5-Amino-1MQ: not a peptide, and so far only tested in mice
A small molecule that blocks the enzyme NNMT cut fat in obese mice and strengthened old mouse muscle, but nobody has published a single study in humans.

5-Amino-1MQ is not a peptide. It's a small synthetic molecule that blocks an enzyme called NNMT. In obese mice it reduced body weight and fat without cutting food intake [4,8], and in old mice it improved muscle repair and grip strength [5,7]. We could find no published human study of any kind: no safety trial, no dosing study, no case series.
What it is
The name is shorthand for 5-amino-1-methylquinolinium. Chemically it is a quinoline ring, a two-ring structure common in drug chemistry, with a methyl group and an amino group attached [3]. There is no amino-acid sequence, which is why it has none on its HPR profile page. It appears on peptide lists mainly because the same online shops sell it.
It was designed by a research group at the University of Texas Medical Branch, who screened a series of quinolinium compounds for their ability to block NNMT and found this family worked at around 1 micromolar in the test tube [3]. The same Texas group wrote nearly all of the published papers on it; some of the later ones list a company, Ridgeline Therapeutics, among the authors' affiliations [8].
What NNMT does
Nicotinamide N-methyltransferase (NNMT) is an enzyme found mostly in the liver and fat tissue. It takes nicotinamide, a form of vitamin B3 that the body uses to make NAD+, and attaches a methyl group, producing a waste product called 1-methylnicotinamide (1-MNA) that is excreted [1].
In 2014, researchers found that NNMT was raised in the fat and liver of obese and diabetic mice, and that switching the gene down in those tissues protected the mice against diet-induced obesity by increasing energy expenditure [1]. Their proposed explanation was that blocking NNMT leaves more nicotinamide available for NAD+ and more methyl donors for other jobs, which shifts cells towards burning energy [1]. That is mechanism theory, based on mouse and cell work.
There is a human link, but only an association. A 2015 study of 199 surgical patients found roughly twice as much NNMT gene expression in the fat of people with type 2 diabetes as in controls, and higher NNMT tracked with worse insulin sensitivity [2]. In the same paper, exercise and bariatric surgery both lowered NNMT in fat [2]. That shows NNMT goes up with insulin resistance in people. It does not show that blocking it helps.
The human evidence
There is none. We searched PubMed and ClinicalTrials.gov and found no published human study of 5-amino-1MQ and no registered trial. Everything below comes from mice or cells.
That matters more than usual here, because 5-amino-1MQ is not an adapted version of a hormone people already make. It's a new chemical. How it is absorbed, where it goes, how long it stays and what it does to other organs in people are all unknown.
What the animal and lab work suggests
All of these findings are in mice or in cultured cells.
In fat cells in a dish. 5-amino-1MQ lowered 1-MNA, raised NAD+ and cut fat production in mouse fat cells, by 50% at 30 µM and 70% at 60 µM [4]. It did not block several related enzymes, suggesting it is selective for NNMT [4].
In obese mice. The 2018 study above was small and short: nine mice per group for 11 days [4]. A 2024 study by the same group gave daily 5-amino-1MQ to diet-induced obese mice for 28 days and reported dose-dependent limits on weight and fat gain, better glucose tolerance and insulin sensitivity, and less fatty liver [8]. It also found the drug reached fat, muscle and liver after injection under the skin in mice [8].
Combined with diet. In obese mice switched to a lean diet, adding an NNMT inhibitor sped up fat loss and brought body composition and liver fat back to levels seen in mice that had never been fattened [6].
In ageing muscle. In 24-month-old mice with an injured leg muscle, twice-daily injections improved muscle stem cell activity, produced nearly twofold larger repaired muscle fibres and raised peak muscle force by about 70% compared with controls [5]. A 2024 study in 22-month-old female mice found about 40% greater grip strength with 5-amino-1MQ alone, 20% with exercise alone and 60% with both [7].
A caution from the genetic studies. Not every mouse study of NNMT agrees. A 2019 study in male mice bred without the NNMT gene found better insulin sensitivity on a high-fat diet but no change in glucose tolerance [9]. That doesn't undermine the drug studies, but it shows the effects of losing NNMT are more mixed than the headline papers suggest.
