D tier · weak
The mouse data are real, internally consistent and replicated across at least three publications from the same group, but there is not a single human study of any kind, the pivotal experiments used injected doses in the 34-40 mg/kg/day range while the product is sold as oral capsules, and the target enzyme has substantial roles in cancer biology that no one has mapped for chronic systemic inhibition in people.
5-amino-1mq
5-Amino-1MQ is a small-molecule, membrane-permeable inhibitor of nicotinamide N-methyltransferase (NNMT) — not a peptide, despite being sold alongside them. In diet-induced obese mice it reduced body weight and white adipose mass without changing food intake, but no human pharmacokinetic, safety or efficacy study has been published.
// we supply this one
available as a research reagent
≥ 98% HPLC · research solution · batch certificate published. Grade D above is our own and is not adjusted because we stock it.
the explanation
5-Amino-1MQ is a small chemical, not a peptide, that blocks an enzyme in fat cells and made obese mice lose fat without eating less. That result is genuine and has been repeated — but only in mice, only by injection, and never once in a person.
regulatory status
Not approved as a drug in any jurisdiction and not an authorised dietary ingredient
5-Amino-1MQ is catalogued and supplied by chemical vendors as a research-grade NNMT inhibitor with no human therapeutic authorisation, no investigational-new-drug programme in the public record, and no appearance on FDA's Category 1 or Category 2 bulk drug substance lists — it is an unapproved synthetic small molecule being sold in the peptide market despite not being a peptide.
how it works · proposed mechanism
5-Amino-1MQ works by blocking a single methyl-transfer reaction, and the interesting claim is that this rebalances two central metabolic currencies at once.
NNMT inhibition in adipocytes
NNMT methylates nicotinamide to 1-methylnicotinamide, consuming S-adenosylmethionine and diverting nicotinamide away from NAD+ salvage. Inhibiting it lowers intracellular 1-methylnicotinamide and raises both NAD+ and SAM in cultured adipocytes.
Lipogenesis suppression
The raised NAD+ and SAM flux is accompanied by suppressed lipogenesis in cultured adipocytes and, in vivo, by smaller adipocytes and reduced white adipose tissue mass. The proposed mechanism is metabolic and epigenetic rather than appetite-mediated.
Food intake is unchanged
Across the mouse studies, treated animals did not eat less than controls, so the weight and fat loss is attributed to altered energy handling rather than reduced consumption. This distinguishes the mechanism from incretin-based agents.
Selectivity, verified in vitro
Methylquinolinium analogues with primary amine substitutions showed high membrane permeability in artificial-membrane and Caco-2 assays and did not inhibit related SAM-dependent methyltransferases or NAD+ salvage pathway enzymes. Selectivity was demonstrated against a defined panel, not against the proteome.
what’s reported
evidence shape
6 sourcesThe composition of the cited literature by study type. This describes the shape of the evidence, not its quality — and it does not by itself set the grade.
⚠ the catch
The entire evidence base is mice injected subcutaneously with 34-40 mg/kg/day, while the consumer product is an oral capsule at a fraction of the allometric equivalent — the route, the exposure and the species are all unbridged, and nothing has ever been measured in a human. Separately, NNMT is not an adipose-specific enzyme: its overexpression drives invasion and metastasis in clear cell renal cell carcinoma through a PI3K/Akt/SP1/MMP-2 pathway, so chronic systemic inhibition of a node this central to methylation and NAD+ metabolism has consequences nobody has characterised in people.
key published findings
- Mouse study (Neelakantan 2018, Biochemical Pharmacology, diet-induced obese mice, 5-amino-1MQ at 20 mg/kg per subcutaneous injection three times daily, ~34 mg/kg/day, 11 days): body weight fell 2.0 ± 0.6 g (~5.1%) in treated animals versus a 0.6 ± 0.4 g gain (~1.4%) in controls; epididymal white adipose tissue mass decreased ~35%; adipocyte size decreased >30% with >40% reduction in adipocyte volume; total cholesterol was ~30% lower; food intake was unchanged and no observable adverse effects were reported.
- Mouse study (Sampson 2021, Scientific Reports, DIO mice, 5-amino-1MQ ~40 mg/kg/day by daily injection plus a reduced-calorie diet, 7 weeks): cumulative body weight loss of 6.3 g in treated animals versus 2.9 g in vehicle controls, with fat mass falling approximately 29.3% versus 2.9% — combining inhibition with caloric restriction normalised body composition toward lean-diet controls.
