5-Amino-1MQ: The Complete Guide
It is sold alongside peptides, but it isn't one. It has a genuinely interesting mechanism and not a single published human trial. Here is what the research actually establishes.
This guide summarizes the published preclinical research on 5-Amino-1MQ and nicotinamide N-methyltransferase inhibition. It is educational only and not a substitute for advice from a qualified healthcare professional. Sources are listed at the end.
Start with the thing almost no page selling this compound says clearly: 5-Amino-1MQ is not a peptide. It has no amino acids in it. It is a small synthetic molecule — a quinolinium ring with a methyl group and an amino group attached — that happens to be sold through the same channels as peptides and discussed in the same conversations.
That distinction is not pedantry. It changes how the compound is absorbed, how it is stored, how it behaves in the body, and how it should be evaluated. If you want a sense of how actual peptides work by comparison, our guide to how peptides work in the body covers that ground.
What 5-Amino-1MQ does have is a clean, specific mechanism and an unusually striking set of mouse results. What it does not have is a single published human trial. This page covers both halves honestly.
What 5-Amino-1MQ Is
The full chemical name is 5-amino-1-methylquinolinium. It is a permanently charged molecule — the nitrogen in its ring carries a positive charge — which means it is always supplied as a salt paired with a negative ion, most commonly iodide, sometimes chloride.
It was not discovered in the body or isolated from tissue. It was designed. A group at the University of Texas Medical Branch screened a series of quinolinium compounds looking for something that would block a specific enzyme, and this one came out of that screen as the most useful combination of potency, selectivity and ability to cross cell membranes.
The salt-weight problem worth knowing about
Because the compound is sold as a salt, the number on the label may not be the amount of active molecule inside. The iodide counter-ion is heavy: roughly 1.89 mg of the iodide salt contains about 1 mg of 5-Amino-1MQ itself. A vial or capsule labelled by salt weight therefore delivers a little over half what a vial labelled by free-base weight would. Reputable suppliers state which basis they are quoting. Many do not. If precision matters to you, ask.
How It Works
5-Amino-1MQ blocks one enzyme: nicotinamide N-methyltransferase, or NNMT. Understanding why that might matter takes one short detour into cellular bookkeeping.
Your cells run two economies that both pass through the same enzyme. The first is the NAD+ salvage pathway — nicotinamide, a form of vitamin B3, gets recycled back into NAD+, the cofactor that powers energy metabolism and sirtuin signalling. The second is the methyl economy — S-adenosylmethionine, or SAM, is the cell's universal methyl donor, used for everything from gene regulation to building polyamines.
NNMT sits between them. It takes nicotinamide, attaches a methyl group borrowed from SAM, and produces 1-methylnicotinamide as waste. Every time it fires, it spends a unit of nicotinamide that could have become NAD+ and a unit of SAM that could have done something else. Block NNMT and both substrates stay in circulation.
Simplified from the published NNMT literature. All of the downstream effects shown have been measured in cells and rodents, not in people.
Selective for NNMT
In enzyme assays it inhibits NNMT at low micromolar concentrations without hitting structurally similar methyltransferases or the NAD+ salvage enzymes themselves.
Suppresses Lipogenesis
In cultured fat cells, blocking NNMT reduced the building of new fat, lowered 1-methylnicotinamide, and raised both NAD+ and SAM.
Raises Polyamine Flux
More available SAM feeds polyamine synthesis and turnover — an energetically expensive cycle that increases oxygen consumption in fat cells.
Membrane Permeable
Unlike most peptides, it crosses cell membranes readily in laboratory assays — the property the original screen was designed to find.
What the Research Shows
The fat story
The groundwork came in 2014, when a Harvard group published in Nature that NNMT is elevated in the fat tissue and liver of obese and diabetic mice, and that knocking it down protected animals against diet-induced obesity. Crucially, the protection came from increased energy expenditure, not reduced eating. That paper made NNMT a target; it did not test 5-Amino-1MQ.
The 2018 follow-up did. Diet-induced obese mice given the compound lost body weight and white fat mass, had smaller fat cells and lower plasma cholesterol — with no change in food intake and no adverse effects observed within the study window. It was the first demonstration that a drug, rather than a genetic manipulation, could reproduce the effect.
