its rate-limiting component: raising NAMPT raised total cellular NAD+, while raising the next enzyme along did not (9).
Ageing is accompanied by a gradual decline in tissue and cellular NAD+ across several model organisms, rodents and humans among them (1). In human pelvic skin from 49 donors spanning newborns to 77-year-olds, tissue NAD+ correlated negatively with age — r = −0.706 in males, r = −0.537 in females (6). Those are correlations across donors of different ages, not a loss followed inside one person over time.
What NAD+ does, and what spends it
01
Redox carrier
In its oxidised form the molecule accepts electrons; in its reduced form, NADH, it releases them. Covarrubias and colleagues describe this as the role that makes NAD+ central to energy metabolism (1). It is a loan rather than a purchase — the molecule cycles between the two states and is not consumed.
02
Enzyme substrate
Sirtuins, CD38 and the poly(ADP-ribose) polymerases are described as NAD+-dependent enzymes that consume the molecule rather than recycle it (1). In the human skin series, PARP activity rose with donor age and correlated inversely with tissue NAD+ (r = −0.639, p = 0.0003) (6).
03
The salvage pathway
Because the second group destroys what the first only borrows, cells resynthesise NAD+ continuously, mostly by salvaging nicotinamide. NAMPT was the rate-limiting component of that pathway in mouse fibroblasts, and it is the step every oral precursor in the trials below is aimed at bypassing (9).
Why the human literature is about precursors
Almost every human trial that reports raising NAD+ did not administer NAD+. It administered a precursor — nicotinamide riboside (NR) or nicotinamide mononucleotide (NMN) — swallowed as a capsule and converted to NAD+ inside the cell. Vendor pages routinely present those results as evidence about NAD+ itself. They are not the same claim, and every figure on this page is labelled with the compound that was actually given.
The distinction is not pedantry. Grant and colleagues infused 750 mg of NAD+ intravenously over six hours into eight men, with three controls, and stated that no data on the fate of directly infused NAD+ in a human cohort were available before their own. Plasma NAD+ did not move for the first two hours — the paper concludes the infused molecule was rapidly and completely removed from plasma over that period — and rose significantly only at the six-hour mark, at the end of the infusion (5).
So the compound in this vial and the compounds in the trials below are related by metabolism rather than by identity. What those trials establish is that oral precursors raise NAD+ in blood. What none of them establishes is what follows when NAD+ itself is supplied.
Whole blood NAD+ after oral nicotinamide riboside, by dose
One trial, 140 healthy overweight adults, 35 per arm, eight weeks. Every bar is the mean increase from that group's own baseline at day 14 — and every bar is nicotinamide riboside taken by mouth, not NAD+, which is why no bar on this chart is drawn as the subject of this page. The trial's placebo group is not drawn: it reported a small but significant decrease from baseline over the 56-day period with no percentage published, and an undrawn baseline is better than an invented one.
Nicotinamide riboside 100 mg
22%
Nicotinamide riboside 300 mg
51%
Nicotinamide riboside 1,000 mg
142%
Sources. (2) Conze D, Brenner C, Kruger CL. Safety and Metabolism of Long-term Administration of NIAGEN (Nicotinamide Riboside Chloride) in a Randomized, Double-Blind, Placebo-controlled Clinical Trial of Healthy Overweight Adults. Sci Rep. 2019;9(1):9772. Figures are the mean percentage increase in whole blood NAD+ at day 14 relative to each group's own baseline — 22 ± 9%, 51 ± 7% and 142 ± 14%. The compound administered was nicotinamide riboside, an oral NAD+ precursor, and not NAD+. NAD+ is not an approved medicine.
What the human trials reported
Blood is where the precursor trials agree. Conze and colleagues randomised 140 healthy overweight adults across placebo and three oral NR doses for eight weeks and reported whole blood NAD+ up 22%, 51% and 142% at 100, 300 and 1,000 mg by day 14, with the increases maintained through the rest of the study (2). Martens and colleagues gave 30 healthy middle-aged and older adults 500 mg of NR twice daily in a 2 × 6-week placebo-controlled crossover and reported NAD+ in peripheral blood mononuclear cells elevated by approximately 60% against placebo (3). Trammell and colleagues, in the first pharmacokinetic trial of oral NR in humans, reported dose-dependent increases across the blood NAD+ metabolome in twelve participants at the same three single doses; a preceding pilot saw blood NAD+ rise as much as 2.7-fold, and that figure rests on a single individual (8).
