5-Amino-1MQ: A Small Molecule With No Human Data

By Evan Marsh, EditorUpdated July 30, 2026Sources: peer-reviewed preclinical literature, ClinicalTrials.gov

Two things about this compound are consistently reported wrong, and both are easy to check. It is not a peptide. And it has never been tested in a human being — not in a published trial, not in a registered one.

The evidence base, stated exactly. A PubMed search for 5-amino-1-methylquinolinium returns three records: a bladder-cancer tumour-microenvironment paper, a HeLa cell-line study, and a mouse microbiome study. ClinicalTrials.gov returns nothing for the compound, nothing for the drug class, and no NNMT inhibitor given to humans in any trial. That is the complete human evidence base: empty.

What it is

5-Amino-1MQ is 5-amino-1-methylquinolinium, a small-molecule inhibitor ofnicotinamide N-methyltransferase (NNMT). It came out of a medicinal chemistry program at the University of Texas Medical Branch, and the paper defining the chemical series was published in the Journal of Medicinal Chemistry in 2017.

Vendors sell it next to BPC-157 and MOTS-c and it inherits the peptide framing by proximity. It is a quinolinium salt. Nothing about peptide handling — bacteriostatic water, reconstitution volumes, cold chain, the injection-only assumption — carries over. It is typically sold as an oral capsule for exactly that reason.

The mechanism, which is genuinely interesting

NNMT methylates nicotinamide to 1-methylnicotinamide. That reaction does two things at once: it consumes S-adenosylmethionine, the cell's main methyl donor, and it pulls nicotinamide out of the salvage pathway that regenerates NAD+. NNMT is highly expressed in adipose tissue, and its expression rises in obesity.

So inhibiting it should, in principle, spare methyl groups and free nicotinamide back toward NAD+ synthesis — a metabolic argument that does not depend on appetite suppression at all. That is a real hypothesis, and it is why the compound gets attention from people who understand the biology rather than just the marketing.

What the animal work found

Model	What was measured	Result
Diet-induced obese mice	Body weight, adipose mass, adipocyte size, cholesterol	All reduced — without a reduction in food intake
24-month-old mice, post-injury, 5 and 10 mg/kg	Muscle fiber cross-sectional area, peak torque	Nearly 2× the fiber area; roughly 70% greater peak torque vs controls
Obese mice plus calorie restriction	Body composition	Normalised composition; effects additive with the diet
Aged mice, with and without exercise	Muscle function	Described as mimicking and adding to exercise effects

Read the first row carefully, because it is the finding the marketing is built on and it is real: the mice lost fat without eating less. If that translated, it would be a genuinely different mechanism from every GLP-1 drug, which all work through appetite.

"If that translated" is doing the load-bearing work in that sentence. Mouse metabolic findings have a long history of not translating, and the compounds that did translate got tested to find out. This one has not been.

Dosing: there isn't one

Capsules are typically sold at 50–150 mg daily. No published study supports those figures. They are not scaled from a human trial, because none exists, and scaling the rodent doses directly is not valid — the mouse studies used 5–10 mg/kg, and naive body-weight conversion across species is exactly the error that dose-finding trials exist to prevent.

There is also no human pharmacokinetic data: no absorption figures, no half-life, no information on what oral dosing actually achieves in blood. A capsule strength printed on a label is a manufacturing decision, not a dosing recommendation.

Safety

Unknown. Animal studies at the doses used did not report significant toxicity, which is the most that can be said. There is no human safety data of any kind — no adverse event reporting, no monitoring guidance, no drug interaction information.

One mechanistic consideration worth naming: NNMT sits on the methylation pathway, and methylation is not a niche process. Sustained inhibition of an enzyme that regulates SAM availability is not obviously benign, and the studies that would characterise it have not been done.

Where it belongs on the evidence ladder

Interesting mechanism, real animal data published in respectable journals, and zero human evidence. That combination is common in this market, and it is usually presented as though the first two imply the third is a formality.

Our fat-loss ranking places 5-Amino-1MQ below every compound with human trial data for that reason. It is not that the mechanism is implausible — it is that "plausible in mice" and "works in people" are separated by exactly the step that has never been taken here.

We do not link a supplier for this one. Our affiliate partner does not stock it, and rather than route you to a different vendor for the sake of a commission, the more useful thing to say is that there is nothing here worth buying on the strength of the evidence. If the mechanism interests you, the compounds on this site with actual human data —the GLP-1 class for fat loss, orMOTS-c if you want the other metabolic story with its limits stated — are where that interest is better spent.

Frequently asked questions

Is 5-Amino-1MQ a peptide?

No. It is a small molecule — 5-amino-1-methylquinolinium, a quinolinium salt. It is sold alongside peptides and grouped with them by most vendors, but chemically it belongs to a different class entirely. That matters because peptide-specific reasoning about stability, reconstitution and injection does not apply to it.

Has 5-Amino-1MQ been tested in humans?

No. There is no published human trial and none registered on ClinicalTrials.gov. The stronger statement is that no NNMT inhibitor of any kind has entered human trials. Every efficacy figure in circulation comes from mice or cell culture.

What does it do in animals?

In diet-induced obese mice, NNMT inhibition reduced body weight and white adipose mass, shrank adipocytes and lowered plasma cholesterol — notably without reducing food intake. In 24-month-old mice given 5 and 10 mg/kg after muscle injury, treated animals regained nearly twice the fiber cross-sectional area and about 70% more peak torque than controls.

What is the human dose?

There is no established human dose, because there is no human study. The 50–150 mg oral capsules commonly sold have no published basis — they are not scaled from a trial, because no trial exists.

Is it FDA approved or regulated?

It has no FDA approval. Unusually for this category it also appears on neither FDA compounding list — not in Category 2 and not among substances nominated and withdrawn. It seems never to have been formally nominated at all.

Sources

Neelakantan H et al. Structure-Activity Relationship for Small Molecule Inhibitors of Nicotinamide N-Methyltransferase. Journal of Medicinal Chemistry, 2017;60(12):5015–5028. PubMed
Neelakantan H et al. Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochemical Pharmacology, 2018;147:141–152. PubMed
Neelakantan H et al. Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. Biochemical Pharmacology, 2019;163:481–492. PubMed
Sampson CM et al. Combined nicotinamide N-methyltransferase inhibition and reduced-calorie diet normalizes body composition and enhances metabolic benefits in obese mice. Scientific Reports, 2021;11(1):5637. PubMed
Dimet-Wiley AL et al. Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice. Scientific Reports, 2024;14(1):15554. PubMed
Babula JJ et al. Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction. Diabetes, Obesity and Metabolism, 2024;26(11):5272–5282. PubMed
Absence of human data verified against PubMed and ClinicalTrials.gov in July 2026.

Related guides

Research use only. 5-Amino-1MQ is not approved for human use and has never been tested in humans. This page summarizes published preclinical research and is not medical advice.