The muscle story
The finding that put this compound on the longevity radar came a year later. NNMT accumulates in skeletal muscle with age while NAD+ falls and muscle stem cells become sluggish. Treating 24-month-old mice with an NNMT inhibitor reactivated those stem cells, produced markedly larger regenerating muscle fibres after injury, and increased peak muscle torque by roughly 70% compared with untreated controls.
Later work found that combining NNMT inhibition with exercise improved endurance and grip strength in aged mice beyond what exercise did alone. That is a more interesting result than it first appears, because it suggests the two are not redundant.
The honest limitation
Every result above is a mouse or a cell culture dish. Not one of them involved a person. And the picture is not uniformly clean even within the animal literature — one study of genetic NNMT loss found improved insulin sensitivity but no change in glucose tolerance, which is a more modest result than the headline version suggests.
The Human Evidence Gap
This deserves its own section, because it is the single most important fact about 5-Amino-1MQ and it is routinely soft-pedalled.
There are no published human clinical trials of 5-Amino-1MQ. Not a completed phase 2, not a phase 1, not a dose-finding study, not a pharmacokinetic paper. A search of trial registries returns no registered human studies of the compound. There is no human safety database, no established human dose, and no clinical evidence of benefit for any condition.
Solid bars mark evidence that exists. Dashed bars mark rungs that have not been climbed.
It is worth being precise about what that does and does not mean. It does not mean the compound is dangerous — nobody has found a signal either way, because nobody has looked properly. It does not mean the mechanism is wrong; the biology is well characterised. It means that anyone taking it is running an experiment with themselves as the only subject, on the basis of results in mice.
Oral vs Injectable
5-Amino-1MQ is unusual among compounds in this catalogue because it is sold both as oral capsules and as a lyophilized powder for reconstitution. The marketing around the two routes has got ahead of the evidence.
| Route | What supports it | What is missing |
|---|---|---|
| Oral | Laboratory permeability assays show the molecule crosses membranes readily, which makes oral absorption plausible | The animal efficacy studies did not use oral dosing; no human absorption data exists |
| Subcutaneous | The mouse fat-loss and muscle studies used injection, so this is the route the efficacy data actually came from | No human dosing equivalence has ever been established between the routes |
The claim you will see most often — that 5-Amino-1MQ is orally bioavailable, so the capsule is as good as the injection — overstates the record. What exists is permeability data suggesting oral absorption is possible, plus animal studies that used injection. No study has directly compared the two in a human, and the doses quoted for each route differ by an order of magnitude, which should tell you how little is settled here.
Dosing in the Research
No human dose has ever been validated. The figures below are what exists, with their provenance attached.
| Source | Dose | Route | Context |
|---|---|---|---|
| Obesity study in mice | 20 mg/kg per day | Subcutaneous | Where the fat-loss result comes from |
| Muscle regeneration in aged mice | 5 or 10 mg/kg twice daily | Subcutaneous | Where the muscle result comes from |
| Tolerability in mice | Up to 60 mg/kg per day | Subcutaneous | No adverse effects observed at that ceiling |
| Community oral convention | 50–150 mg daily, morning | Oral capsule | Not derived from any published study |
| Community injectable convention | Substantially lower than the oral figures | Subcutaneous | No published basis for the conversion between routes |
Two things about that table deserve emphasis. The mouse doses were given to animals of about 25 grams; scaling them to a person is an approximation at best, and different scaling conventions give very different answers. And the gap between the oral and injectable community figures has no published justification at all — it is convention layered on convention.
Side Effects & Safety
There is no controlled human safety data. What the animal work offers is that no adverse effects were observed in mice at doses up to roughly three times the effective dose, over study windows of days to weeks. That is genuinely reassuring as far as it goes, which is not very far.
What is reported anecdotally
- Sleep disruption — the most consistently mentioned effect, and the reason most community protocols specify morning dosing.
- Headache and nausea, particularly at the upper end of the oral range.
- Injection-site irritation where the subcutaneous route is used.
