A small-molecule NNMT enzyme inhibitor, not a peptide, that reduced fat mass in obese mice. No human studies exist.
Also called 5-amino-1-methylquinolinium, 5A1MQ, NNMT inhibitor
5-Amino-1MQ is not a peptide. It is a small synthetic molecule, a methylquinolinium, built at the University of Texas Medical Branch in Galveston to block an enzyme called nicotinamide N-methyltransferase, or NNMT. It shows up on peptide sites because it is sold through the same research-chemical channels and is usually discussed alongside fat-loss peptides.
NNMT is unusually active in the fat tissue and liver of obese mice and people. It takes nicotinamide, a form of vitamin B3, and tags it with a methyl group so it gets excreted. Blocking NNMT leaves more nicotinamide to be recycled into NAD+ and keeps more SAM, the body's main methyl donor. In cultured fat cells 5-Amino-1MQ raised NAD+ and cut fat production. In obese mice on a high-fat diet, injections three times a day for 11 days took off about 5% of body weight while untreated mice gained 1.4%, and shrank belly fat pads by about 35%, with no change in how much the mice ate.
That is the whole evidence base: cells and mice, nearly all from one research group whose founder started Ridgeline Therapeutics to develop NNMT inhibitors. No human has been given 5-Amino-1MQ in a published study, so its dose, safety, and whether it works in people are unknown. The capsules and injections sold online are unapproved, it is not on any FDA compounding list, and under WADA's S0 rule for unapproved drugs athletes should treat it as prohibited.
Not technically a peptide. 5-Amino-1MQ is listed here because it is discussed and used alongside peptides, but it is not built from amino acids joined by peptide bonds.
What it binds to, and what happens inside the body after that, step by step.
5-Amino-1MQ blocks NNMT, the enzyme that methylates nicotinamide using SAM as the methyl donor. With NNMT blocked, fat cells make less 1-methylnicotinamide, keep more NAD+ and SAM, and in mouse and cell studies make less new fat. It did not inhibit related methyltransferases or the NAD+ salvage enzymes NAMPT and SIRT1 at the concentrations tested.
Human results and animal results are kept apart below. A result in rats tells you a mechanism is plausible. It does not tell you what happens in a person.
All data come from cells and mice: lower body weight, smaller fat pads, better glucose tolerance and less fatty liver in diet-induced obese mice, and better muscle regeneration in old injured mice. Nearly every study comes from the Watowich and Neelakantan group at UTMB and the company built around it. There are no published human studies of any kind.
No human studies are among the key studies for 5-Amino-1MQ. Everything known comes from animals or cells.
Diet-induced obese mice, 9 per group; cultured 3T3-L1 adipocytes
20 mg/kg injected three times daily for 11 days: mice lost about 5.1% of body weight versus a 1.4% gain on saline, belly fat fell about 35% and cholesterol about 30%, with no change in food intake.
Read the studyDiet-induced obese mice, 28 days of once-daily dosing
5A1MQ dose-dependently limited weight and fat gain, improved glucose tolerance and insulin sensitivity, reduced fatty liver and normalized ALT and AST.
Read the studyDiet-induced obese mice switched to a lean diet
Adding the NNMT inhibitor to a diet switch produced faster fat loss and brought body composition and liver fat to the level of lean control mice.
Read the study24-month-old mice with chemically injured leg muscle
At 5 to 10 mg/kg, regenerating muscle fibers were nearly 2-fold larger and peak muscle torque about 70% higher than in untreated old mice.
Read the studyMice with NNMT knocked down in fat and liver
The study that established NNMT as an obesity target: knockdown raised energy expenditure, fat-tissue NAD+ and SAM, and prevented diet-induced obesity.
Read the studyThese are questions the published research has not answered.
No product containing 5-Amino-1MQ is approved as a medicine by the FDA.
Not approved anywhere and no registered human trial was found on ClinicalTrials.gov. Sold online as a research chemical and as oral capsules marketed like a supplement, which FDA has not authorized. Not named on the WADA Prohibited List, but S0 bans any pharmacological substance with no current government approval for human therapeutic use, which covers it; athletes should check GlobalDRO.
No human half-life has been published for 5-Amino-1MQ, so we do not draw a clearance curve. Half-lives quoted online for it are usually estimates from animal data.
No human study or approved label has published a dose for 5-Amino-1MQ, so there is no table to show.
No dose of 5-Amino-1MQ has been tested in a published human study or approved on a label. Numbers that circulate online come from animal studies scaled up by guesswork or from sellers. We do not reproduce them.
Which symptoms are expected and which mean stop and get help: side effects and red flags.
Tap a claim to see what the studies found.
Obese mice lost about 5% of body weight in 11 days without eating less, but it has never been tested in people.
It raised NAD+ inside cultured fat cells and fat-tissue NAD+ rose with NNMT knockdown in mice. Nobody has measured NAD+ in people taking it.
It is a small quinolinium molecule with a molecular weight of about 159, not a chain of amino acids.
In old mice with chemically injured muscle, it improved repair and strength. There are no data on muscle growth in healthy animals or in people.
Oral pharmacokinetics were measured only in mice, and all mouse efficacy studies used injections.
These pairings come up often. Almost none have been tested together in a trial, and the evidence note on each says so plainly.
The idea is to supply NAD+ precursors while blocking the enzyme that diverts nicotinamide out of the NAD+ recycling loop.
EvidenceNo study has tested this pairing in animals or people.
Mice switched to a lean diet lost more fat and liver fat when the NNMT inhibitor was added.
EvidenceMouse data only, from the developing research group.
Pairs an NNMT inhibitor with an AMPK-activating peptide, both promoted for fat loss.
EvidenceNever studied together; each has only mouse data.
Supplied as a dry powder or in capsules. No pharmaceutical stability data are published; suppliers generally list cool, dry, dark storage.
No validated stability data for solutions.
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