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5-Amino-1-methylquinolinium (5A1MQ)
A grey-market research chemical with NO human trials of any kind — every result below is from mice or cells. 5-Amino-1MQ is a small-molecule inhibitor of the enzyme nicotinamide N-methyltransferase (NNMT), not a peptide (it's grouped here with research peptides by category convention). In diet-induced-obese mice, an NNMT inhibitor limited fat-mass gain and improved glucose tolerance — a genuinely interesting preclinical signal. But it has never been tested in a single human, it is not an approved drug or a regulated dietary supplement, and it is sold online with no quality control. Its long-term safety and its effects on human NAD+/methylation metabolism are completely unknown. This entry exists to inform, not to recommend.
Research peptide — not a dietary supplement
5-Amino-1MQ is a research compound, not a regulated dietary supplement. It is typically administered by injection and sold “for research use only.” The evidence below is largely preclinical (animal and in-vitro) or early-stage, so no evidence score is assigned. This page is provided for transparency and education — it is not a recommendation to use. Consult a qualified healthcare provider, and be aware that purity, dosing, and legal status vary by jurisdiction.
What the evidence says
Most 5-Amino-1MQ studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality studies published 2014–2025.
Based on 7 studies
Confidence
Low confidenceBy outcome
An intriguing preclinical NNMT-inhibitor story with consistent fat-loss and glucose benefits in obese mice, but zero human trials of any kind — no safety, no pharmacokinetics, nothing.
5-Amino-1MQ (5-amino-1-methylquinolinium, '5A1MQ') is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT) — despite being grouped here with research peptides, it is a synthetic small molecule, not a peptide.
NNMT is a cytosolic enzyme that methylates nicotinamide (vitamin B3) using S-adenosylmethionine (SAM) as the methyl donor, producing 1-methylnicotinamide (MNAM) and S-adenosylhomocysteine.
Because nicotinamide is a precursor of NAD+ and SAM is the cell's universal methyl donor, NNMT sits at the intersection of NAD+ metabolism, one-carbon/methylation balance, and polyamine flux.
The therapeutic hypothesis comes from mouse genetics: a 2014 Nature paper (Kraus et al.) showed that knocking down Nnmt in white adipose tissue and liver protected mice from diet-induced obesity by raising cellular energy expenditure, increasing tissue SAM and NAD+, and driving polyamine flux.
That made NNMT an attractive pharmacological target, and 5-amino-1MQ is one of the chemical-probe NNMT inhibitors used to test the idea in vivo.
The most directly relevant study (Babula et al., 2024, Diabetes Obes Metab) dosed diet-induced-obese (DIO) mice with 5A1MQ once daily for 28 days and reported dose-dependent reductions in body-weight and fat-mass gain, improved oral glucose tolerance and insulin sensitivity, lower hyperinsulinaemia, and attenuated hepatic steatosis — alongside a pharmacokinetic profile showing systemic exposure and distribution to adipose, muscle, and liver.
A related study combined 5-amino-1-methylquinolinium with a low-fat-diet switch and saw dramatic adiposity/weight loss in DIO mice plus a distinct gut microbiome. Other NNMT-inhibitor chemotypes (e.g.
JBSNF-000028, AMO-NAM) reproduce metabolic and cardiac benefits in mouse models, and reviews frame NNMT as a candidate target for metabolic syndrome. Here is the honest, load-bearing caveat: ALL of this is preclinical.
There has never been a published human trial of 5-amino-1MQ — not a phase-I safety study, not a pharmacokinetic study, nothing.
It is not approved by any regulator, it is not a lawful dietary-supplement ingredient, and the material sold online is an unregulated grey-market research chemical with no guarantee of identity, purity, or sterility.
Manipulating NNMT activity also perturbs NAD+ and cellular methylation — pathways whose long-term modulation in humans is unstudied, and where unintended effects (on methylation-dependent gene regulation, polyamine balance, or downstream metabolism) cannot be ruled out.
The evidence here is therefore UNSCORED: an intriguing mouse-and-cell story with zero human data, sandboxed out of all goal- and stack-based recommendations.
5-Amino-1MQ is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), the enzyme that methylates nicotinamide using SAM to form 1-methylnicotinamide. Inhibiting it is proposed to spare nicotinamide (a NAD+ precursor) and SAM. Demonstrated only in cell and mouse systems — never measured in humans.
In mice, NNMT knockdown raised adipose SAM and NAD+ levels, increased polyamine flux, and augmented cellular energy expenditure. This is the proposed route from enzyme inhibition to a leaner metabolic phenotype — established in rodent models, with no human confirmation.
By raising energy expenditure in white adipose tissue and liver, NNMT inhibition limited diet-induced fat-mass gain and improved insulin sensitivity in obese mice. Whether any of this translates to humans is entirely unknown — there are no human data.
How 5-Amino-1MQ works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Avoid — there are no human trials, no approved use, and no quality-controlled product. The mouse evidence does not justify human self-experimentation.
Avoid — interactions on the NAD+/methylation axis are unstudied and unpredictable.
Avoid entirely — completely unstudied.
