5-Amino-1MQ
5-Amino-1-methylquinolinium · NNMT inhibitor · Research-grade reference material
Identity
- Molecular formula
- C10H11IN2 (iodide salt)
- Molecular weight
- ~286.11 g/mol (iodide salt)
- CAS number
- Inconsistent across chemical databases — confirm against COA and PubChem CID 950107, not CAS alone
Research Background
5-Amino-1MQ is studied as a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme that methylates nicotinamide using S-adenosylmethionine (SAM) as the methyl donor. NNMT activity sits at the intersection of cellular methylation capacity and NAD+ salvage pathway biology, and its role in adipose tissue metabolism has made it a target of interest in metabolic research (Roberti, Fernández, and Fraga).
Lab-tested research material
Mechanism
By inhibiting NNMT, 5-Amino-1MQ is studied for preserving intracellular SAM and nicotinamide pools that would otherwise be consumed by the methylation reaction, shifting adipose tissue toward greater energy expenditure. In diet-induced obese mice, an NNMT inhibitor of this class reduced body weight and fat mass and increased energy expenditure without changing food intake, identifying NNMT as a potential metabolic target for obesity research.
NNMT catalyses the methylation of nicotinamide using S-adenosylmethionine (SAM) as methyl donor, producing 1-methylnicotinamide and SAH. It therefore sits at the intersection of two pathways: it consumes nicotinamide (a NAD⁺ precursor) and it consumes SAM (the cell's principal methyl donor). Inhibiting it is a way to probe both simultaneously. All findings below derive from cell-culture and rodent models. There are no human data.
NNMT inhibition. Blocks the methylation drain on nicotinamide and SAM, with reported downstream effects on NAD⁺ salvage and methyl-donor availability.
Adipocyte models. In 3T3-L1 preadipocyte culture, reported to inhibit differentiation and reduce lipid accumulation across a micromolar concentration range.
Diet-induced obesity models. Neelakantan et al. (2019) reported reduced weight gain, decreased fat mass and smaller adipocytes in high-fat-diet mice without differences in food intake — mechanistically distinct from appetite-mediated compounds.
Metabolic parameters. Improved glucose tolerance and insulin sensitivity reported in obese rodent models.
Tissue context. NNMT is highly expressed in white adipose tissue and liver, and elevated expression has been observed in obese adipose tissue — the rationale for adipose as the primary research target.
Proposed mechanism investigated in preclinical (in-vitro / rodent) models. Schematic only; not a claim of established human effect.
State of the Evidence
Research Evidence: based on 1 study cited, most recent 2022. Source: “NNMT Inhibitor in Diet-Induced Obese Mice: Effects on Body Weight, Body Fat, and Energy Expenditure,” Scientific Reports, 2022 (PMID 35013352). Research in diet-induced obese mice found that NNMT inhibition with a small-molecule inhibitor related to 5-amino-1MQ significantly reduced body weight and fat mass and increased energy expenditure, identifying NNMT as a potential metabolic target for obesity. Whether this effect occurs in humans has not been studied.
What the Literature Supports — and What It Doesn’t
The position here is simple and should not be overstated: 5-Amino-1MQ is a preclinical research tool. Its mechanism is coherent and its rodent data are internally consistent, but the human column of the evidence table is empty.
Evidence at a glance
No published human clinical trials exist. Every reported effect on body composition, glucose tolerance and adipocyte biology comes from mouse or cell studies.
Metabolic targets have a poor translation record. Multiple prior anti-obesity mechanisms succeeded in rodents and failed in human trials; rodent adipose findings are weak predictors of human outcomes.
The compound belongs to a traceable medicinal-chemistry lineage of methylquinolinium NNMT inhibitors, which is a genuine strength for research provenance.
Reported quantitative effects vary substantially between secondary sources; rely on the primary publications rather than aggregated figures when designing experiments.
Appropriate characterization: a selective small-molecule NNMT inhibitor useful as a research tool for probing methylation flux, NAD⁺ salvage and adipocyte metabolism — with no human evidence and no established translational relevance.
Regulatory & status notes
Selected references
- 1. Kraus D, et al. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature. 2014. (foundational NNMT target validation)
- 2. 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 / Cell Chem Biol. 2019.
- 3. Pharmacokinetics and tissue distribution characterization of 5A1MQ in mice. 2024.
Safety Information
Research-use compound with limited human data. No established clinical contraindications. This is an investigational compound with limited human data and has not been evaluated by the FDA for safety in this context. Consult a qualified clinician. For research and educational purposes only, not for human or veterinary use.
Related Compounds
For research and educational purposes only. Not for human or veterinary use.