Where the theoretical risks actually sit
Blood glucose. NNMT inhibition improved glucose handling in animal models. Combining it with metformin, insulin or a sulfonylurea has never been studied, and additive glucose-lowering is mechanistically plausible. Anyone on glucose-lowering medication should involve their prescriber. Methylation. This compound deliberately changes how the cell spends its methyl-donor pool. The downstream consequences of doing that for months — on gene regulation, on homocysteine, on anything else methylation touches — have not been characterised in humans at all. This is the risk that has no data and no easy reassurance. NAD+ precursors. Stacking with NMN or NR is common on the logic that one adds substrate while the other stops it being wasted. That logic is plausible and completely untested. Pregnancy and breastfeeding. No data — avoid.
Athletes
5-Amino-1MQ is not named individually on the WADA Prohibited List. It is still captured, because WADA's S0 category prohibits at all times any pharmacological substance with no current approval by a governmental health authority for human therapeutic use — which describes this compound exactly. Treat it as prohibited and confirm with your national anti-doping organisation.
How It Compares
5-Amino-1MQ gets shelved with several things it is not much like. The distinctions matter.
| Compound | What it does | Human evidence | Key difference |
|---|---|---|---|
| 5-Amino-1MQ | Blocks NNMT; preserves NAD+ and SAM | None — no trials at all | A small molecule, not a peptide; no appetite effect |
| NAD+ and precursors | Adds substrate to the NAD+ pool directly | Human trials exist; results mixed | Supplies NAD+ rather than stopping its loss |
| MOTS-c | Activates AMPK via a different route | None interventional; genetic data only | A peptide, and explicitly WADA-banned by name |
| GLP-1 drugs | Reduce appetite and slow gastric emptying | Large phase 3 trials; approved | Work through eating less; proven weight outcomes |
| Metformin | Multiple metabolic effects including AMPK | Decades of trials; approved | Actually a medicine, with known risks and benefits |
If the goal is documented weight loss, the honest answer is that the GLP-1 class is the one with the trial data — see our guide on how GLP-1 peptides work for weight loss. What makes 5-Amino-1MQ interesting is not that it is better; it is that it targets something different, and does so without touching appetite. Whether that translates into anything measurable in a human remains the open question.
Where It Stands Legally
5-Amino-1MQ is not approved as a medicine by the FDA, the EMA, or Costa Rica's Ministerio de Salud, and it is not a scheduled controlled substance. It is sold as a research chemical.
One point of difference from the peptides discussed elsewhere in the Info Center is worth noting. In July 2026 the FDA's Pharmacy Compounding Advisory Committee reviewed seven peptides for the 503A bulk substances list, generating a lot of coverage. 5-Amino-1MQ was not among them and is not on that list. It sits outside that process entirely — which means there is no compounding-pharmacy pathway for it, and no regulatory review currently underway that would change its status.
Practically, that puts sourcing quality entirely on the buyer. There is no pharmaceutical manufacturing standard applied to a research chemical, and identity and purity vary by supplier. Our guide to research peptides versus pharmaceutical peptides and the notes on purity and certificates of analysis apply here with more force than usual.
Common Questions
Is 5-Amino-1MQ a peptide?
No. It contains no amino acids and is not built from them. It is a synthetic small molecule of the quinolinium class. It is grouped with peptides commercially, not chemically, and that grouping causes real confusion about storage, absorption and how to think about the evidence.
Does it cause weight loss in humans?
Unknown. It caused fat loss in obese mice without reducing food intake, which is a real and repeatable finding. Whether that happens in a person has never been tested. Anyone telling you it produces a specific amount of weight loss in humans is extrapolating from rodents.
Does it suppress appetite?
No, and that is the most interesting thing about it. The animal fat loss occurred with food intake unchanged, which means it works through energy expenditure rather than eating less. This is the opposite of how the GLP-1 drugs work, and it is why the two are sometimes discussed as complementary — though no study has tested that combination.
Should it be taken with NMN or NR?
This is the most common stacking question and it has a satisfying-sounding rationale: the precursor supplies raw material for NAD+ while 5-Amino-1MQ stops that material being methylated away. Nothing has tested it. It is a reasonable hypothesis, not a validated protocol, and combining two unstudied interventions doubles the uncertainty rather than halving it.