- In vitro (Neelakantan 2018): methylquinolinium analogues with primary amine substitutions showed high permeability in parallel artificial membrane and Caco-2 assays, did not inhibit related SAM-dependent methyltransferases or NAD+ salvage enzymes, reduced intracellular 1-methylnicotinamide, and raised intracellular NAD+ and S-adenosylmethionine while suppressing lipogenesis in cultured adipocytes.
- Mouse study (Dimet-Wiley 2022, Scientific Reports): NNMT inhibition combined with dietary restriction produced greater weight reduction than diet alone and established a distinct gut microbiome signature, with decreased Erysipelatoclostridium and increased Lactobacillus relative abundance.
- Cancer biology (Tang 2011, Carcinogenesis): NNMT overexpression markedly enhanced invasive capacity in clear cell renal cell carcinoma cells via a PI3K/Akt/SP1/MMP-2 pathway, and NNMT knockdown reduced tumour growth and metastasis in vivo — establishing that the target enzyme sits in a pathway with substantial oncological consequences in either direction.
- Translational status (Puleo 2026, Trends in Pharmacological Sciences): a review of 'emerging opportunities for NNMT inhibitor clinical translation' assesses medicinal-chemistry progress and therapeutic promise — the framing itself confirms that no NNMT inhibitor, 5-Amino-1MQ included, has reached clinical validation.
limitations of the evidence
- There are zero human studies of 5-Amino-1MQ — no pharmacokinetics, no dose-finding, no safety cohort, no efficacy trial — so nothing about human exposure, clearance or tolerability is known.
- The pivotal in vivo data used subcutaneous injection; oral bioavailability of a permanently charged quaternary quinolinium cation in humans has not been established, which directly undermines the capsule products on the market.
- The mouse work originates predominantly from a single research group and set of collaborators, so independent replication of the in vivo body-composition effect is limited.
- Selectivity was demonstrated against a defined panel of structurally related methyltransferases and NAD+ salvage enzymes, not against broad off-target screening, and NNMT itself is expressed well beyond adipose tissue including liver, kidney and multiple tumour types.
documented safety signals
- No human safety data of any kind exist for this compound.
- NNMT is causally implicated in cancer cell invasion and metastasis, with overexpression driving MMP-2 activation via PI3K/Akt/SP1 in renal carcinoma — a target with pleiotropic roles in tumour biology whose chronic pharmacological inhibition in humans is uncharacterised.
- The enzyme sits at the junction of NAD+ salvage and S-adenosylmethionine-dependent methylation, so sustained inhibition would be expected to perturb global methylation and one-carbon metabolism in tissues beyond adipose; no toxicology study addressing this has been published.
- Products are marketed within the peptide category despite the compound being a synthetic small-molecule quinolinium salt, indicating a supply chain with poor characterisation of what is actually being sold.
- Reported absence of 'observable adverse effects' in mice refers to an 11-day study in a single species with no formal toxicology endpoints.
identity
| full name | 5-amino-1-methylquinolinium (commonly supplied as the iodide salt) |
| category | Metabolic |
| modality | small molecule |
| formula | C10H11IN2 (iodide salt); C10H11N2+ cation |
| molar mass | 286.11 g/mol |
| cas | 42464-96-0 |
laboratory handling
| storage | Solid material is stored at -20 °C, desiccated and protected from light, in a tightly sealed container; solutions in aqueous buffer or DMSO are aliquoted and stored at -20 °C to -80 °C for laboratory use and protected from light, with repeated freeze-thaw cycles avoided. |
| solubility | As a quaternary quinolinium salt it is water-soluble and dissolves readily in aqueous buffers and saline; DMSO is used for concentrated laboratory stock solutions, which are then diluted into aqueous media. |
| co-studied with | The one combination with supporting data is not another compound at all: in mice, pairing NNMT inhibition with a reduced-calorie diet produced substantially greater fat-mass reduction than either intervention alone. |
Handling information describes laboratory practice for a research reagent. It is not a preparation guide for use in humans.
the receipts
6 citedSigma-Aldrich / Merck KGaA · 2024 · official
Carcinogenesis · 2011 · peer-reviewed
Trends in Pharmacological Sciences · 2026 · review
Biochemical Pharmacology · 2018 · preclinical
Scientific Reports · 2021 · preclinical
Scientific Reports · 2022 · preclinical
others in Metabolic