5-Amino-1MQ, short for 5-amino-1-methylquinolinium, is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT); it is not a peptide. Cell and mouse studies use it to test how NNMT inhibition changes 1-methylnicotinamide, NAD+- and SAM-linked metabolism, body-composition, liver, and tissue-repair endpoints. The selected evidence remains preclinical and does not establish human weight loss, safety, efficacy, dosing, or a treatment protocol.
The central question in 5-Amino-1MQ research is narrower than most search results suggest: what changes when a defined NNMT inhibitor is introduced into a specified biochemical assay, cell system, or animal model? A useful answer must distinguish direct 5-Amino-1MQ studies from genetic NNMT studies, other inhibitor chemotypes, and reviews of the target.
Apex-specific research boundary: Apex Laboratory supplies 5-Amino-1MQ as a research-grade chemical reagent for in-vitro research only. It is not a peptide, pharmaceutical formulation, supplement, or weight-loss product; it is not for human consumption and is not represented here as a treatment or administration product.
- 5-Amino-1MQ is a small molecule, not a peptide; chemical form and counterion are therefore material identity fields.
- NNMT transfers a methyl group from SAM to nicotinamide, producing 1-methylnicotinamide and SAH.
- Direct 5-Amino-1MQ evidence includes enzyme/cell work and several mouse studies; genetic NNMT knockdown and other NNMT inhibitors are supporting target context, not interchangeable compound evidence.
- The selected literature does not establish controlled human weight-loss efficacy, general safety, a dose, or a treatment protocol.
What Is 5-Amino-1MQ?
5-Amino-1MQ is the common shorthand for 5-amino-1-methylquinolinium, a small-molecule NNMT inhibitor. It contains no amino-acid chain and is not a peptide. The “amino” in its chemical name describes a functional group, not membership in the peptide class.
Neelakantan et al. (2017) screened N-methylated quinolinium, isoquinolinium, pyridinium and benzimidazolium/benzothiazolium analogues in an NNMT structure-activity program spanning a greater than 1000-fold range of inhibitory activity, and identified quinoliniums as the promising scaffold at low-micromolar potency (IC50 ≈ 1 µM in the reported enzyme assay). The later 2018 Biochemical Pharmacology paper identified 5-amino-1-methylquinolinium as a selective, membrane-permeable tool compound and tested it in biochemical, adipocyte, and diet-induced-obese mouse systems.
The name alone is incomplete as a material record. A supplier or paper should specify the chemical form being tested, including a counterion or salt when applicable. A molecular-weight or CAS field for one form should not be assigned automatically to another. For that reason the identity record below states which form each value belongs to, instead of presenting one universal number as though every material labeled “5-Amino-1MQ” were chemically identical.
Reagent identity record
| Field | Value | Form qualifier |
|---|---|---|
| Chemical name | 5-amino-1-methylquinolinium (5A1MQ) | Quaternary cation, so the material ships as a salt and the counterion belongs in the record |
| Molecular formula | C10H11N2+ | Cation only (PubChem CID 950107); a salt adds the counterion to the empirical formula |
| Molecular weight | ~158–159 Da (159.21 for the cation) | Cation basis. The Apex product record lists 158.2 Da for that same cation on a different rounding convention; any salt form is heavier by its counterion |
| CAS number | Not assigned in this record — pending supplier-COA confirmation | The catalog-listed 5467-79-8 is a documented mismatch: PubChem resolves that registry number to 6-methoxyquinoline-2-carbonitrile (CID 230481), a different compound |
| Amino-acid sequence | None | Not a peptide; the molecule contains no amino-acid residues, so no sequence field exists for it |
| Purity specification | ≥99% by HPLC | Supplier specification with per-lot ESI-MS identity confirmation; a documentation claim, not a biological-activity claim |
What Does NNMT Do?
Nicotinamide N-methyltransferase is a cytosolic enzyme that transfers a methyl group from S-adenosylmethionine (SAM) to nicotinamide. The reaction produces 1-methylnicotinamide (1-MNA) and S-adenosylhomocysteine (SAH). NNMT therefore sits at an intersection between nicotinamide handling and methyl-donor metabolism.
Pissios (2017) reviewed NNMT as more than a vitamin-B3 clearance enzyme and described its connections to NAD+ precursor availability and methylation biology; as a narrative synthesis it reports no quantitative endpoint of its own. A review is useful for pathway synthesis, but target plausibility must still be separated from the effects of one inhibitor in one model.
