
Weight and fat mass in obese mice
Daily 5A1MQ for 28 days limited body weight and fat gain in diet-induced obese mice.4

5-amino-1-methylquinolinium, 5A1MQ, NNMT inhibitor
Obese mice given 5-Amino-1MQ lost fat without eating less. It sits on peptide menus, yet it contains no amino acids at all.
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5-Amino-1MQ is a small molecule, not a peptide, that blocks NNMT, an enzyme fat cells use to dispose of vitamin B3 and methyl groups. Blocking it raised NAD+ and SAM, two key energy and methylation molecules, in fat cells. In obese mice it limited weight and fat gain and improved insulin sensitivity and fatty liver. No human trials have been published.
Medically reviewed by Robert Lufkin, MD (opens in a new tab)
Chief Medical Officer, Vitals Vault · Updated · 9 sources
It blocks one enzyme in fat cells that is linked to obesity in mice.
In cell tests, the compound got inside cells and blocked that one enzyme without hitting similar ones.1
In fat cells, blocking it raised two chemicals that help run the cell’s energy and settings.1
Treated fat cells made less new fat, and treated obese mice carried smaller fat cells.1
All of the supporting data are from cells and mice, some of it from the company developing the compound.
In fat cells, blocking the enzyme raised two energy chemicals, and treated cells made less new fat.1
Shows a mechanism
In 28 days, obese mice gained less weight and fat, with better insulin sensitivity and less liver fat.4
Shows an effect in a body
No human efficacy or safety trials have been published. The compound has not been given to people.5
Shows it works in people
The University of Texas group behind the original compounds has published several mouse studies. A 2024 paper from Ridgeline Therapeutics, a company founded by one of the authors, reported benefits for body composition and liver health in obese mice. The authors disclosed that relationship. Independent confirmation, and any human data, are still missing.145
The full guide to 5-Amino-1MQ
In a paper published in early 2018, a team in Galveston, Texas, gave obese mice on a high-fat diet a small molecule that blocks a single enzyme. The mice ate the same total amount of food as untreated mice. They still lost weight. Their white fat stores shrank, their fat cells got smaller and their blood cholesterol fell, with no observable side effects.
That family of molecules produced 5-Amino-1MQ, short for 5-amino-1-methylquinolinium. It is often sold and discussed alongside peptides, but it belongs to a different class. Peptides are chains of amino acids. 5-Amino-1MQ contains none. It is a small ring-shaped compound, much closer to an ordinary pill drug than to BPC-157 or semaglutide.
The distinction matters for more than accuracy. Small molecules and peptides are generally made, absorbed, cleared and tested differently, so what you know about one class tells you little about the other. To understand 5-Amino-1MQ, start with the enzyme it blocks and with a discovery about that enzyme in a Boston lab.13
NNMT, nicotinamide N-methyltransferase, does a simple chemical job. It attaches a methyl group to nicotinamide, a form of vitamin B3. The methyl group comes from SAM, S-adenosylmethionine, the main methyl donor inside cells. The product, 1-methylnicotinamide, is mainly how the body clears surplus vitamin, though it has some biological activity of its own.
In 2014, researchers at Beth Israel Deaconess Medical Center and Harvard Medical School went looking for genes that track insulin action in fat. They compared fat from mice engineered to lack or overproduce Glut4, the transporter that lets insulin move glucose into fat cells. Of all the genes they examined, Nnmt moved most strongly in the opposite direction to Glut4.
NNMT levels were higher in the fat and liver of obese and diabetic mice. When the team knocked the enzyme down in fat and liver, mice on a fattening diet were protected from obesity, because their cells burned more energy. Their fat held more SAM and more NAD+, and a fuel-burning cycle involving molecules called polyamines sped up. The paper, published in Nature, turned a vitamin-clearing enzyme into a drug target.6
Think of NNMT as a drain in the cell’s chemistry. Each time it works, it pours away one methyl group from SAM and one molecule of nicotinamide that could have been recycled into NAD+, the coenzyme cells use to turn food into energy. In the fat of obese and diabetic mice, that drain runs faster than normal.
5-Amino-1MQ plugs the drain. In cultured fat cells, methylquinolinium inhibitors lowered 1-methylnicotinamide and raised both NAD+ and SAM, and the cells made less new fat. The compounds crossed cell membranes well and did not block related methyl-transferring enzymes or the enzymes that recycle NAD+, which is what good selectivity looks like at this stage.
Why would more NAD+ and SAM change body fat? The Harvard work offers one route. Higher SAM changed histone methylation, a chemical mark on the proteins that package DNA, and that switched on the enzymes driving the polyamine cycle, which spends energy. More NAD+ also feeds SIRT1, a sensor that links a cell’s energy state to its genes. The result, in mice, was fat cells that spent more fuel.