The muscle studies are small. The 2019 injury study used 10 to 13 mice per group given 5 or 10 mg/kg twice a day [5]. The 2024 exercise study used 35 female mice split across four groups, treated once daily at 10 mg/kg for eight weeks [7]. Those are respectable numbers for mouse work, but they are the kind of results that often shrink or vanish when someone else repeats them.
| Study | Model | What changed |
|---|---|---|
| Neelakantan 2018 [4] | Obese mice, 11 days | Less weight and white fat, lower cholesterol |
| Neelakantan 2019 [5] | 24-month-old mice with muscle injury | Better muscle repair, about 70% more force |
| Sampson 2021 [6] | Obese mice on a lean diet | Faster fat loss, normalised liver fat |
| Dimet-Wiley 2024 [7] | 22-month-old female mice | Grip strength up about 40% alone, 60% with exercise |
| Babula 2024 [8] | Obese mice, 28 days | Less weight and fat gain, better insulin sensitivity, less fatty liver |
How much weight to put on this
Three features of this evidence should make anyone cautious. First, almost all the positive studies come from one research group and its associated company [4–8], and we found no independent replication of the headline fat-loss or muscle results with 5-amino-1MQ. Second, the doses were given by injection in milligrams per kilogram of mouse, and mouse doses don't convert to human doses by simple scaling. Third, several of the studies used only males or only females [7,9], so we don't know whether the effects hold in both sexes.
None of that means the idea is wrong. NNMT is a plausible target, and the human association with insulin resistance is real [2]. It means the drug sits at the stage where a pharmaceutical company would normally start formal toxicology and a first-in-human safety trial, and that hasn't happened in public.
Safety and side effects
In humans, nothing is known. No human safety data have been published.
In mice, the authors reported no observable adverse effects at the doses used [4], and a small dose-escalation step in two mice tolerated up to 60 mg/kg a day [4]. Short mouse studies, typically days to weeks with a handful of animals per group, are not designed to find rare or slow-developing harms, and they cannot rule out problems in people.
There is also a theoretical question the mouse papers do not answer. NNMT is one of the routes the body uses to clear excess nicotinamide and to manage its supply of methyl groups [1]. What happens to those systems when the enzyme is blocked for months, in a human liver, is untested.
Legal and regulatory status
| Where | Status |
|---|---|
| US | Not an FDA-approved drug and not tested in any registered clinical trial. |
| UK | Not a licensed medicine. |
| Sport | Not named on the 2026 WADA Prohibited List [10]. The list's catch-all S0 section bans substances with no regulatory approval for human therapeutic use, so athletes should treat it as off-limits. |
Because it is sold as a research chemical, there is no pharmaceutical standard for what a given product contains.
What we still don’t know
- Whether 5-amino-1MQ is absorbed, distributed and cleared in people the way it is in mice [8].
- Whether it changes weight, fat or muscle in humans at all.
- What a safe dose would be, if there is one. No human dose has ever been tested.
- What long-term NNMT blockade does to the liver and to methyl-group balance [1].
- Whether raised NNMT in people with diabetes is a cause of insulin resistance or just a marker of it [2].
Educational content only — not medical advice. Many peptides discussed on HPR are not approved for human use. Talk to a qualified clinician before making any decision about your health.

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References
- [1]Kraus D, Yang Q, Kong D, et al.. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature 2014. doi:10.1038/nature13198
- [2]Kannt A, Pfenninger A, Teichert L, 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. doi:10.1007/s00125-014-3490-7
- [3]Neelakantan H, Wang HY, Vance V, et al.. Structure-activity relationship for small molecule inhibitors of nicotinamide N-methyltransferase. J Med Chem 2017. doi:10.1021/acs.jmedchem.7b00389
- [4]Neelakantan H, Vance V, Wetzel MD, et al.. Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochem Pharmacol 2018. doi:10.1016/j.bcp.2017.11.007
- [5]Neelakantan H, Brightwell CR, Graber TG, et al.. Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. Biochem Pharmacol 2019. doi:10.1016/j.bcp.2019.02.008
- [6]Sampson CM, Dimet AL, Neelakantan H, et al.. Combined nicotinamide N-methyltransferase inhibition and reduced-calorie diet normalizes body composition and enhances metabolic benefits in obese mice. Sci Rep 2021. doi:10.1038/s41598-021-85051-6
- [7]Dimet-Wiley AL, Latham CM, Brightwell CR, et al.. Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice. Sci Rep 2024. doi:10.1038/s41598-024-66034-9
- [8]Babula JJ, Bui D, Stevenson HL, et al.. Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction. Diabetes Obes Metab 2024. doi:10.1111/dom.15879
- [9]Brachs S, Polack J, Brachs M, et al.. Genetic nicotinamide N-methyltransferase (Nnmt) deficiency in male mice improves insulin sensitivity in diet-induced obesity but does not affect glucose tolerance. Diabetes 2019. doi:10.2337/db18-0780
- [10]World Anti-Doping Agency. The 2026 Prohibited List. WADA 2026. www.wada-ama.org/en/prohibited-list
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