Inhibition can be evaluated at several levels. A biochemical assay asks whether a compound inhibits purified NNMT. A cell study can ask whether 1-MNA or related metabolites change in a membrane-intact system. An animal study adds exposure, distribution, physiology, and model-specific endpoints. These layers are connected, but success at one layer does not prove success at the next.
Why Is NNMT a Research Target?
The target rationale predates 5-Amino-1MQ. Riederer et al. (2009) showed that mouse 3T3-L1 adipocytes and both human and murine adipose-tissue explants express enzymatically active NNMT, and that homocysteine secretion from those cultures fell when the tissue was treated with the NNMT product-inhibitor 1-methylnicotinamide; that abstract reports no quantitative result for the change, so no magnitude is carried over. Kraus et al. (2014) used antisense Nnmt knockdown in adipose tissue and liver of mice and reported protection against diet-induced obesity via increased cellular energy expenditure, higher adipose SAM and NAD+, altered histone H3K4 methylation, and increased polyamine flux — directions stated in the abstract with no single quantitative finding attached.
That 2014 paper is important target-validation evidence, but it did not test 5-Amino-1MQ. Genetic knockdown changes expression over a different time course and can affect tissues differently from a small molecule. Treating genetic evidence as if it were direct compound evidence is one of the most common errors in 5-Amino-1MQ summaries.
Human observational work also belongs to the target lane. Kannt et al. (2015) examined adipose NNMT expression and circulating 1-MNA across three human cohorts: 199 patients undergoing abdominal surgery, 60 people in a 12-week exercise programme, and 55 patients in a two-step bariatric-surgery programme. Patients with type 2 diabetes carried roughly twofold higher NNMT expression in omental and subcutaneous white adipose tissue than controls, and in that group plasma 1-MNA tracked adipose NNMT expression (women r = 0.59, men r = 0.61, both p < 0.001), while in insulin-resistant individuals adipose NNMT mRNA tracked insulin sensitivity inversely (r = 0.64, p < 0.001; replicated in a second cohort, n = 60, r = 0.78, p < 0.001). Association with a metabolic phenotype does not show that pharmacological inhibition improves that phenotype in people.
What Have 5-Amino-1MQ Studies Found?
Enzyme, adipocyte, and diet-induced-obesity models
The most direct early compound paper is Neelakantan et al. (2018). The authors tested 5-Amino-1MQ and related inhibitors in enzyme-selectivity experiments, differentiated adipocytes, and a diet-induced-obesity mouse model. In adipocytes the compound lowered intracellular 1-MNA while raising intracellular NAD+ and SAM and suppressing lipogenesis; in high-fat-diet mice, systemic treatment reduced body weight and white adipose mass, decreased adipocyte size, and lowered plasma total cholesterol without changing total food intake. The abstract states those directions but reports no quantitative outcome, so no effect size is quoted here.
The study supports three bounded claims: 5-Amino-1MQ inhibited NNMT in the reported assay; it changed selected metabolite readouts in the studied adipocytes; and it changed selected phenotypes in the mouse model. It does not establish a human weight-loss effect, a safe exposure range, or a protocol.
Aged-muscle and regeneration context
Neelakantan et al. (2019) dosed 24-month-old mice with a small-molecule NNMT inhibitor at 5 or 10 mg/kg for one week after a barium-chloride injury to the tibialis anterior, and at 10 mg/kg for three weeks in a second arm. Treated mice showed elevated muscle-stem-cell proliferation and fusion, nearly 2-fold greater regenerating myofiber cross-sectional area, and peak tibialis-anterior torque roughly 70% higher than saline controls. The abstract identifies the material as an NNMT inhibitor rather than establishing that every commercial 5-Amino-1MQ form is equivalent. The paper is therefore supporting inhibitor-class context unless the exact study material is reconciled from the full methods.
Diet, microbiome, and liver-metabolic models
Dimet-Wiley et al. (2022) combined a low-fat-diet switch with 5-amino-1-methylquinolinium — one of the few papers to name the compound explicitly in its abstract — in diet-induced-obese mice and analyzed cecal microbiome differences, reporting lower Erysipelatoclostridium and higher Lactobacillus relative abundance in treated animals; the abstract gives no quantitative result for those abundance shifts. Diet and inhibitor status were both experimental variables, so a microbiome or body-composition observation cannot be assigned to the compound without respecting the factorial design.