That makes 5-Amino-1MQ a different strategy from the NAD+ precursor supplements many people already take. Those add raw material, such as forms of vitamin B3, to the top of the pipeline. An NNMT inhibitor tries to stop raw material leaking out of it, and in the mouse work it raised SAM at the same time, which precursors do not aim to do.
This is a mechanism worked out in mice and cell dishes, and it is a neat one. It also shows that blocking NNMT reaches into gene regulation inside fat tissue, which is exactly why long-term effects deserve careful study before anyone calls the compound benign.61
The most detailed study came in 2024. Diet-induced obese mice received 5-Amino-1MQ once a day for 28 days. Higher doses limited weight and fat gain more, a dose-dependent pattern that strengthens the case. Glucose tolerance and insulin sensitivity improved, and abnormally high insulin levels came down.
The liver results stood out. Treated mice had less liver fat, fewer inflammatory immune cells in the liver, smaller and lighter livers, and lower liver triglycerides. ALT and AST, the two liver enzymes doctors use as a first check on liver stress, returned to normal. After injection under the skin, the compound reached fat, muscle and liver in high amounts.
A 2022 study tested something closer to real life. Obese mice were switched from a Western diet to a low-fat diet, with or without the inhibitor. The diet change alone did not restore lean body composition in the study period. With the inhibitor added, weight and fat quickly returned to the levels of lean mice of the same age, and the treated mice developed a distinct gut microbiome.
Two cautions sit beside these results. They are all in mice. And the 2022 and 2024 papers come from Ridgeline Therapeutics, a company founded by one of the authors, a relationship the authors disclosed. The cited studies of this compound share investigators, so they do not show independent replication.43
NNMT also rises in skeletal muscle with age, where it has been linked to weaker NAD+ recycling and to muscle stem cells that drift into senescence, a state in which cells stop dividing. In 2019 the Galveston group asked whether blocking it could help old muscle heal.
They injured a leg muscle in 24-month-old mice, which is old age for a mouse, and treated them with the group’s NNMT inhibitor for one or three weeks. Muscle stem cells multiplied and fused more, the regenerating fibers were nearly twice as large in cross-section, and peak torque of the injured muscle was about 70 percent higher than in untreated mice. Longer treatment produced still larger fibers.
It is one study, in mice, after an acute injury. It does say something interesting about the target. If NNMT sits where energy metabolism meets cell aging, fat loss may not be the only reason to keep watching this field. Older adults lose muscle and heal slowly after injury, and a compound that helped aged muscle stem cells would matter far beyond weight, if the effect ever held up in people.2
No human trial of 5-Amino-1MQ has been published. There is human data on its target, and it may be the most useful part of the whole story. In 2015 a German team measured NNMT in fat tissue from 199 people having abdominal surgery. People with type 2 diabetes had more NNMT in their fat, and among insulin-resistant people, the more NNMT their fat made, the less sensitive to insulin they were.
The same study followed people through change. In 60 people on a 12-week exercise program, and in 55 going through bariatric surgery, NNMT in fat fell as insulin sensitivity improved. After surgery, the blood level of NNMT’s product, 1-methylnicotinamide, fell too. The enzyme this compound is meant to block was already being turned down by exercise and surgical weight loss.
The picture is not tidy. In a 2019 study, mice bred without NNMT were not simply protected from obesity; results depended on sex and diet, and insulin sensitivity improved without better glucose tolerance. In a human weight-loss study, NNMT in fat actually rose while blood 1-methylnicotinamide fell. NNMT may be a marker that moves with metabolic health as much as a lever that drives it.
That leaves an open question worth holding as a hypothesis. If exercise and weight loss already turn this dial in people, an inhibitor would need to show that it adds something on top, and no human study has tested that yet. The trial that would settle it is easy to describe, with people on the same exercise program randomized to the inhibitor or a placebo with insulin sensitivity and fat NNMT measured before and after.78
From published controlled studies, nothing. A 2026 review of NNMT inhibitors in Trends in Pharmacological Sciences says early compounds were held back by weak engagement with the target inside cells, poor bioavailability and unknown safety. Newer compounds address some of those issues, and the review frames clinical testing as the next step for the field.
Who has studied 5-Amino-1MQ matters too. Most of the published work on it comes from one research group and the company founded by one of its members, and the authors of the 2026 review are themselves inventors on a patent for a different NNMT inhibitor. Disclosed interests are normal in drug development. They are also a good reason to wait for independent replication.
