NAD+ vs 5-Amino-1MQ
NAD+ is the coenzyme itself, while 5-Amino-1MQ is a small molecule that blocks NNMT, an enzyme that diverts nicotinamide, an NAD+ building block, away from the NAD+ salvage pathway. One adds to the NAD+ pool; the other is studied for slowing a drain on it, with most of its research in fat tissue and obesity models. Neither is a peptide. Here is how they compare, what the research on each shows, and where the human evidence stands.
Findings
- NNMT methylates nicotinamide using SAM as the methyl donor; knocking it down in fat and liver protected mice against diet-induced obesity by raising energy expenditure, with higher adipose SAM and NAD+ (2014).
- 5-Amino-1MQ is a membrane-permeable methylquinolinium NNMT inhibitor. In adipocytes it raised intracellular NAD+ and SAM and suppressed fat formation (2018).
- In diet-induced obese mice, 11 days of 5-amino-1MQ reduced body weight and white fat mass, shrank fat cells by more than 30% and lowered cholesterol by about 30%, with no change in food intake (2018).
- NAD+ has human data, mostly through precursors: nicotinamide riboside raised blood-cell NAD+ by about 60% over placebo in a randomised crossover trial in adults aged 55 to 79 (2018).
What is NAD+?
Nicotinamide adenine dinucleotide is a coenzyme for redox reactions and an essential cofactor for sirtuins, CD38 and poly(ADP-ribose) polymerases, linking it to energy metabolism, DNA repair, chromatin remodelling and senescence. Tissue and cellular NAD+ declines gradually with age in rodents and in humans (Covarrubias et al., Nat Rev Mol Cell Biol, 2021). Cells keep their supply up largely by recycling nicotinamide, which the NAD+-consuming enzymes release, back into NAD+ through the salvage pathway. That recycling step is where NNMT, and so 5-Amino-1MQ, comes in. More background is in NAD+ Is Not a Peptide.
The human research
In a 2 × 6-week randomised, double-blind, placebo-controlled crossover trial, 30 healthy adults aged 55 to 79 were randomised and 24 completed. Nicotinamide riboside was well tolerated and raised NAD+ in peripheral blood mononuclear cells by about 60% compared with placebo (Martens et al., Nat Commun, 2018). A 10-week randomised, double-blind trial of nicotinamide mononucleotide in postmenopausal women with prediabetes and overweight or obesity increased muscle insulin sensitivity, insulin signalling and remodelling, with no change on placebo (Yoshino et al., Science, 2021). NAD+ itself was given by 6-hour intravenous infusion to 8 healthy men in a 2019 pilot; plasma NAD+ did not rise for the first 2 hours as it was cleared, then reached about 400% of baseline by 6 hours (Grant et al., Front Aging Neurosci, 2019). See NAD+ Restoration: What the Research Shows.
What is 5-Amino-1MQ?
5-Amino-1MQ (5-amino-1-methylquinolinium) is a small aromatic molecule from a series of NNMT inhibitors developed at the University of Texas Medical Branch. Its target, nicotinamide N-methyltransferase, attaches a methyl group from S-adenosylmethionine (SAM) to nicotinamide, producing 1-methylnicotinamide. That reaction uses up both nicotinamide, the NAD+ precursor, and SAM, the cell’s main methyl donor (Kraus et al., Nature, 2014). The compound’s background is in 5-Amino-1MQ: What the NNMT Research Actually Covers.
Why NNMT became a target
In 2014, NNMT emerged as the gene most strongly regulated in fat tissue of mice engineered to lack or overexpress the Glut4 glucose transporter. NNMT expression was raised in fat and liver of obese and diabetic mice, and knocking it down protected against diet-induced obesity by increasing energy expenditure, with higher SAM and NAD+ in fat tissue (Kraus et al., 2014). In people, NNMT expression in white fat and plasma 1-methylnicotinamide tracked insulin resistance across a surgical cohort of 199 patients, and both exercise and bariatric surgery reduced fat-tissue NNMT (Kannt et al., Diabetologia, 2015).
The 5-Amino-1MQ studies
In the 2018 study that characterised it, 5-amino-1MQ crossed membranes readily, did not inhibit related methyltransferases or the NAD+ salvage enzymes, and in cultured fat cells lowered 1-methylnicotinamide, raised NAD+ and SAM, and suppressed lipogenesis. Diet-induced obese mice treated for 11 days lost body weight and white fat mass progressively; adipocyte size fell by more than 30% and total cholesterol by about 30%, while food intake was unchanged and no adverse effects were observed (Neelakantan et al., Biochem Pharmacol, 2018).
The same group then turned to ageing muscle. In 24-month-old mice with an injured leg muscle, 5-amino-1MQ increased muscle stem cell activity, produced nearly 2-fold larger regenerating fibres and raised peak torque by about 70% (Neelakantan et al., Biochem Pharmacol, 2019). In mice given 5-amino-1MQ from 22 to 24 months of age, grip strength was about 40% higher than in sedentary controls, and combined with exercise the gain reached 60% (Dimet-Wiley et al., Sci Rep, 2024). No human trial of 5-Amino-1MQ has been published.