Tissue is where they stop agreeing. Elhassan and colleagues gave twelve men aged 70 to 80 one gram of NR daily for 21 days in a placebo-controlled double-blind crossover. The muscle NAD+ metabolome shifted — nicotinamide clearance products and nicotinic acid adenine dinucleotide both rose — but the NAD+ concentration in the muscle itself did not: 210 pmol/mg on NR against 197 pmol/mg on placebo, p = 0.22. Muscle mitochondrial bioenergetics were unaffected, while specific circulating inflammatory cytokines fell (7).
The one functional endpoint to have moved comes from NMN rather than NR. Yoshino and colleagues randomised 25 postmenopausal women with prediabetes, overweight or obese, to 250 mg of oral NMN daily or to placebo for ten weeks. The rate of insulin-stimulated glucose disposal per kilogram of fat-free mass was 25 ± 7% greater after the ten weeks than before them (p < 0.01), and did not change in the placebo group (4). That is a before-and-after comparison inside a treated group of thirteen, in one population, on one endpoint.
NAD+, the precursors that were actually studied, and SS-31
Three columns for three different things. The first is the molecule this page is about. The second is what almost every human trial cited here administered instead. The third is the other longevity compound in this catalogue, included because it is also aimed at mitochondrial function and reaches it by an entirely different route. Nothing in this table is a head-to-head result — the studies share no endpoint, no population and no unit, and the table is deliberately qualitative for that reason.
| Parameter | NAD+ | NR and NMN | SS-31 |
|---|---|---|---|
| Molecular class | Dinucleotide coenzyme — not a peptide | Vitamin B3 derivatives and precursors of NAD+ — not peptides | Synthetic tetrapeptide |
| Role described in the cited work | Redox electron carrier, and substrate for sirtuins, CD38 and the PARPs (1) | Converted to NAD+ inside the cell, largely through the salvage pathway (1)(9) | Binds cardiolipin in the inner mitochondrial membrane and protects cristae structure (10) |
| Largest human study cited here | Pilot infusion study, 11 men, one 6-hour session (5) | Randomised, double-blind, placebo-controlled, 140 adults, 8 weeks, NR (2) | MMPOWER-3, phase 3, 218 participants, 24 weeks double-blind (11) |
| What that study measured | Plasma and urine NAD+ and its metabolites during and after infusion (5) | Whole blood NAD+ and other NAD+ metabolites (2) | Six-minute walk distance and a total fatigue score (11) |
| What it reported | No change in plasma NAD+ or its metabolites until after 2 hours (5) | Whole blood NAD+ up 22%, 51% and 142% at 100, 300 and 1,000 mg (2) | The double-blind part did not meet its primary endpoints (11) |
| Administration in the cited studies | Intravenous infusion (5) | Oral capsules (2)(3)(4)(7)(8)(12) | Daily subcutaneous injection (11) |
| Evidence stage in the literature cited here | A single pharmacokinetic cohort (5) | Several randomised placebo-controlled trials, mostly measuring NAD+ in blood (2)(3)(7)(8) | Preclinical mechanism (10) and one completed phase 3 (11) |
| Approval status | Not an approved medicine | Not approved medicines; nicotinamide riboside chloride is generally recognised as safe for use in foods (2) | Elamipretide is approved in the United States as FORZINITY, subcutaneous, to improve muscle strength in Barth syndrome (13) |
Sources. (2) Conze D, Brenner C, Kruger CL. Safety and Metabolism of Long-term Administration of NIAGEN (Nicotinamide Riboside Chloride) in a Randomized, Double-Blind, Placebo-controlled Clinical Trial of Healthy Overweight Adults. Sci Rep. 2019;9(1):9772. (5) Grant R, Berg J, Mestayer R, et al. A Pilot Study Investigating Changes in the Human Plasma and Urine NAD+ Metabolome During a 6 Hour Intravenous Infusion of NAD+. Front Aging Neurosci. 2019;11:257. (10) Birk AV, Liu S, Soong Y, et al. The mitochondrial-targeted compound SS-31 re-energizes ischemic mitochondria by interacting with cardiolipin. J Am Soc Nephrol. 2013;24(8):1250–1261. (11) Karaa A, Bertini E, Carelli V, et al. Efficacy and Safety of Elamipretide in Individuals With Primary Mitochondrial Myopathy: The MMPOWER-3 Randomized Clinical Trial. Neurology. 