Section 01
What it's used for
Raising blood NAD+ levels
Clinical trials in people show that taking NMN increases blood levels of NAD+, a molecule cells need to produce energy, by 40 to 100 percent compared with levels measured before supplementation began in the trials.
▸Clinical wording
- Clinical trials show NMN supplementation increases blood NAD+ levels by 40-100%
- Shown to improve age-related biomarkers including telomere length and epigenetic age
- Supports sirtuin activation — a key pathway in longevity and caloric restriction mimicry
Muscle insulin response in a trial
In a randomized trial of prediabetic women given 250 mg a day for 10 weeks, NMN improved how muscle responded to insulin, measured with a specialized clamp test. It did not improve blood sugar tolerance or fasting glucose.
▸Clinical wording
A randomized clinical trial in prediabetic women (250 mg/day for 10 weeks) found that NMN improved muscle insulin sensitivity, measured by hyperinsulinemic-euglycemic clamp and insulin signaling. The trial did not report an improvement in oral glucose tolerance or fasting glucose, and no other clinical trial demonstrating improved glucose tolerance from NMN was found.
Aerobic capacity and endurance
NMN is studied for improving aerobic capacity, the body's ability to use oxygen during exercise, and how efficiently muscles use that oxygen, both of which relate closely to physical endurance and overall performance.
▸Clinical wording
- Improves aerobic capacity and muscle oxygen utilization
- Enhances exercise endurance in both animal models and human trials
- Supports muscle NAD+ levels and post-exercise recovery
Brain function: no human trial yet
NMN's potential to support thinking and brain energy use is discussed in lab research and vendor material, but no published human trial has shown improved cognitive function from NMN. Results in this area have often been mixed or null.
▸Clinical wording
NMN's potential to support cognitive function and brain energy metabolism is discussed in preclinical, mechanistic, vendor, and community material. No published human clinical trial demonstrating improved cognitive function or brain energy metabolism from NMN supplementation was found, and review articles note that functional and cognitive outcomes in this area have been heterogeneous and often null.
Blood vessel health
NMN is studied for supporting the elasticity of blood vessels and the health of the endothelium, the thin inner lining that lines blood vessels and helps regulate blood flow and circulation throughout the body.
▸Clinical wording
- Supports vascular elasticity and endothelial function
- Reduces arterial stiffness in aging
- Improves cardiac energy metabolism
Section 02
Mechanism of Action
One step away from the finished molecule
- NMN needs only one enzymatic step to become NAD+, skipping the pathway's usual bottleneck enzyme (NAMPT).
- In high-fat-fed mice that bottleneck was severely compromised in liver, fat and muscle, and NMN restored NAD+ there.
- One enzyme of this family sits inside mitochondria and is the only known NAD+-making enzyme found there.
▸Clinical wording
NMNAT-catalysed conversion to NAD+ downstream of NAMPT
NMN sits one enzymatic step below NAD+: NMNAT enzymes adenylylate it to NAD+, so supplying NMN bypasses NAMPT, the rate-limiting enzyme that produces NMN from nicotinamide. Yoshino and colleagues showed that NAMPT-mediated NAD+ biosynthesis is severely compromised in liver, white adipose tissue and skeletal muscle of high-fat-fed mice, and that NMN restored NAD+ in these tissues (Cell Metabolism, 2011). Nikiforov and colleagues localised NMNAT3 to the mitochondrial matrix, where NMN together with ATP serves as its substrate — the only known NAD+-synthesising enzyme residing inside the organelle (Journal of Biological Chemistry, 2011).
How it gets into cells is disputed
- One group showed a surface enzyme (CD73) strips a phosphate from NMN so it enters as nicotinamide riboside.
- Isotope labelling led another group to conclude cells require that conversion before uptake and NAD+ synthesis.
- A direct transporter was later proposed in the mouse gut, and another team formally challenged that assignment.