So, in the published record, the human evidence gap is complete, with no safety data, no dosing data and no efficacy data. Anything you read about how people feel on it is anecdote, and the product behind the anecdote is unverified.543
The 2018 mouse study reported no observable adverse effects and no change in food intake. That is reassuring as far as it goes, which is a short study in one species looking for obvious problems. The later 28-day study measured liver markers that improved, but it was designed to test metabolic effects rather than toxicity, and none of the studies cited here looked at months or years of exposure.
Three features of the biology argue for caution in people. Blocking NNMT changes SAM levels and histone methylation in fat, so it reaches into how genes are switched on and off. NNMT is also active in cancer biology, which the 2026 review discusses alongside its metabolic roles. And NAD+ and methyl balance are shared by many tissues. Mouse studies have measured effects in liver and muscle, but broader effects and long-term safety in people are unknown.
The product is a further question. Supplements labeled 5-Amino-1MQ are not reviewed by FDA for identity, purity or amount before sale, and nothing ties a given bottle to the compound used in the mouse papers.
Talk to a clinician first if you take diabetes medicine, have liver or kidney disease, are pregnant or breastfeeding, or have a history of cancer.16542
The 2024 mouse study tracked blood glucose, insulin and liver enzymes, alongside tissue and body-composition measures no blood test can copy. In people, HbA1c adds average blood sugar over about three months, and fasting insulin shows how hard the pancreas is working to keep it there. A high insulin alongside a normal glucose can be an early hint of insulin resistance, though fasting insulin alone does not make the diagnosis.
ALT and AST are the liver enzymes that normalized in the treated mice. In people they give a first look at liver stress, and fatty liver is common with insulin resistance. They do not measure liver fat on their own, but they give a clinician a baseline to read later results against.
Vitals Vault does not offer 5-Amino-1MQ. A clinician can choose metabolic and liver tests around your own risks, and these markers give that review its context. A baseline before any change and a retest a few months later turn a hopeful guess into something you can actually read, though fat loss itself needs its own measurement.4
5-Amino-1MQ is not an FDA-approved drug, and it does not appear on FDA’s compounding safety page, current as of April 22, 2026. Products sold to consumers are unregulated, and their contents are not verified before sale.
A 2026 review describes NNMT inhibitors as a field still moving toward clinical translation, with safety profiles still being established. Until a sponsor runs human trials, there is no approved form to prescribe.95
5-Amino-1MQ is a selective, cell-permeable small molecule aimed at a real target. In obese mice it trimmed fat gain, improved insulin sensitivity and reduced liver fat, and an earlier inhibitor study saw weight loss without a drop in food intake. In people, its target tracks with insulin resistance and fell with exercise and bariatric surgery in one study, though it rose during weight loss in another. What is missing is any evidence that the compound itself helps humans.
If NNMT interests you, the most useful step is to measure what it influences, insulin, glucose and liver enzymes, and to work the levers already shown to lower it in people. The next question worth asking is whether an inhibitor adds anything to a body that is already exercising, and only a human trial can answer it.4178
No human study has measured how long 5-Amino-1MQ takes to act, so there is no evidence-based timeline. The mouse studies ran for about four weeks, which is a mouse timescale and should not be read as a human one.
The human study with the clearest timing involved exercise. In a 12-week training program, NNMT in fat fell as insulin sensitivity improved. A baseline and a retest of insulin, HbA1c and liver enzymes over a similar window is the most reliable way to see your own metabolism change.47
Kraus et al., 20146
Animal study · Mice on a high-fat diet, NNMT knocked down in fat and liver
Protected against diet-induced obesity by raising energy use; more SAM and NAD+ in fat
Limits: Antisense knockdown, not 5-Amino-1MQ; mice
Neelakantan et al., 20181
Cell and animal study · Fat cells; diet-induced obese mice
Inhibitors raised NAD+ and SAM; mice lost weight and fat with no change in food intake
Limits: Mice; short study
Neelakantan et al., 20192
Animal study · 24-month-old mice after muscle injury
Nearly twice the fiber size and about 70 percent more peak torque
Limits: Acute injury model in mice
Dimet-Wiley et al., 20223
Animal study · Obese mice switched to a low-fat diet
Inhibitor plus diet restored lean body composition faster than diet alone
Limits: Mice; company-affiliated authors
Babula et al., 20244
Animal study, 28 days · Diet-induced obese mice
Less weight and fat gain, better insulin sensitivity, less liver fat, normal ALT and AST
Limits: Mice; company-affiliated authors
Kannt et al., 20157
