For research purposes only. Not for human use. 5-Amino-1MQ is a preclinical small molecule with no approved use in any species. Nothing here is medical advice or an administration protocol.
What 5-Amino-1MQ Is
5-Amino-1MQ (5-amino-1-methylquinolinium; abbreviated 5A1MQ in the primary literature) is a small, positively charged quinolinium compound that inhibits nicotinamide N-methyltransferase (NNMT). It is not a peptide. It appears on this platform because it is sold alongside metabolic research peptides and is often stacked with them in study designs, but its chemistry, handling and evidence base are those of a small-molecule enzyme inhibitor.
NNMT is a cytosolic enzyme that transfers a methyl group from S-adenosylmethionine (SAM) onto nicotinamide, producing 1-methylnicotinamide (1-MNA) and S-adenosylhomocysteine. Because nicotinamide is a precursor of NAD+ and SAM is the cell's universal methyl donor, NNMT sits at a junction between NAD+ availability, methylation capacity and energy metabolism. It is expressed most strongly in liver and white adipose tissue, and its expression in fat rises with obesity and insulin resistance (Roberti et al., 2021).
Why NNMT Became a Drug Target
The case for NNMT as an obesity target was made in a 2014 Nature paper from the Kahn laboratory. Screening white adipose tissue from mice with adipose-specific Glut4 knockout or overexpression, the authors found Nnmt was the most strongly reciprocally regulated gene. Knocking down NNMT with antisense oligonucleotides protected mice from diet-induced obesity, and the mechanism involved increased polyamine flux and higher cellular energy expenditure: NNMT inhibition in adipocytes raised oxygen consumption in a manner dependent on the polyamine enzymes ODC, SSAT and PAO. The authors described NNMT as a regulator of histone methylation, polyamine flux and NAD+-dependent SIRT1 signalling (Kraus et al., 2014).
That paper used a genetic tool, not a drug. The small-molecule programme that produced 5-Amino-1MQ developed methylquinolinium scaffolds designed to be selective, membrane-permeable NNMT inhibitors suitable for in vivo work.
Preclinical Evidence for 5-Amino-1MQ
Cellular selectivity and mechanism. The 2018 Biochemical Pharmacology paper characterised a series of methylquinolinium NNMT inhibitors. Analogues with primary amine substitutions crossed membranes readily in PAMPA and Caco-2 assays, and did not inhibit related SAM-dependent methyltransferases or enzymes of the NAD+ salvage pathway. In cultured adipocytes the inhibitors reduced intracellular 1-MNA, increased NAD+ and SAM, and suppressed lipogenesis (Neelakantan et al., 2018).
Diet-induced obese mice. In the same paper, systemic treatment of diet-induced obese mice with a potent NNMT inhibitor reduced body weight and white adipose mass, decreased adipocyte size and lowered plasma total cholesterol, without changing total food intake and without observable adverse effects. The lack of a food-intake effect distinguishes this mechanism from the incretin class, where weight loss is driven mainly by reduced appetite.
Extended metabolic characterisation. A 2024 study in Diabetes, Obesity and Metabolism administered 5A1MQ daily to diet-induced obese mice for 28 days. Treatment dose-dependently limited body-weight and fat-mass gains, improved oral glucose tolerance and insulin sensitivity, suppressed hyperinsulinaemia, and reduced hepatic steatosis, macrophage infiltration, liver weight and liver triglyceride content; circulating alanine transaminase normalised. The paper also established plasma pharmacokinetics and tissue distribution after intravenous, oral and subcutaneous dosing, reporting high systemic exposure and distribution to adipose, muscle and liver (Diabetes Obes Metab, 2024).
Aged muscle. A 2019 study treated 24-month-old mice with an NNMT inhibitor and reported activation of senescent muscle stem cells and improved regeneration after injury, framed as the first evidence that NNMT inhibition can rescue age-related deficits in muscle stem-cell function (Neelakantan et al., 2019).
Diet combination and the microbiome. When 5-amino-1-methylquinolinium was combined with a switch from high-fat to low-fat diet in diet-induced obese mice, adiposity and weight normalised to lean age-matched controls faster than diet switch alone; the follow-up microbiome study found the diet switch, not the inhibitor, drove most of the caecal microbiome differences (Scientific Reports, 2022).
What the Evidence Does Not Yet Show
Every efficacy result above is from mice or cultured cells. A 2024 review of NNMT as a metabolic-syndrome target states that clinical trials focusing on NNMT have not been documented (Frontiers in Pharmacology, 2024), and a 2026 review in Trends in Pharmacological Sciences notes that early NNMT inhibitors were limited by insufficient target engagement, poor bioavailability and unknown safety profiles, with newer compounds only beginning to address those gaps (Trends Pharmacol Sci, 2026). No human pharmacokinetic, safety or efficacy data for 5-Amino-1MQ exist in the peer-reviewed literature as of September 2026.
Claims found on vendor pages that 5-Amino-1MQ "burns fat without diet or exercise," "raises NAD+ like NMN," or has a defined human dose are not supported by any published study. The NAD+ increase reported in the 2018 paper was measured inside cultured adipocytes; whether systemic NAD+ changes in animals or people has not been shown.