▸Clinical wording
Extracellular dephosphorylation to nicotinamide riboside
How NMN crosses the plasma membrane is contested. Grozio and colleagues showed that the ecto-5'-nucleotidase CD73 dephosphorylates extracellular NMN to nicotinamide riboside, which then enters cells (Journal of Biological Chemistry, 2013). Using isotope labelling, Ratajczak and colleagues concluded that mammalian cells require conversion of extracellular NMN to NR for cellular uptake and NAD+ synthesis (Nature Communications, 2016). A direct sodium-dependent transporter, Slc12a8, was later proposed in the murine jejunum and ileum (Grozio et al., Nature Metabolism, 2019); Schmidt and Brenner published a formal challenge to that assignment in the same journal.
Metabolic and blood vessel changes in mice
- In diabetic mice NMN restored NAD+ and activated a maintenance enzyme (SIRT1), improving liver insulin sensitivity.
- Gene activity linked to oxidative stress, inflammation and the daily body clock normalised in those mice.
- In aged mice vessel dilation and aortic stiffness measures returned toward the levels of young animals.
- Those aged mice also showed reversed collagen accumulation and lower markers of oxidative damage.
▸Clinical wording
SIRT1-dependent metabolic and vascular effects
In diet- and age-induced diabetic mice, NMN restored NAD+ and activated SIRT1, improving hepatic insulin sensitivity and normalising gene expression related to oxidative stress, inflammatory response and circadian rhythm (Yoshino et al., Cell Metabolism, 2011). In aged mice, NMN restored endothelium-dependent dilation to the level of young animals, normalised aortic pulse wave velocity and elastic modulus, reversed collagen accumulation, and restored vascular SIRT1 activity as read out by acetylation of NFκB p65, alongside reduced superoxide production and nitrotyrosine (de Picciotto et al., Aging Cell, 2016).
An enzyme that eats the precursor
- NMN is also a substrate for degradation, so a consuming enzyme competes with any supplied precursor.
- In mice one enzyme (CD38) rises with age in liver, fat, spleen and muscle and degrades NMN.
- Mice lacking that enzyme maintained higher NAD+ during ageing and preserved mitochondrial function.
- This helps explain why NAD+ pools fall with age even though the building machinery stays intact.
▸Clinical wording
CD38 as the principal NMN-degrading enzyme in ageing
NMN is also a substrate for degradation, which places a consuming enzyme in competition with any supplied precursor. Camacho-Pereira and colleagues found that CD38 expression and enzymatic activity rise with age in mouse liver, adipose tissue, spleen and skeletal muscle, and identified CD38 as the main enzyme degrading NMN in vivo (Cell Metabolism, 2016). CD38-knockout mice maintained higher NAD+ during ageing and preserved mitochondrial function, an effect the authors traced at least in part to regulation of SIRT3 activity. This helps explain why NAD+ pools fall with age despite intact synthetic machinery.
Long mouse studies, one narrow human trial
- Twelve months of oral NMN in mice suppressed age-associated weight gain and raised energy expenditure and activity.
- The same mice showed better insulin sensitivity, eye function, bone density and muscle metabolism, without observable toxicity.
- The human evidence is far narrower: one trial in prediabetic women found increased muscle insulin sensitivity.
- That trial drew a published comment in the same journal questioning baseline differences between the groups.
▸Clinical wording
Long-term rodent phenotypes and a single human trial
Twelve months of oral NMN in C57BL/6N mice suppressed age-associated weight gain, raised energy expenditure and physical activity, improved insulin sensitivity, eye function and bone density, and enhanced mitochondrial oxidative metabolism in skeletal muscle without observable toxicity (Mills et al., Cell Metabolism, 2016). The human evidence is far narrower: in prediabetic women, NMN increased muscle insulin sensitivity and upregulated platelet-derived growth factor receptor beta and other muscle-remodelling genes (Yoshino et al., Science, 2021). That trial drew a published Comment in the same journal questioning baseline differences between groups (Brenner, Science, 2021).
Section 03
Biological Pathways
No data for this section yet.
