5-amino-1MQ: benefits, dosage, side effects and what the research shows

5-amino-1MQ (5-amino-1-methylquinolinium) is a small organic molecule that inhibits nicotinamide N-methyltransferase, or NNMT, an enzyme found mainly in the liver and in fat tissue. It came out of a drug-discovery programme at the University of Texas Medical Branch, where researchers screened a series of methylquinolinium and related compounds and found that quinoliniums blocked NNMT at low micromolar concentrations ^[1]. A follow-up paper singled out 5-amino-1MQ as a membrane-permeable, selective inhibitor and tested it in obese mice ^[2].

Despite the name it is often sold under, 5-amino-1MQ is not a peptide. A peptide is a short chain of amino acids; 5-amino-1MQ is a single fused-ring molecule with a molecular weight of about 159 and contains no amino acids at all. The word “amino” in its name refers to an amine group attached to the ring, not to an amino acid.

It appears on PepFinder because the stores that sell research peptides also sell it, usually as capsules or as a powder in injectable vials, and because shoppers search for it as the “5-amino-1MQ peptide”. We list it so that buyers can compare prices and testing in the same place, and so that the evidence behind the marketing is set out plainly.

NNMT attaches a methyl group to nicotinamide, one form of vitamin B3, using S-adenosylmethionine (SAM) as the methyl donor. The product, 1-methylnicotinamide, is then broken down and excreted. For years this was seen as a simple clearance route for excess vitamin B3, but work since 2014 has linked NNMT to wider control of metabolism in fat and liver ^[10].

The key study was published in Nature in 2014. Researchers at Harvard found that NNMT was one of the genes most strongly switched on in the fat tissue of insulin-resistant mice, and that its expression rose in the fat and liver of obese and diabetic mice. Knocking NNMT down in fat and liver protected mice from diet-induced obesity by raising energy expenditure. Blocking NNMT increased levels of SAM and NAD+ in fat tissue and speeded up a cycle of polyamine production and breakdown that burns energy ^[3]. Nicotinamide is a building block for NAD+, so an enzyme that uses up nicotinamide competes with NAD+ production.

As a 5-amino-1MQ NNMT inhibitor, the compound binds the site on the enzyme where nicotinamide normally sits ^[1]. In fat cells grown in the laboratory it lowered 1-methylnicotinamide, raised NAD+ and SAM inside the cells, and suppressed fat production. It did not inhibit related methyltransferase enzymes or the enzymes of the NAD+ salvage pathway that were tested ^[2]. The researchers proposed that more NAD+ and SAM, the cell’s key energy and methyl-group carriers, explains its effects. That proposal comes from cell and mouse data and has not been tested in people.

There is some human evidence that NNMT itself matters in metabolism. In a German study of 199 surgical patients, NNMT expression in fat tissue was about twice as high in people with type 2 diabetes as in controls and tracked insulin resistance, and it fell after an exercise programme or bariatric surgery ^[11]. This is an association between the enzyme and disease. It does not show that blocking the enzyme with a drug helps people.

Searches for what 5-amino-1MQ does usually lead to the same short list of claims: fat loss, better blood sugar control, stronger muscles in old age, and “more NAD+”. Each traces back to a handful of mouse studies, most of them from one research group and its spin-out company, Ridgeline Therapeutics, whose founder and employees are named as authors and declare that interest ^[5][8][9]. The sections below take each area in turn and give the species, dose and route used.

No study has tested 5-amino-1MQ in people. That means there is no human evidence on any of the 5-amino-1MQ benefits described below, on how quickly anything happens, or on its side effects.

The first animal test was short. Mice made obese on a high-fat diet received 5-amino-1MQ by injection under the skin three times a day for 11 days. Treated mice lost weight progressively, their main abdominal fat pad was about 35% lighter than in untreated obese mice, fat cells were more than 30% smaller, and total cholesterol was about 30% lower. Food intake did not differ significantly between groups, and the authors reported no observable adverse effects ^[2].

A 2021 study combined the inhibitor with a switch from a Western-style diet to a lean diet. Mice given both lost weight and fat faster than mice given the diet change alone, and their body composition and liver fat returned to the levels of mice that had never been obese ^[5]. A companion analysis found that this combination produced a distinct gut bacteria profile ^[6]. In both papers the comparison was with the diet change alone, so what the inhibitor contributed is the extra effect on top of a better diet.

The largest mouse study, published in 2024, gave obese mice 5-amino-1MQ once a day for 28 days at two doses while they stayed on a high-fat diet. The compound limited further weight and fat gain rather than causing weight loss: by the end, control mice had gained 4.7 g of fat and high-dose mice 1.3 g. The high dose also improved glucose tolerance and insulin sensitivity, reduced liver fat and liver weight, and brought liver enzymes back towards normal, again without changing food intake ^[8].