How do NAD+ and 5-Amino-1MQ compare side by side?
| Question | NAD+ | 5-Amino-1MQ |
|---|---|---|
| What is it? | Dinucleotide coenzyme | Small-molecule methylquinolinium |
| Is it a peptide? | No | No |
| Main research area | Energy metabolism, ageing, sirtuin and PARP biology | Obesity, fat tissue, aged muscle repair |
| Mechanism | Is the cofactor; consumed by sirtuins, PARPs, CD38 | Blocks NNMT, sparing nicotinamide and SAM |
| Human evidence | Precursor RCTs; one IV NAD+ pilot | None published; human NNMT data are observational |
| Forms we supply | 500 mg vial; nasal spray (250 mg and 500 mg) | 50 mg vial |
Is 5-Amino-1MQ an NAD+ booster?
Partly, and locally. In fat cells, blocking NNMT raised intracellular NAD+ along with SAM (Neelakantan et al., 2018), and knocking NNMT down raised adipose NAD+ in mice (Kraus et al., 2014). The authors proposed that more NAD+ and SAM flux may explain the effect, but the 2014 work also tied NNMT to histone methylation and polyamine flux, so NAD+ is one of several pathways involved. Supplying NAD+ adds to the pool everywhere it reaches; 5-Amino-1MQ conserves it where NNMT is active, which in the research means fat, liver and aged muscle.
Which one fits which research question?
- NAD+ levels, sirtuin and PARP activity, and age-related NAD+ decline: NAD+, which has the human pharmacology and precursor trial record.
- Fat-cell metabolism, diet-induced obesity models and methyl-donor (SAM) balance: 5-Amino-1MQ, the NNMT-specific tool.
- Aged muscle regeneration and strength: 5-Amino-1MQ has the aged-mouse studies; NAD+ precursors have human muscle insulin-sensitivity data.
Can NAD+ and 5-Amino-1MQ be studied together?
Yes, and the pairing has a clear rationale: one supplies the cofactor and the other reduces a route by which its precursor is lost. A design using both can separate the effect of adding NAD+ from that of sparing nicotinamide and SAM. That rationale comes from each compound’s own literature; we found no published study of the combination. For a different pairing see 5-Amino-1MQ vs MOTS-c and NAD+ vs MOTS-c.
How are NAD+ and 5-Amino-1MQ supplied?
NAD+ comes as a 500 mg lyophilised vial and as a ready-mixed NAD+ Nasal Spray (0.175 mL per press) in 250 mg and 500 mg bottles; the NAD+ spray is also part of the Cognitive Clarity Spray Stack. 5-Amino-1MQ comes as a 50 mg lyophilised vial. Vials are reconstituted with bacteriostatic water: see the NAD+ reconstitution guide and the 5-Amino-1MQ reconstitution guide. Certificates of analysis are on the lab reports page, and every order ships from within Canada by Canada Post Xpresspost.
NAD+ and 5-Amino-1MQ are supplied for laboratory research use only. The 5-Amino-1MQ studies above were done in cells and mice; the NAD+ human studies used pharmaceutical or supplement-grade preparations.
Frequently asked questions
What is the difference between NAD+ and 5-Amino-1MQ?
NAD+ is the coenzyme used in energy metabolism and by sirtuins and PARP enzymes. 5-Amino-1MQ is a small molecule that inhibits NNMT, an enzyme that uses up nicotinamide, an NAD+ precursor, and SAM, the main methyl donor. Neither is a peptide.
Does 5-Amino-1MQ increase NAD+?
In cultured fat cells, 5-amino-1MQ raised intracellular NAD+ and SAM (2018), and NNMT knockdown raised adipose NAD+ in mice (2014). It has not been shown to raise NAD+ in people, as no human trial has been published.
Is 5-Amino-1MQ a peptide?
No. It is a methylquinolinium, a small aromatic molecule. NAD+ is not a peptide either; it is a dinucleotide coenzyme.
Can NAD+ and 5-Amino-1MQ be studied together?
Yes. One supplies the cofactor and the other reduces the loss of its precursor through NNMT, so a design using both can separate those two effects. No published study has tested the combination.
Where can I buy NAD+ and 5-Amino-1MQ in Canada?
Vistara Labs supplies NAD+ as a 500 mg vial and a ready-mixed nasal spray, and 5-Amino-1MQ as a 50 mg vial, shipped from within Canada by Canada Post Xpresspost.
Product details from vistaralabs.ca, October 2026. Sources: Covarrubias AJ et al. NAD+ metabolism and its roles in cellular processes during ageing. Nat Rev Mol Cell Biol. 2021. PMID 33353981. Martens CR et al. Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults. Nat Commun. 2018. PMID 29599478. Yoshino M et al. Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. Science. 2021. PMID 33888596. Grant 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. PMID 31572171. Kraus D et al. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature. 2014. PMID 24717514. Kannt A et al. Association of nicotinamide-N-methyltransferase mRNA expression in human adipose tissue and the plasma concentration of its product, 1-methylnicotinamide, with insulin resistance. Diabetologia. 2015. PMID 25596852. Neelakantan H et al. Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochem Pharmacol. 2018. PMID 29155147. Neelakantan H et al. Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. Biochem Pharmacol. 2019. PMID 30753815. Dimet-Wiley AL et al. Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice. Sci Rep. 2024. PMID 38969654.
More on this: Weight Loss & Metabolism Research.
All products supplied by Vistara Labs are intended for laboratory research use only. They are not drugs, are not approved for human or veterinary use, and are not intended to diagnose, treat, cure or prevent any condition. Nothing on this page constitutes medical advice or guidance for use in humans.