Section 04
Dosage Information
| Route / system | Context | Range studied | Limitation |
|---|---|---|---|
| Oral — dose-ranging trials | Randomised trials in healthy adults, 250–900 mg a day | 250–900 mg daily for 30–90 days — about 3–13 mg/kg at 70–90 kg. Blood NAD+ rose at every dose; 250 mg for 12 weeks raised it 2.6-fold. | Blood NAD+ is a marker of the molecule's own metabolism. No trial showed that raising it changes anything the person taking the capsule would notice. |
| Oral — physical-function trial | Manufacturer-run trial, healthy adults aged 40–65 | 600 and 900 mg a day for 60 days improved 6-minute walk distance and self-rated health; 300 mg a day did not improve walking. | The sponsor sells the product. Gains were against each person's own start, on the softest measures in the field, and no independent group has repeated them. |
| Oral — metabolic trial | 10-week trial, 25 prediabetic postmenopausal women | 250 mg a day — 2.8–3.6 mg/kg at 70–90 kg. Muscle insulin sensitivity rose about 25%; liver, fat, weight and body composition did not. | Twenty-five women in one narrow metabolic state, and what moved was a laboratory measurement — not weight, not blood sugar, not anything they could feel. |
| Oral — safety ceiling | Highest dose ever formally tested for safety | 1250 mg once daily for 4 weeks in 31 healthy adults aged 20–65 — about 14–18 mg/kg. No dose has been studied beyond about 12 weeks. | Four weeks of blood work says nothing about years of daily use. After the FDA lifted its 2022 exclusion in 2025, capsules are supplements: labels go unchecked. |
| Subcutaneous / intranasal | Products sold outside any trial | No human study has given NMN either way. Circulating injection figures — 50–200 mg two or three times a week — are NAD+ protocols. | Every human NMN number comes from swallowing it. An injected dose has no absorption or safety data, and borrowing NAD+ figures assumes the two behave alike. |
Results
Syringe Fill Level (100u syringe)
Set positive values for: Recommended dose per kg.
Research Use Only. This information is for educational and research purposes only. Not intended for medical advice or self-medication.
Section 05
Protocols
- Protocol 01
NAD+ Restoration Protocol
Protocol for restoring cellular NAD+ levels using one of three interchangeable approaches: direct NAD+ administration, NMN supplementation, or Nicotinamide Riboside (NR). Choose ONE approach based on your budget, preferred route, and goals. NAD+, NMN, and NR all raise NAD+ levels — they are alternatives, not a stack. NAD+ levels decline ~50% between ages 40-60, contributing to aging, cognitive decline, and metabolic dysfunction. Restoring NAD+ supports DNA repair, mitochondrial function, sirtuin activation, and cellular energy production.
- Focus
- Anti-Aging
- Level
- Beginner
- Duration
- Ongoing
Section 06
Stability & Storage
Storing the product
NMN is kept in a cool, dry place away from light. It is relatively stable at room temperature, though refrigeration is preferred for long-term storage.
After opening
Once opened, the container is resealed to keep moisture out, since exposure degrades the compound. No fixed expiry is specified; shelf life after opening depends on the batch and storage conditions.
Section 07
Side Effects & Precautions
Generally well tolerated at doses up to 1200 mg/day in clinical trials. Mild side effects may include nausea, digestive discomfort, and headache. No serious adverse effects reported in published human trials.
Section 08
Regulatory Status
FDA / United States
Lawful supplement again since 2025
On 29 September 2025 FDA responded to a citizen petition and concluded NMN meets the definition of a dietary supplement after all, ending a dispute that ran since 2022.
2022 exclusion
A reversed drug-preclusion call
FDA had ruled NMN excluded from the supplement definition because Metro International Biotech studied it as an investigational drug (MIB-626) before it was marketed as a supplement; the agency reversed itself once it found evidence of NMN supplements on the US market as early as 2017.
European Union
Not yet authorised as a food
NMN is a Novel Food under EU law; EFSA gave a positive safety opinion in May 2026 for up to 300 mg a day as a niacin source, but the compound still has no entry on the EU's Novel Food list, so it cannot yet be lawfully sold there.
China
Banned from food and supplements
The National Health Commission has refused to approve NMN as a new food ingredient, cross-border e-commerce platforms have been barred from selling it since June 2021, and customs has issued repeated risk alerts against it since.
WADA
Not on the Prohibited List
NMN does not appear anywhere in WADA's 2026 Prohibited List, under S0, S2 or any other category.
Regulatory status differs by country and keeps changing fast — NMN swung from excluded to reinstated in the US within three years. Being sold online is not proof that a product is authorised where you live; check the current rules before buying or using it.