A newer direct study, Babula et al. (2024), dosed diet-induced-obese mice with 5A1MQ once daily for 28 days. Treatment dose-dependently limited body-weight and fat-mass gain, improved oral glucose tolerance and insulin sensitivity, and suppressed hyperinsulinaemia; liver histology showed attenuated hepatic steatosis and macrophage infiltration with correspondingly lower liver weight, size and triglyceride, and circulating alanine transaminase, aspartate transaminase and ketone bodies normalised. Plasma pharmacokinetics and tissue distribution were characterised separately after intravenous, oral and subcutaneous dosing, with distribution to adipose, muscle and liver after subcutaneous administration. It remains a mouse study; its endpoints are not human effect estimates.
What Have Other NNMT Interventions Shown?
These sources sit in the NNMT target lane, not the 5-Amino-1MQ compound lane. Each row keeps its figure attached to the exact intervention, model and species that produced it.
| Intervention | Model | Species | Endpoint | Reported result | Source |
|---|---|---|---|---|---|
| Glucose deprivation (no inhibitor) | 3T3-L1 adipocytes in culture | Mouse cell line | NNMT mRNA and protein | 2-fold increase; reproduced by phloretin and 2-deoxyglucose, blocked by mTOR activation | PMID 32112869 |
| Genetic Nnmt knockout | High-fat diet, males | Mouse | Insulin sensitivity vs glucose tolerance | Insulin sensitivity strongly improved; glucose tolerance not improved. The abstract reports no quantitative endpoint for either measure | PMID 30552109 |
| 1-methylnicotinamide plus SAH bound to NNMT | Ternary X-ray crystal structures | Monkey and mouse enzyme | Active-site geometry | Solved at 2.30 Å (monkey) and 1.88 Å (mouse); product trapped in the substrate pocket, consistent with feedback inhibition | PMID 28720493 |
| JBSNF-000028, a tricyclic NNMT inhibitor — not the methylquinolinium scaffold | Diet-induced obesity | Mouse | Plasma, liver and adipose 1-MNA; glucose tolerance; body weight | 1-MNA, glucose and body weight all reduced, but the glucose effect persisted in NNMT-knockout mice, so part of it is not attributable to NNMT. No quantitative result is given in the abstract | PMID 36104373 |
What Is Direct Compound Evidence?
Direct evidence requires the tested material to be 5-Amino-1MQ and the claim to match the model and endpoint. A paper on Nnmt knockdown supports the target. A paper on another inhibitor supports the inhibitor class or pathway. A 5-Amino-1MQ adipocyte study supports a cell-level statement. A 5-Amino-1MQ mouse study supports a model-specific animal statement. None can be relabeled as controlled human evidence.
| Evidence source | What it can support | What it cannot support by itself |
|---|---|---|
| Genetic Nnmt knockdown | NNMT target biology and pathway plausibility in the studied system | 5-Amino-1MQ potency, exposure, selectivity, safety, or effect |
| Biochemical inhibition assay | Inhibition under the reported enzyme-assay conditions | Cell entry, tissue exposure, organism outcome, or human effect |
| Adipocyte study | Cellular metabolite and target-linked observations in that system | Weight loss or safety in animals or people |
| Mouse DIO study | Model-specific body-composition, metabolic, liver, or exposure endpoints | A human weight-loss percentage, dose, safety profile, or treatment claim |
| Review article | Synthesis of target and inhibitor literature | New experimental proof |
Compound form is part of directness. If a paper used one counterion and a supplier provides another, the materials may differ in total molecular weight, elemental composition, solubility, and mass-spectrometric expectations. The article title “5-Amino-1MQ” is not enough to erase those distinctions.
What Does the Human Evidence Show?
The selected PubMed source set contains human observational evidence about NNMT and metabolic phenotypes, but no controlled human outcome study of 5-Amino-1MQ. That means the article can discuss target relevance and preclinical findings; it cannot supply a human efficacy estimate, adverse-event rate, dose, treatment duration, or clinical protocol.
This gap is especially important because online pages frequently convert mouse body-composition findings into a “fat-loss” promise. Mouse diet models differ from human obesity in physiology, exposure, comorbidity, behavior, and outcome measurement. Even a well-controlled animal study is a preclinical result, not a substitute for a randomized human trial.
Regulatory status: 5-Amino-1MQ has no FDA, EMA, NMPA or other regulatory approval anywhere globally, for any indication. It is not a pharmaceutical, a dietary supplement, or a weight-loss product. The 2024 NNMT target review by Sun et al. records that clinical trials focusing on NNMT had not been documented as of writing; that review and the Park et al. (2024) survey of NNMT across liver, obesity, diabetes, cardiovascular and other disease contexts are both narrative syntheses that report no quantitative endpoint of their own.