Taken together, 5-amino-1MQ weight loss in mice was modest on its own and larger when paired with a diet change. None of these results has been shown in people, and mouse obesity models respond to many compounds that later fail or cause problems in human trials. Approved weight-loss medicines such as semaglutide reached the market only after large human trials, which is the stage 5-amino-1MQ has not begun.

NNMT is also more active in ageing muscle, and the same group tested whether blocking it helps old muscle repair. In 24-month-old mice with an injected muscle injury, 5-amino-1MQ at 5 or 10 mg/kg increased muscle stem cell activity, produced muscle fibres nearly twice the cross-sectional area of untreated controls, and increased the injured muscle’s peak force by about 70% ^[4].

A 2024 study treated 22-month-old female mice with 5-amino-1MQ, a weighted running-wheel programme, or both, for eight weeks. Sedentary mice given the compound had about 40% greater grip strength than sedentary controls, exercised mice had about 20% greater grip strength, and mice given both had about 60% greater grip strength ^[9]. The authors described the compound as mimicking and adding to the effects of exercise on muscle in old mice. This is the basis for comparisons with so-called exercise mimetics such as SLU-PP-332, which works by a different mechanism.

Other groups have tested NNMT inhibitors in aged mice and a model of poor blood flow to the legs, reporting better grip strength or muscle strength ^[17][18]. Those papers describe their compound as an “NNMT inhibitor” rather than naming it in the abstract, so they support the NNMT idea rather than 5-amino-1MQ specifically.

Beyond weight, the 2024 obese-mouse study reported a 73% reduction in one type of liver fat build-up and less inflammatory cell infiltration in the liver at the higher dose ^[8]. A 2026 study in human kidney biopsies and mice linked NNMT to ageing of kidney tubule cells and scarring, and found that selective NNMT inhibition protected senescent kidney cells, kidney organoids and mice ^[13].

In a laboratory study, 5-amino-1MQ slowed the growth of HeLa cervical cancer cells without apparently affecting a non-cancer human kidney cell line ^[12]. A result in a cell dish at chosen concentrations says nothing about cancer prevention or treatment in people.

No. A search of ClinicalTrials.gov on 24 September 2026 for “5-amino-1MQ”, “5-amino-1-methylquinolinium” and “NNMT inhibitor” returned no registered studies ^[14]. We also found no human study of the compound in PubMed. Every figure on this page comes from mice, rats or cells.

People searching “clinicaltrials.gov 5-amino-1MQ” are often checking claims made on product pages. If a seller says the compound is “clinically proven” or “tested in humans”, ask for the trial registration number. We could not find one. Our methodology page explains how we treat claims we cannot verify.

Because there are no human trials, there is no controlled answer to how long 5-amino-1MQ takes to work or what results to expect. In mice, weight and fat changes were measured over 11 to 28 days ^[2][8], and muscle effects over one to eight weeks ^[4][9].

5-amino-1MQ before and after photos, forum threads and Reddit reports cannot fill that gap. They are uncontrolled, the product’s identity and strength are rarely tested, and people usually change diet, training or other drugs at the same time. The diet-switch mouse study is a reminder that diet alone produces a large part of the change ^[5]. Whether 5-amino-1MQ does work in people is an open question.

Almost all of the efficacy research used injections under the skin (subcutaneous) ^[2][8][9]. Sellers offer both 5-amino-1MQ capsules and powder for 5-amino-1MQ injection, and the difference matters because the two routes behave very differently in the published pharmacokinetic studies.

In rats, a study that developed a blood test for the compound gave it intravenously and by mouth and reported an oral bioavailability of 38.4%, with an elimination half-life of about 3.8 hours after intravenous dosing and 6.9 hours after oral dosing ^[7]. In mice, the 2024 study found the opposite picture: after an oral dose of 30 mg/kg, blood levels peaked at only 14.5 ng/mL after four hours, and oral bioavailability was 3.5%. Subcutaneous dosing gave high blood levels and good distribution to fat, muscle and liver ^[8]. The authors linked the poor oral uptake to slow and limited absorption from the gut rather than poor solubility, since the compound dissolves readily in water.

So on 5-amino-1MQ oral vs injection, the only direct comparisons are in rodents, the two species disagreed on how well oral doses were absorbed, and neither tells us about people. There are no published data on 5-amino-1MQ tablets or capsules in humans. The effect studies that produced the headline findings used injection.

All published doses are from rodents, given by injection unless stated. In the first obesity study, mice received 20 mg/kg three times a day under the skin for 11 days, which the authors calculated as about 34 mg/kg per day of the parent compound ^[2]. In the 2024 obesity study, mice received 10 or 32 mg/kg once daily under the skin for 28 days, and only the higher dose clearly reduced liver fat ^[8]. The muscle-injury study used 5 or 10 mg/kg ^[4], and the eight-week ageing study used 10 mg/kg once daily under the skin ^[9]. Pharmacokinetic studies used single doses of 5 mg/kg intravenously, 25 mg/kg under the skin and 30 mg/kg by mouth in mice ^[8].