2023;101(3):e238–e252; design and outcome details from ClinicalTrials.gov NCT03323749. (13) FORZINITY (elamipretide hydrochloride) injection, for subcutaneous use. Prescribing information. Stealth Biotherapeutics Inc.; initial U.S. approval 2025. Cited elsewhere on this page: (1) Covarrubias AJ, Perrone R, Grozio A, Verdin E. NAD+ metabolism and its roles in cellular processes during ageing. Nat Rev Mol Cell Biol. 2021;22(2):119–141. (3) Martens CR, Denman BA, Mazzo MR, et al. Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults. Nat Commun. 2018;9(1):1286. (4) Yoshino M, Yoshino J, Kayser BD, et al. Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. Science. 2021;372(6547):1224–1229. (6) Massudi H, Grant R, Braidy N, et al. Age-associated changes in oxidative stress and NAD+ metabolism in human tissue. PLoS One. 2012;7(7):e42357. (7) Elhassan YS, Kluckova K, Fletcher RS, et al. Nicotinamide Riboside Augments the Aged Human Skeletal Muscle NAD+ Metabolome and Induces Transcriptomic and Anti-inflammatory Signatures. Cell Rep. 2019;28(7):1717–1728.e6. (8) Trammell SA, Schmidt MS, Weidemann BJ, et al. Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. Nat Commun. 2016;7:12948. (9) Revollo JR, Grimm AA, Imai S. The NAD biosynthesis pathway mediated by nicotinamide phosphoribosyltransferase regulates Sir2 activity in mammalian cells. J Biol Chem. 2004;279(49):50754–50763. (12) Irie J, Inagaki E, Fujita M, et al. Effect of oral administration of nicotinamide mononucleotide on clinical parameters and nicotinamide metabolite levels in healthy Japanese men. Endocr J. 2020;67(2):153–160. Apart from (5), every human study cited on this page administered an NAD+ precursor by mouth rather than NAD+. NAD+ is not an approved medicine.
What the cited literature does and does not show
- Oral nicotinamide riboside raised whole blood NAD+ dose-dependently in 140 adults, and the increase held for the eight weeks of the trial (2).
- Oral nicotinamide riboside raised NAD+ in peripheral blood mononuclear cells by approximately 60% against placebo in 30 adults (3).
- Oral nicotinamide riboside did not raise the NAD+ concentration of skeletal muscle in men aged 70 to 80 — 210 pmol/mg against 197 pmol/mg on placebo, p = 0.22 — although other metabolites in that tissue did rise (7).
- One functional endpoint moved: muscle insulin sensitivity in 25 prediabetic postmenopausal women given nicotinamide mononucleotide, reported as a 25 ± 7% before-and-after change within the treated group (4).
- The decline of NAD+ with age in humans appears here as a correlation across donors of different ages, in one tissue, in one series of 49 people (6).
- The single study in which NAD+ itself was administered measured where the molecule went, not what it did (5).
- Among the studies cited on this page, none administered NAD+ and measured a clinical outcome.
What Peptio ships
A sealed vial of lyophilised powder, in a 100 mg or a 500 mg size. Both are the same material; the difference is the mass in the vial, not the concentration — concentration is set later, by how much solvent is added.
Each batch is released against a certificate of analysis from an independent issuer, and the batch number printed on the vial matches the number on that certificate. Checking those two against each other is the most useful thing to do with a delivery. The purity, form, storage condition and molecular weight recorded for the current batch are in the specifications above.
Handling is the same as for every other compound in the catalogue. The handling protocol below covers storage temperatures, solvent choice and the concentration calculation.
Research use only
NAD+ is not an approved medicine. Peptio is not a pharmacy and supplies it for research use only — not for human or veterinary consumption. Read every figure on this page with the compound attached to it: apart from the single infusion study, each human trial cited here administered a precursor by mouth — nicotinamide riboside or nicotinamide mononucleotide — and not NAD+. Those results describe what happened to the participants of those trials, and none of it is guidance for use in people.