Section 09
Research Studies
- [1]Nicotinamide mononucleotide, a key NAD+ intermediate, treats the pathophysiology of diet- and age-induced diabetes in miceYoshino J, Mills KF, Yoon MJ, Imai S. · Cell Metabolism · 2011
- [2]Pathways and subcellular compartmentation of NAD biosynthesis in human cells: from entry of extracellular precursors to mitochondrial NAD generationNikiforov A, Dölle C, Niere M, Ziegler M. · Journal of Biological Chemistry · 2011
- [3]CD73 protein as a source of extracellular precursors for sustained NAD+ biosynthesis in FK866-treated tumor cellsGrozio A, Sociali G, Sturla L, et al. · Journal of Biological Chemistry · 2013
- [4]NRK1 controls nicotinamide mononucleotide and nicotinamide riboside metabolism in mammalian cellsRatajczak J, Joffraud M, Trammell SAJ, et al. · Nature Communications · 2016
- [5]Slc12a8 is a nicotinamide mononucleotide transporterGrozio A, Mills KF, Yoshino J, et al. · Nature Metabolism · 2019
- [6]Absence of evidence that Slc12a8 encodes a nicotinamide mononucleotide transporterSchmidt MS, Brenner C. · Nature Metabolism · 2019
- [7]Nicotinamide mononucleotide supplementation reverses vascular dysfunction and oxidative stress with aging in micede Picciotto NE, Gano LB, Johnson LC, et al. · Aging Cell · 2016
- [8]CD38 dictates age-related NAD decline and mitochondrial dysfunction through an SIRT3-dependent mechanismCamacho-Pereira J, Tarragó MG, Chini CCS, et al. · Cell Metabolism · 2016
- [9]Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in miceMills KF, Yoshida S, Stein LR, et al. · Cell Metabolism · 2016
- [10]Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic womenYoshino M, Yoshino J, Kayser BD, et al. · Science · 2021
- [11]Comment on "Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women"Brenner C. · Science · 2021
Section 10
Frequently Asked Questions
Blood NAD+ rises reliably across every dose tested, from 250 mg to 1250 mg daily. Functional results are thinner: a manufacturer-run 60-day trial found 600-900 mg improved 6-minute walk distance and self-rated health but 300 mg did not, and a 250 mg, 10-week trial in prediabetic women raised muscle insulin sensitivity about 25% while leaving glucose tolerance, weight and body composition unchanged. No independent group has replicated the walking-distance result.
NMN sits one enzymatic step closer to NAD+, converted directly by NMNAT enzymes, while nicotinamide riboside (NR) needs an extra phosphorylation by NRK1/2 first. How NMN actually gets into cells is contested, though: one line of evidence shows the enzyme CD73 dephosphorylates extracellular NMN back down to NR before uptake, meaning much of an NMN dose may act as NR anyway, while a proposed direct NMN transporter (SLC12A8) has been challenged in a formal published rebuttal.
Dose-ranging trials used 250-900 mg daily for 30-90 days; the highest dose formally tested for safety was 1250 mg once daily for 4 weeks in 31 adults. No trial has run past about 12 weeks, and no study has given NMN by injection or nasal spray in humans - every dosing figure above comes from swallowing it.
NMN is sold as a dietary supplement in most countries and is not approved as a drug anywhere. In the US the FDA's classification wavered after a 2022 move that would have excluded it from the supplement category on the grounds it was under investigation as a drug; that exclusion was lifted in 2025, after which it returned to being sold as a supplement.
No carcinogenicity study of NMN has been published, and none of the cited human trials reported a cancer signal - but none ran long enough, or was designed, to detect one either. CD38, the enzyme that degrades NMN in the body, rises with age, which is a metabolic detail rather than evidence either way on cancer risk.
It is kept in a cool, dry place away from light and is relatively stable at room temperature, though refrigeration is preferred for long-term storage. No fixed expiry after opening is specified; shelf life depends on the specific product and how it has been stored.
No - every human trial cited in NMN's own research record dosed it alone, including the ones that raised blood NAD+ and the ones that moved insulin sensitivity or walking distance. Pairing NMN with resveratrol is a research tradition from earlier mouse studies rather than something tested in these human trials.