Compound reference
5-Amino-1MQ
Also known as 5-Amino-1-methylquinolinium
5-Amino-1MQ is a small-molecule NNMT inhibitor (not a peptide) sold as a fat-loss and longevity research compound. Its metabolic and muscle data in mice are real and reproducible — but the evidence is entirely preclinical, there are no human trials, and reviewers describe it as a limited-potency tool compound that may not become a drug.
- CAS
- 42464-96-0
- Formula
- C₁₀H₁₁N₂⁺ (cation; supplied as the iodide salt)
- Molar mass
- 159.2 g/mol (cation); 286.1 g/mol (iodide salt)
Research compound; not FDA-approved as a drug.
Mode of action
5-Amino-1MQ (5-amino-1-methylquinolinium) is worth stating plainly at the outset: it is a small molecule, not a peptide, despite being marketed and sold alongside research peptides. It is an inhibitor of nicotinamide N-methyltransferase (NNMT), a cytosolic enzyme that transfers a methyl group from S-adenosyl-L-methionine (SAM) to nicotinamide, producing 1-methylnicotinamide (1-MNA). That reaction sits at the junction of two important currencies: it consumes a precursor that feeds the NAD⁺ salvage pathway, and it spends a methyl group from the SAM pool.
By binding NNMT's nicotinamide site (with modest, micromolar potency), 5-Amino-1MQ lowers 1-MNA, raises intracellular NAD⁺ and SAM, and stabilizes the activity of the NAD⁺-dependent deacetylase SIRT1. In fat cells the net effect is a metabolic shift away from lipogenesis and storage and toward energy expenditure, with downstream anti-inflammatory effects (reduced NF-κB signaling and pro-inflammatory cytokines). Importantly, it is reported to be selective — it does not inhibit other SAM-dependent methyltransferases or the NAD⁺-salvage enzymes — which is what makes it a clean research tool for interrogating NNMT biology.
Main intended effect
Metabolic: reducing fat mass and body weight and improving insulin sensitivity and fatty-liver measures, with emerging interest in muscle function and aging.
Areas of interest
The core interest is metabolic — obesity, type 2 diabetes, metabolic syndrome, and non-alcoholic fatty liver disease. A newer and, for the consumer market, compelling strand is skeletal muscle and aging (sarcopenia). NNMT inhibition is also being explored across fibrosis, inflammation, and several cancers. In practice 5-Amino-1MQ is sold as a fat-loss and longevity "research compound," frequently described — inaccurately — as a peptide.
Evidence for intended effects
The preclinical evidence is genuinely solid and reproducible across groups — but it is entirely preclinical. The foundational work showed that 5-Amino-1MQ reverses diet-induced obesity in mice, reducing body weight, white adipose mass, adipocyte size, and plasma cholesterol without changing food intake. A later study confirmed dose-dependent reductions in fat mass with improved glucose tolerance, insulin sensitivity, and hepatic steatosis. And a 2024 study extended the story to muscle: in aged mice, NNMT inhibition raised grip strength by about 40% on its own and roughly 60% combined with exercise — a striking result that underpins much of the longevity-market enthusiasm.
Two caveats are essential. First, there are no human trials of 5-Amino-1MQ — none of the metabolic or muscle findings have been tested in people. Second, the pharmacologists working on this target are themselves cautious about this particular molecule: a 2026 review describes 5-Amino-1MQ as an invaluable tool compound whose limited in-vitro and in-vivo potency suggests it may not be a viable clinical candidate, with newer, more potent and orally bioavailable NNMT inhibitors better positioned for translation. In other words, what is sold today is the early research tool, not an optimized drug.
| Strand | What exists | Tier |
|---|---|---|
| Obesity / metabolic | Diet-induced obese mice: weight, adiposity, insulin sensitivity, fatty liver | Strong preclinical |
| Muscle / aging | Aged mice: grip strength, fiber size (with exercise) | Preclinical |
| Mechanism | NNMT inhibition → ↑NAD⁺/SAM, SIRT1; selective | Well characterized |
| Human | None | No trials |
Studied amounts (literature dosing context)
In mice, effective regimens were given by subcutaneous injection — for example about 20 mg/kg three times daily in the original obesity study, and 5–30 mg/kg/day in later work. A notable detail: those studies found high systemic exposure by subcutaneous dosing but poor oral bioavailability — which sits awkwardly against the oral capsules and sublingual products marketed to consumers. There is no established human dose. These are animal-study figures only, and this page does not provide dosing guidance.