Human observational study · 199 surgical patients; 60 exercisers; 55 bariatric patients
Fat NNMT tracked insulin resistance and fell with exercise and surgery
Limits: Association only; no inhibitor given
Brachs et al., 20198
Animal and human study · NNMT knockout and knockdown mice; people losing weight
Mixed, sex- and diet-specific effects; fat NNMT rose during human weight loss
Limits: Complicates the simple target story
It is a small molecule, 5-amino-1-methylquinolinium, with no amino acids. It is often sold next to peptides, but it is a small molecule rather than a peptide, and its absorption and clearance have only been studied in animals.31
In the 2018 obese-mouse study, total food intake did not change while weight and fat fell. The earlier NNMT knockdown work suggests one possible reason, higher energy use in fat cells.16
It limited weight and fat gain in obese mice, mostly in studies from one group and its company. No human trial has tested whether it does anything in people.45
Fat NNMT does track insulin resistance in people, but mice without NNMT showed mixed results, and NNMT in fat rose during human weight loss. It may be a marker as much as a cause.78
In mice, 5A1MQ was given by injection and by mouth. Supplement products sold to people are unregulated, and their purity and amounts vary.4
There is no FDA-approved dose of 5-Amino-1MQ and no typical human dose, because it has not been tested in people. Doses used online are scaled from mouse studies, which is not a safe basis for a human dose. Your clinician decides whether any use makes sense.5
No dose of 5-Amino-1MQ has been published from a study in people, an FDA label or a clinical practice report, so there is no typical human dose to show. All published dosing comes from animal studies, which this page does not use. A clinician decides any use.
Already have a prescribed dose? The peptide dosage calculator turns it into the units to draw on an insulin syringe.
No dose has been published from studies in people yet, so there is no typical dose to show. A prescribing clinician decides whether 5-Amino-1MQ fits and how it is given.
A clinician makes the call. These are the questions they will ask first.
Vitals Vault peptide care starts with a blood panel and a licensed clinician, and ends with a retest.
Get early access to peptide careIn obesity, the chemistry inside fat tissue shifts. The enzyme this compound blocks has been linked to obesity and diabetes, which made it an attractive drug target.
Whether that link is a cause or a bystander in people is unproven, and no human trial has tested the compound. Habits that move fat mass and insulin are the levers you can check with labs today.54
A blood test before you start and a retest after shows what actually changed for you. It is how Vitals Vault approaches every treatment.
No. 5-Amino-1MQ is not an FDA-approved drug and does not appear on FDA’s compounding safety page (current as of April 22, 2026). A 2026 review of NNMT inhibitors describes the field as preclinical and notes that safety profiles are still being established.95
2018
Small-molecule NNMT inhibitors reduce body weight and fat mass in diet-induced obese mice.1
2019
An NNMT inhibitor improves regeneration of aged mouse muscle.2
2022
5-amino-1-methylquinolinium plus a low-fat diet restores lean body composition in obese mice faster than diet alone.3
2024
A 28-day study reports better fat mass, insulin sensitivity and liver markers in obese mice treated with 5A1MQ.4
April 2026
FDA’s compounding safety page is updated; 5-Amino-1MQ does not appear on it.9

5-Amino-1MQ is studied for fat mass, insulin sensitivity and fatty liver in obese mice. It is not a peptide. It is a small molecule that blocks the enzyme NNMT, and it is not FDA-approved for any use.
No. It is a small-molecule NNMT inhibitor, 5-amino-1-methylquinolinium. It has no amino acid chain, but sellers often list it with peptides.
In obese mice it limited body weight and fat gain, improved glucose tolerance and reduced liver fat. No human trial has confirmed these effects.
It blocks NNMT, which raises NAD+ and SAM in fat cells and slows new fat production in cell and mouse studies.
Mouse studies reported no observable adverse effects, but no human safety data have been published. NNMT also plays roles outside metabolism, so long-term effects are unknown.
There is no FDA-approved dose and no typical human dose, because it has not been tested in people. Online doses are scaled from mouse studies. Your clinician decides whether any use makes sense.
5-Amino-1MQ is a small molecule that blocks an enzyme in fat cells, with mouse data only. AOD-9604 is a growth hormone fragment that reached human obesity trials and did not beat placebo on its primary endpoint. Neither is approved.
No. It is not an FDA-approved drug and does not appear on FDA’s April 2026 compounding safety page.
Not at this time. Vitals Vault is opening clinician-led peptide care that starts with a blood test, and 5-Amino-1MQ is not part of it. Join the peptides waitlist to hear what is offered.

Vitals Vault is opening peptide care that starts with your blood work, is prescribed by licensed US clinicians and ends with a retest. Join the waitlist to hear first.