Handling and storage
Every compound Peptio ships arrives as a sealed vial of lyophilised powder. Freeze-drying is what keeps it stable in transit: with the water removed and the vial closed, the peptide keeps far longer than it would in solution. The protocol below applies to all of them, and it is the same protocol whichever compound is in the vial.
The steps that matter most happen in the first few minutes after a vial is opened, and in how the prepared solution is labelled afterwards. A vial with no recorded solvent volume is a vial with no known concentration, and no amount of care later recovers that.
From delivery to prepared solution
01
Inspect on arrival
Check that the crimp seal and stopper are intact and that the powder cake is dry and unbroken. Compare the batch number printed on the vial with the number on the certificate of analysis. A cake that has slumped into a film, or a vial that arrives loose in its packaging, is worth photographing before anything else is done to it.
02
Equilibrate before opening
Let a vial taken from cold storage stand sealed until it reaches room temperature. Opening cold glass in a warm room pulls condensation onto it, and moisture is the one thing a desiccated powder is being protected from.
03
Add the solvent
Direct the solvent slowly down the inner wall of the vial rather than onto the cake, then let it dissolve on its own and swirl gently until the solution runs clear. This takes a minute or two, and it is not helped by shaking.
04
Label, then refrigerate
Write the date, the solvent and the exact volume added onto the vial before it goes anywhere. Keep the prepared solution cold and out of direct light, and check that it is still clear each time it is used.
Quick reference
- Form
- Lyophilised powder in a sealed, stoppered vial
- Solvent
- Bacteriostatic water where the vial will be drawn from more than once; sterile water where it will not
- Typical reconstitution volume
- 1–3 mL, chosen to give the concentration the work calls for
- Storage before reconstitution
- −20 °C, desiccated and protected from light
- Storage after reconstitution
- 2–8 °C, protected from light, in the original stoppered vial
- In transit
- Short periods at 2–8 °C are expected; that is what the insulated mailer is for
- Once opened
- Record the date on the vial. How long a prepared solution stays usable depends on the solvent and the storage temperature, so the date is the only reliable reference point.
Handling
| Correct | Common mistake |
|---|---|
| Direct the solvent down the inner wall of the vial and let the cake dissolve on its own. | Drive the solvent onto the powder in a fast stream. |
| Swirl gently until the solution runs clear. | Shake or vortex the vial — mechanical agitation and foaming degrade peptide structure. |
| Let a vial from cold storage reach room temperature while it is still sealed. | Open a vial straight out of the freezer, and pull condensation into a product that is kept dry on purpose. |
| Label every prepared vial with the date, the solvent and the volume added. | Rely on memory — two vials that look identical at 2–8 °C can hold two different concentrations. |
| Draw through the stopper with a fresh sterile needle each time. | Prise off the crimp seal; an open vial cannot be kept sterile. |
| Keep prepared solution cold and shielded from light between uses. | Leave a reconstituted vial standing at room temperature on the bench. |
| Look at the solution before every use and confirm it is clear. | Use a solution that has turned cloudy or thrown a visible particle. |
Solvent volume sets the concentration
The mass of peptide in a vial is fixed at manufacture. The only variable is how much solvent goes in, and it changes every measurement that follows — 2 mL instead of 1 mL halves the concentration. Confirm the vial's usable capacity before adding anything, since a 2 mL vial will not take 3 mL, and write down the volume you actually added.
Working out the concentration
- Concentration (mg/mL) = peptide mass in the vial (mg) ÷ solvent volume added (mL).
- A 5 mg vial with 1 mL of solvent gives 5 mg/mL. The same vial with 2 mL gives 2.5 mg/mL.
- A 10 mg vial with 2 mL of solvent also gives 5 mg/mL — the same concentration from twice the mass.
- Volume (mL) = mass required (mg) ÷ concentration (mg/mL).
- 1 mg/mL is 1,000 micrograms per mL. Convert once, at the start, and hold one unit for the whole calculation.
Questions
About NAD+
Delivery
- One delivery option at checkout: standard, 3–5 working days.
- Orders ship in an insulated mailer.
- Delivery is free on orders over €150.00.
- See the Shipping page for the delivery terms in full.
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