Research profile · Small molecule
5-amino-1MQ
Also known as 5-amino-1-methylquinolinium
Overview
A small-molecule enzyme inhibitor, not a peptide, with no human data of any kind.
- Category
- Small molecule
- Highest evidence level identified
- Animal evidence
- Last scientifically reviewed
- 20 August 2026
- Last regulatory review
- 20 August 2026
Mechanism under investigation
Despite being marketed and retailed alongside peptides, 5-amino-1MQ is a small molecule and not a peptide: it is a permanently charged quinolinium cation with no peptide bond or amino-acid residue. It is a small-molecule inhibitor of nicotinamide N-methyltransferase, an enzyme that transfers a methyl group from S-adenosylmethionine to nicotinamide. The proposed mechanism is that in adipose tissue this enzyme acts as a methyl sink, and that inhibiting it preserves methyl-donor and cofactor pools and shifts metabolism away from fat storage. The original investigators frame this tentatively, and none of it has been demonstrated in a human being.
Research areas
- Metabolic research
- Enzyme inhibition
These are fields in which the compound has been investigated. Listing a field is not a statement that anything was demonstrated within it.
Current evidence
In-vitro evidence
Cells, tissues or biochemical systems outside a living organism.
Real and reasonably solid. Structure-activity work identified the chemical scaffold as an inhibitor, and in cultured adipocytes the inhibitors reduced the enzyme’s product, increased cofactor levels and suppressed fat synthesis. Potency is in the micromolar range, which is weak by modern drug-discovery standards.
Animal evidence
Studies in living non-human animals.
Real, consistent, and entirely rodent. In diet-induced obese mice, enzyme inhibition reduced body weight and white adipose mass and decreased adipocyte size without changing food intake. A nuance worth noting: the foundational obesity paper refers throughout to a class of inhibitors rather than naming this specific compound, which is named explicitly only in follow-on papers.
- Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice (opens doi.org in a new tab)
- Combined nicotinamide N-methyltransferase inhibition and reduced-calorie diet normalizes body composition in obese mice (opens doi.org in a new tab)
Human observational evidence
Studies observing people without assigning an intervention.
None. Every record returned by literature searches is a review, a cell-culture study or a rodent study. No cohort, no case series, no case report, and no human pharmacokinetic data of any kind.
Clinical-trial evidence
Studies assigning an intervention to human participants.
None registered anywhere. Verified across three registries, with a deliberately broader control query confirming the search machinery worked — so the zero results are real rather than an artefact. The two records that surfaced measure the target enzyme only as a biomarker and administer no inhibitor.
Study limitations
- Rodent-only evidence in vivo, largely in diet-induced obese mice — a model that has produced many obesity findings which failed to translate to humans.
- No human pharmacokinetics whatsoever. As a permanently charged molecule, its absorption and distribution cannot safely be inferred from mouse data.
- Almost all in vivo work originates from one laboratory holding the relevant patents, so independent replication is minimal.
- Micromolar potency leaves meaningful target engagement in humans an open question.
- It is routinely sold and discussed as a peptide. It is not one, and that misdescription travels with most of the surrounding claims.
UK regulatory context
Experimental — not authorised for human use in the UK
A compound appearing in research literature that holds no UK authorisation for human use in any indication.
Source: The Human Medicines Regulations 2012, regulation 46 — prohibition on sale or supply of an unauthorised medicinal product (opens legislation.gov.uk in a new tab) (legislation.gov.uk)
Regulatory classification is jurisdiction-specific. A compound authorised elsewhere is not thereby authorised in the UK, and a supplier’s description of a substance does not determine how it is classified in law. See safety and regulation for the framework and the authoritative sources.
Safety and interpretation
Human safety data are absent entirely: no trials, no pharmacokinetic studies, no surveillance covering it and no published case reports. The frequently repeated claim that it is well tolerated derives solely from a mouse study observing no obvious adverse effects over short dosing, which is a statement about mice. The target enzyme is expressed in the liver and other tissues beyond adipose, and the consequences of sustained systemic inhibition in humans are entirely uncharacterised.
References
- Regulator or official body
legislation.gov.uk, 2012 · accessed 20 August 2026
No UK marketing authorisation and no UK novel food authorisation, so there is no lawful route to sale as a food or supplement in Great Britain either.
- Primary researchCitation not yet verified
Neelakantan H, et al.. Journal of Medicinal Chemistry, 2017 · doi:10.1021/acs.jmedchem.7b00389
Bibliographic record and abstract confirmed via Europe PMC; the publisher page blocks automated access.
- Primary researchCitation not yet verified
Neelakantan H, et al.. Biochemical Pharmacology, 2018 · doi:10.1016/j.bcp.2017.11.007
The foundational obesity paper. Refers to a class of inhibitors rather than naming this compound specifically. Bibliographic record confirmed via Europe PMC.
- Primary researchCitation not yet verified
Sampson CM, et al.. Scientific Reports, 2021 · doi:10.1038/s41598-021-85051-6
Bibliographic record confirmed via Europe PMC.
- Reporting standard
US National Library of Medicine · accessed 20 August 2026
Confirms this is a small molecule rather than a peptide.