NNMT Beyond Metabolism
NNMT research has broadened well past obesity, which affects how the target is likely to be developed. A 2025 Nature paper found that NNMT in cancer-associated fibroblasts drives complement secretion and recruitment of immunosuppressive myeloid cells; NNMT knockout impaired tumour growth in ovarian, breast and colon models, and a newly developed potent inhibitor reduced tumour burden and restored checkpoint-blockade efficacy (Nature, 2025). This is a different inhibitor from 5-Amino-1MQ and a different application, but it signals that the medicinal-chemistry effort around NNMT is accelerating, and that the compound sold today as a research chemical is an early-generation tool rather than a clinical candidate.
Platform Market Data: 5-Amino-1MQ Listings
The Peptides.SO listings table holds 10,922 priced listings across 119 suppliers (prices checked 24–25 September 2026). 5-Amino-1MQ is one of the most widely stocked non-peptide compounds on the platform.
| Product row | Listings | Suppliers | Median list price | Interquartile range | Median at sale |
|---|---|---|---|---|---|
| 5-Amino-1MQ (all sizes) | 89 | 62 | $79.99 | $58.00 – $135.00 | $75.00 |
| 5-Amino-1MQ 5 mg | 7 | 7 | $34.99 | — | — |
| 5-Amino-1MQ 10 mg | 11 | 11 | $60.00 | — | — |
| 5-Amino-1MQ 50 mg | 20 | 16 | $170.50 | — | — |
The 62 suppliers is nearly three times the number listing semaglutide (23), though fewer than list MOTS-c (95), so availability is not a constraint. The vial-size distribution is wide (5 mg to 125 mg) and about half of the listings do not pin a size in the product URL, so a raw price comparison across suppliers is only meaningful once the milligram amount is confirmed. The cost calculator does that conversion; live prices and stock are on the 5-Amino-1MQ product page.
Because 5-Amino-1MQ is a small molecule rather than a peptide, the relevant certificate of analysis is different: HPLC or LC-MS purity of the quinolinium salt, identity by mass spectrometry or NMR, and a statement of the counter-ion (chloride or iodide salts are both sold). Peptide-specific tests such as endotoxin are less informative here. The supplier checklist covers what to look for.
Handling Notes for Laboratory Use
5-Amino-1MQ is supplied as a powder, usually the chloride or iodide salt. It is water-soluble and, unlike peptides, is not sensitive to freeze-thaw or proteolysis, but quinolinium compounds are light-sensitive and solutions should be protected from light. Store powder dry at room temperature or refrigerated as the supplier specifies. The peptide calculator works for small-molecule concentrations too, given the molecular weight of the salt form on the certificate. These are handling notes for laboratory material only.
Related Compounds and Reading
- •MOTS-c, a mitochondrial-derived peptide studied for exercise-like metabolic effects
- •MOTS-c vs 5-Amino-1MQ vs tesamorelin
- •Tesofensine, another non-peptide compound sold in the same market
- •Semaglutide research overview for the incretin mechanism this compound is often contrasted with
- •The stack builder for planning multi-compound in vitro or animal study designs
Frequently Asked Questions
Is 5-Amino-1MQ a peptide?
No. It is a methylquinolinium small molecule. It is grouped with peptides commercially because it is sold to the same research market.
What does NNMT inhibition do in cells?
It reduces production of 1-methylnicotinamide, sparing nicotinamide for NAD+ synthesis and SAM for methylation and polyamine synthesis. In adipocytes this raised NAD+ and SAM and suppressed lipogenesis.
Did the mouse studies show reduced food intake?
No. The 2018 study reported reduced body weight and fat mass without a change in total food intake, which is the main mechanistic difference from GLP-1-class compounds.
Has 5-Amino-1MQ been tested in humans?
No published human trial exists. Reviews in 2024 and 2026 both state that clinical trials of NNMT inhibitors have not been documented.
Is it the same as the NNMT inhibitor in the 2025 Nature cancer paper?
No. That paper developed a separate, newer compound. 5-Amino-1MQ is an early-generation tool inhibitor from the 2018 methylquinolinium series.
What should a certificate of analysis for 5-Amino-1MQ show?
Purity by HPLC or LC-MS, identity by mass spectrometry or NMR, and the salt form. Peptide-style endotoxin or sequence data are not the relevant tests.
References
1. Roberti A, et al. Nicotinamide N-methyltransferase: At the crossroads between cellular metabolism and epigenetic regulation. Mol Metab. 2021. PMID 33453420
2. Kraus D, et al. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature. 2014. PMID 24717514
3. Neelakantan H, et al. Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochem Pharmacol. 2018. PMID 29155147
4. Babula JJ, et al. Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction. Diabetes Obes Metab. 2024. PMID 39161060
5. Neelakantan H, et al. Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. Biochem Pharmacol. 2019. PMID 30753815
6. Dimet-Wiley A, et al. Reduced calorie diet combined with NNMT inhibition establishes a distinct microbiome in DIO mice. Sci Rep. 2022. PMID 35013352
7. Sun WD, et al. Nicotinamide N-methyltransferase (NNMT): a novel therapeutic target for metabolic syndrome. Front Pharmacol. 2024. PMID 38919254
8. Puleo N, et al. Emerging opportunities for nicotinamide N-methyltransferase (NNMT) inhibitor clinical translation. Trends Pharmacol Sci. 2026. PMID 42067476
9. Heide J, et al. NNMT inhibition in cancer-associated fibroblasts restores antitumour immunity. Nature. 2025. PMID 40702186
Research Disclaimer
5-Amino-1MQ is sold for laboratory research only. It has no approved use, no human safety data and no established dose in any species outside the specific study designs cited above. This article does not recommend or describe administration to people or animals.