Safety and regulatory status
Short mouse studies reported no obvious adverse effects and no change in food intake, but there is no human safety data, no chronic-toxicity characterization, and no pharmacokinetic data in people. 5-Amino-1MQ is not approved as a drug in any jurisdiction; it is sold as a research-use-only compound and consumer "nootropic"/fat-loss product, so any given product is of unverified identity and purity. Its frequent labeling as a "peptide" is simply incorrect — it is a small-molecule enzyme inhibitor.
Sources
Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice
Neelakantan and colleagues synthesized and tested a series of membrane-permeable small-molecule NNMT inhibitors, including the lead compound 5-amino-1MQ, in 3T3-L1 adipocytes (0.1–60 µM in vitro) and in diet-induced obese C57BL/6 mice (20 mg/kg subcutaneous three times daily for 11 days). NNMT inhibition depleted intracellular 1-methylnicotinamide, raised NAD+ and SAM levels, suppressed lipogenic differentiation, and reduced epididymal white adipose tissue mass without affecting food intake. Treated animals showed significant body weight reduction and lower plasma total cholesterol versus saline controls. The compounds displayed high selectivity, not inhibiting related SAM-dependent methyltransferases. No adverse effects were observed over the short treatment window, though chronic toxicity data and human pharmacokinetics are absent.
Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction
Ye and colleagues evaluated the NNMT inhibitor 5-amino-1MQ in a 28-day diet-induced obesity study in male C57Bl/6J mice receiving once-daily dosing (pharmacokinetic profiling used 5–30 mg/kg subcutaneous). Treatment dose-dependently limited body weight and fat mass gains without reducing food intake or lean mass, improved oral glucose tolerance and insulin sensitivity, and suppressed hyperinsulinemia. Liver weight, triglyceride content, and NAFLD activity scores were reduced, and circulating ALT, AST, and ketone levels were normalized. Subcutaneous dosing conferred high systemic exposure with distribution to adipose, muscle, and liver, whereas oral bioavailability was poor. All findings are from a murine model; human efficacy and safety remain unestablished.
Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice
Preclinical study (Dimet-Wiley and colleagues, Scientific Reports 2024) testing the NNMT inhibitor 5-amino-1MQ, alone and combined with exercise, in aged mice. NNMT inhibition in sedentary aged mice increased grip strength by roughly 40% relative to sedentary controls — larger than the gain from exercise alone — and the combination of inhibitor plus exercise produced an additive improvement of about 60%. Treatment also improved intramyocellular lipid content and, when combined with exercise, increased gastrocnemius fiber cross-sectional area, supporting NNMT inhibition as a candidate approach for age-related muscle loss (sarcopenia). All findings are in aged mice; there is no human muscle data.
Roles of Nicotinamide N-Methyltransferase in Obesity and Type 2 Diabetes
Narrative review published in BioMed Research International (2021) synthesizing preclinical evidence on nicotinamide N-methyltransferase (NNMT) as a therapeutic target for obesity and type 2 diabetes. The authors survey oligonucleotide knockdown studies and small-molecule NNMT inhibitors — including compounds in the class that encompasses 5-amino-1MQ — demonstrating that NNMT inhibition increases energy expenditure, reduces white adipose mass, improves insulin sensitivity, and normalizes fasting blood glucose in animal models. The review concludes that NNMT represents a mechanistically distinct, promising target for metabolic disease but acknowledges that the exact signaling mechanisms downstream of NNMT inhibition remain incompletely understood. A critical stated limitation is that no human clinical trials targeting NNMT had been reported as of publication, leaving clinical translation entirely unestablished.
Emerging opportunities for nicotinamide N-methyltransferase (NNMT) inhibitor clinical translation
Review (Puleo, Allega, Niemann, and Lengyel, Trends in Pharmacological Sciences 2026) surveying NNMT as a target across metabolic syndrome, organ fibrosis, and cancer, and the state of NNMT-inhibitor drug development. It recaps that 5-amino-1MQ improves insulin sensitivity and reduces body weight, adiposity, cholesterol, and liver steatosis in diet-induced obese mice and reduces fibrosis in kidney models — but characterizes 5-amino-1MQ primarily as an invaluable tool compound whose limited in-vitro and in-vivo potency suggests it may not itself be a viable clinical candidate. Newer NNMT inhibitors with nanomolar cellular potency and oral bioavailability are described as more promising for translation. Useful for distinguishing the early tool compound sold today from the optimized inhibitors still in development.
https://www.sciencedirect.com/science/article/abs/pii/S0165614726000866