Evidence boundary: This guide does not provide administration, dose, cycle, stack, route, or self-experimentation guidance. Those details would imply a human-use framework that the selected evidence does not establish and that is outside the intended use of Apex research reagents.
What Does Research Grade Mean for 5-Amino-1MQ?
“Research grade” should describe documentation and intended use, not therapeutic quality. A reproducible material record should identify the supplier-defined chemical form, counterion or salt when applicable, batch identifier, test date, identity method, expected analyte or adduct, chromatographic method, purity calculation, and acceptance criteria.
HPLC and mass spectrometry answer different questions. HPLC can support chromatographic purity under the stated method and detection conditions. Mass spectrometry can support the mass identity of the detected species. Neither method alone proves chemical form, comprehensive impurity identity, target inhibition, biological activity, sterility, safety, or efficacy.
The Apex COA-reading guide and HPLC explainer provide a general analytical framework, even though 5-Amino-1MQ is not a peptide. Researchers evaluating the current material can review the 5-Amino-1MQ product record and the lot-specific COA archive. Before deployment, the current product record and COA should be checked for an explicit, internally consistent statement of chemical form, counterion, expected mass, and tested analyte.
Frequently Asked Questions
Is 5-Amino-1MQ a peptide?
No. 5-Amino-1MQ is a small organic molecule, 5-amino-1-methylquinolinium. The “amino” in its name describes a chemical functional group; it does not make the compound an amino-acid chain or peptide.
What enzyme does 5-Amino-1MQ inhibit?
It is studied as an inhibitor of nicotinamide N-methyltransferase, or NNMT. NNMT transfers a methyl group from SAM to nicotinamide, producing 1-methylnicotinamide and SAH.
Does 5-Amino-1MQ increase NAD+?
Cell and mouse studies report NAD+-linked metabolic observations under specific conditions, and genetic NNMT knockdown studies provide target context. That does not establish that every material, tissue, species, or person will show the same result.
Does 5-Amino-1MQ cause weight loss?
Several mouse studies report body-composition and metabolic endpoints in diet-induced-obesity models. The selected source set does not contain a controlled human outcome study that establishes human weight loss, efficacy, or safety.
Is genetic NNMT knockdown evidence the same as 5-Amino-1MQ evidence?
No. Genetic knockdown supports the biological target, while a small molecule has its own potency, selectivity, exposure, distribution, and off-target questions. The two evidence lanes are related but not interchangeable.
What should a 5-Amino-1MQ COA show?
A useful record should identify the exact chemical form and counterion, batch, test date, expected analyte or adduct, identity method, chromatographic method, purity basis, and acceptance criteria. HPLC purity and mass identity should remain separate claims.
Is 5-Amino-1MQ approved by the FDA?
No. 5-Amino-1MQ has no FDA, EMA, NMPA or other regulatory approval anywhere globally, for any indication. It is not a medicine, a dietary supplement or a weight-loss product, and published NNMT target reviews record no documented clinical trial programme against the enzyme.
References
- Riederer et al. (2009). Adipose tissue as a source of NNMT and homocysteine. PMID 18996527.
- Kraus et al. (2014). Nnmt knockdown in diet-induced obesity. PMID 24717514.
- Kannt et al. (2015). Human adipose NNMT expression, 1-MNA, and insulin resistance. PMID 25596852.
- Pissios (2017). NNMT beyond vitamin-B3 clearance. PMID 28291578.
- Neelakantan et al. (2017). Structure-activity relationship for small-molecule NNMT inhibitors. PMID 28548833.
- Neelakantan et al. (2018). Selective membrane-permeable NNMT inhibitors in cells and diet-induced-obese mice. PMID 29155147.
- Neelakantan et al. (2019). Small-molecule NNMT inhibition in aged-muscle regeneration models. PMID 30753815.
- Dimet-Wiley et al. (2022). Reduced-calorie diet, 5-Amino-1MQ, and the microbiome in DIO mice. PMID 35013352.
- Sun et al. (2024). Nicotinamide N-methyltransferase (NNMT): a novel therapeutic target for metabolic syndrome. PMID 38919254.
- Babula et al. (2024). 5A1MQ in obesity-related metabolic dysfunction in mice. PMID 39161060.
- Park et al. (2024). Exploring NNMT: from metabolic pathways to therapeutic targets. PMID 39604638.
Research Use Disclaimer
This article is educational research context, not medical advice. Apex Laboratory materials are sold strictly for in-vitro research use. They are not for human or veterinary use, are not intended to diagnose, treat, cure, or prevent disease, and are not represented as pharmaceutical products, supplements, or weight-loss products.