5-Amino-1MQ acts on the NNMT/NAD+/methylation axis. Combining it with NAD+ precursors (NR, NMN, niacin, nicotinamide) has never been studied in humans; metabolic interactions are theoretically plausible and unpredictable.
There are no human drug-interaction data of any kind. Effects on methylation-dependent metabolism are unknown, so interactions cannot be predicted.
Tip: No human has ever been studied — the side-effect profile in people is genuinely unknown. This is itself the warning.
Tip: NNMT inhibition perturbs cellular methylation and NAD+ balance; long-term human consequences are unstudied.
Tip: Grey-market material has no identity/purity/sterility guarantees; contaminants are possible.
The current evidence for 5-Amino-1MQ is insufficient to assign an evidence score, based on 7 indexed studies. A grey-market research chemical with NO human trials of any kind — every result below is from mice or cells. 5-Amino-1MQ is a small-molecule inhibitor of the enzyme nicotinamide N-methyltransferase (NNMT), not a peptide (it's grouped here with research peptides by category convention). In diet-induced-obese mice, an NNMT inhibitor limited fat-mass gain and improved glucose tolerance — a genuinely interesting preclinical signal. But it has never been tested in a single human, it is not an approved drug or a regulated dietary supplement, and it is sold online with no quality control. Its long-term safety and its effects on human NAD+/methylation metabolism are completely unknown. This entry exists to inform, not to recommend. Representative study: PMID 24717514.
The commonly studied dose of 5-Amino-1MQ is No legitimate or recommended dose — 5-amino-1MQ is an unapproved grey-market research chemical with no human dosing data and no quality control. We do NOT provide a dosing protocol. The only published dosing is in mice (once-daily for 28 days in diet-induced-obese animals), which does not translate to a human dose.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
Timing is flexible for 5-Amino-1MQ — consistent daily use matters more than the time of day. There is no validated human dosing schedule because the compound has never been tested in humans.
5-Amino-1MQ should be used with caution — talk to a healthcare provider before taking it. The most commonly reported side effects are unknown human side-effect profile, unknown effects on NAD+/methylation/polyamine metabolism, harm from an unregulated, impure product. Use caution if any of these apply to you: Not an approved medicine and not a regulated dietary supplement — unapproved grey-market research chemical; do not self-source; No human safety data exists — every safety conclusion would be an extrapolation from mice; Pregnancy and breastfeeding (entirely unstudied).
Semaglutide
Mostly mechanism / observationalAn FDA-approved GLP-1 receptor agonist (Ozempic/Rybelsus for type 2 diabetes, Wegovy for chronic weight management) with genuinely strong, large-RCT evidence for glycemic control and substantial weight loss, plus a cardiovascular-outcomes benefit. Honest appraisal: this is a real prescription medicine with real efficacy AND real risks — a boxed warning for thyroid C-cell tumors, pancreatitis and gallbladder risk, very common GI side effects, and growing concern about grey-market/compounded versions. It is included here for reference only, not as a supplement and not auto-recommended.
Tirzepatide
Mostly mechanism / observationalAn FDA-approved prescription medication (Mounjaro for type 2 diabetes, Zepbound for obesity and obstructive sleep apnea), not a dietary supplement. Honest appraisal: in head-to-head phase-3 trials it is the most effective approved weight-loss drug to date — up to ~21% body-weight loss over 72 weeks and superior to semaglutide — but it is a real medicine with real risks: a boxed warning for thyroid C-cell tumors, common GI side effects, and pancreatitis/gallbladder signals. Do not source or use it outside a prescription.
Liraglutide
Mostly mechanism / observationalAn FDA-approved, once-daily GLP-1 receptor agonist (Victoza for type 2 diabetes, Saxenda for chronic weight management). Honest appraisal: a real prescription medicine with genuinely strong large-RCT evidence for glycemic control and moderate weight loss, plus a cardiovascular-outcomes benefit (LEADER). It also carries real risks — a boxed warning for thyroid C-cell tumors, pancreatitis and gallbladder risk, very common GI side effects, and lean-mass loss with weight loss. Included here for reference only; it is NOT a supplement and is not auto-recommended.
Orforglipron
Mostly mechanism / observationalAn investigational ORAL, non-peptide small-molecule GLP-1 receptor agonist for obesity and type 2 diabetes — the headline is the convenience of a once-daily pill (no injection, no cold chain, no food/water restrictions) delivering GLP-1-class glycemic and weight benefit. Honest appraisal: the phase-2 data are strong and the first phase-3 read-outs (ATTAIN/ACHIEVE) are promising, but it is INVESTIGATIONAL and not yet approved as a general weight-loss medicine, has the full GLP-1-class side-effect burden (very common dose-dependent nausea/vomiting/diarrhea, higher discontinuation than injectables in some comparisons), and the expected thyroid C-cell class warning and long-term outcomes are unsettled. It is NOT a dietary supplement; listed here for reference only.
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Reviewed by Dr. Baher Al Hakim · Last reviewed June 2026 · evidence from 7 studies · how we score · editorial policy
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
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