No human 5-amino-1MQ dosage has been established, because no human study exists. Animal doses in mg/kg should not be converted into human doses, and PepFinder does not recommend any dose, per day or per injection. Online 5-amino-1MQ dosage charts, subcutaneous dosing protocols and per-day capsule schedules are not based on human research.

Questions about reconstitution are arithmetic rather than dosing. A 50 mg vial dissolved in 2.5 mL of liquid contains 20 mg per mL, and on a U-100 insulin syringe (100 units per mL) each unit then holds 0.2 mg. A 10 mg vial in 1 mL gives 10 mg per mL, or 0.1 mg per unit. A 5-amino-1MQ dosage calculator does the same sum for any vial size and volume, and our guide to bacteriostatic water covers the diluent usually supplied.

There are no human safety data, so the honest answer on 5-amino-1MQ side effects is that nobody knows what they are in people. The animal reports are short and small. The 11-day mouse study reported no observable adverse effects and no change in food intake ^[2]. The 28-day study reported normalised liver enzymes, but also found that the high dose lowered total white blood cell count, with lymphocytes down 31% and monocytes down 50% compared with controls ^[8]. The authors did not discuss this as harm, and its meaning is unclear, but it is the kind of signal a formal safety programme would examine.

The broader biology gives reasons for caution. NNMT sits at the junction of vitamin B3 handling and the body’s main methyl-donor supply ^[3][10], and in the tissues where it is high, blocking it changes SAM, NAD+ and histone methylation. Effects of long-term inhibition on these systems in people are unknown. The only toxicity data are from mice and rats over weeks, and none of the studies was a formal toxicology study of the kind regulators require before first human use.

The main practical risks are the ones common to any unlicensed product: wrong identity, wrong amount, contamination and, for injectables, sterility and endotoxin. Our guides to third-party peptide testing and how to read a COA explain what a lab report can confirm. Because 5-amino-1MQ is a small molecule rather than a peptide, a COA should show a purity method suited to small molecules and a mass matching about 159 for the cation.

Stacking 5-amino-1MQ with NAD+ or NAD+ precursors is often promoted on the idea that one raises NAD+ supply while the other stops nicotinamide being diverted away from it. The first half of that idea has some cell and mouse support: 5-amino-1MQ raised NAD+ inside fat cells ^[2], and raising NAD+ in old or diseased animals has improved several health measures ^[15].

No study has tested 5-amino-1MQ together with NAD+, nicotinamide riboside, NMN or any other precursor, in animals or people. There is no evidence that the combination works better, and no basis for combined doses.

MOTS-c is a real peptide, 16 amino acids long, encoded in mitochondrial DNA. In mice it prevented diet-induced obesity and insulin resistance through a different pathway, activating the energy sensor AMPK ^[16]. It is often sold next to 5-amino-1MQ because both are marketed for metabolism.

The two have never been compared or combined in a published study. Their proposed mechanisms differ, one blocking an enzyme and the other acting as a signalling peptide, and neither has published human efficacy data. Claims that they work well together are not based on research.

The half-life of 5-amino-1MQ in people is unknown. In rats the elimination half-life was about 3.8 hours after intravenous and 6.9 hours after oral dosing ^[7]; in mice it was about 14.8 hours after an oral dose, which reflected slow absorption ^[8], and a pharmacokinetic study summarised in the 2024 ageing paper reported a half-life of around 7 hours after subcutaneous dosing, with no build-up after repeat doses ^[9].

Rat plasma samples of the compound were stable under standard storage and handling conditions in the laboratory ^[7]. For vials and capsules, the usual practice is to keep them cool, dry and away from light, and to refrigerate a vial once it has been mixed. See how to store peptides; the same principles apply to small molecules sold alongside them.

5-amino-1MQ is not an approved medicine in the UK, US, EU, Canada, Australia or New Zealand, and no company has registered a human trial of it ^[14]. We did not find a regulator statement that names it specifically. How each country treats unapproved substances sold as “research chemicals” is covered on our legal status pages, including the UK and Australia.

We have not confirmed whether 5-amino-1MQ is named on the World Anti-Doping Agency Prohibited List. Tested athletes should check with their national anti-doping organisation before using any unapproved substance.

PepFinder does not sell 5-amino-1MQ. You can compare 5-amino-1MQ prices across research suppliers, including 5-amino-1MQ UK suppliers and 5-amino-1MQ prices in Australia, where imported unapproved products are regulated. The most searched sizes are 50 mg and 10 mg vials, alongside capsule packs.

Look for batch-specific third-party results rather than a generic certificate, and see which vendors use third-party tested batches. Our guide on how to spot a fake peptide supplier lists the warning signs, and our news page covers regulator actions as they happen.