Why do protocols say morning dosing?
Because sleep disruption is the most frequently reported effect, and the convention developed to avoid it. It is a practical response to user reports rather than a finding from any study of the compound's timing.
What is the half-life?
There is no published human pharmacokinetic study, so any specific number you see is either extrapolated from rodents or invented. Figures in the range of a few hours circulate, but they are not from human data and should not be used to plan anything.
Why does NNMT come up in cancer research?
The enzyme is overexpressed in several tumour types, and NNMT inhibitors have been examined in cell-line work on ovarian, osteosarcoma and Merkel cell cancers as a research tool. That is an active laboratory field and nothing more — it is not a claim about treating anything, and it does not mean this compound is safe or unsafe for someone with a cancer history. Anyone in that situation should be talking to their oncologist before adding anything.
How should it be stored?
As a small molecule rather than a peptide, it is generally more stable than the lyophilized peptides in this catalogue, but sealed vials should still be kept cool and protected from light, and any reconstituted solution refrigerated. Our tropical climate storage guide and reconstitution guide cover the practical side.
What does Peptides Costa Rica stock, and what does it cost?
5-Amino-1MQ is listed as a 5 mg vial. Current pricing and live stock are on the 5-Amino-1MQ product page, and five or more vials of the same product carry an automatic 15% discount. Because oral and injectable formats are dosed very differently, message us about the format before ordering rather than assuming a conversion.
Is it legal in Costa Rica?
It is sold here as a research compound, the same framework used in most countries with an active market for these substances, and it is not approved as a finished pharmaceutical drug by the Ministerio de Salud, the FDA or the EMA. Our FAQ page covers ordering and delivery within Costa Rica.
Questions about 5-Amino-1MQ?
We would rather tell you what the evidence does and doesn't support than sell you something that doesn't fit your goal. Ask us anything — including whether a compound with more human data would serve you better.
Contact Us on WhatsAppImportant disclaimer: The information in this guide is general educational content only. It is not medical advice, a prescription, or a personalized recommendation. 5-Amino-1MQ is a synthetic small molecule, not a peptide. It is not approved by the FDA, the EMA, or Costa Rica's Ministerio de Salud as a finished pharmaceutical drug for human use, is not on the FDA's 503A bulk drug substances list, and is sold as a research compound intended for laboratory and scientific study. It is not a treatment for obesity, type 2 diabetes, sarcopenia, or any other condition. No human clinical trial of 5-Amino-1MQ has been published or registered, and no human pharmacokinetic or safety data exists; all efficacy findings described here come from rodent and cell-culture studies. Dosing figures discussed reflect what is reported in published animal research and in community use; they are not endorsements of those doses for any specific individual, and no dose has ever been validated in a person. The compound is designed to alter cellular methyl-donor metabolism, and the long-term consequences of doing so in humans have not been characterised. It may plausibly add to the effect of glucose-lowering medication including metformin, insulin and sulfonylureas; no interaction studies exist. No safety data exists for pregnancy, breastfeeding, or long-term use. 5-Amino-1MQ falls within WADA's S0 non-approved substances category and should be treated as prohibited in tested sport. Always consult a qualified healthcare professional before beginning any protocol. Products sold by Peptides Costa Rica are intended for laboratory and research purposes only.
- Nature (Kraus et al., 2014): NNMT is elevated in white adipose tissue and liver of obese and diabetic mice; knockdown protects against diet-induced obesity through increased energy expenditure rather than reduced food intake.
- Biochemical Pharmacology (Neelakantan et al., 2018): The defining 5-Amino-1MQ paper — selective, membrane-permeable NNMT inhibitors reversed high-fat-diet-induced obesity in mice with no change in food intake.
- Biochemical Pharmacology (Neelakantan, Brightwell, Graber et al., 2019): NNMT inhibition reactivated senescent muscle stem cells and improved regenerative capacity and peak torque in 24-month-old mice.
- Scientific Reports (Dimet-Wiley et al., 2024): NNMT inhibition combined with exercise improved endurance and grip strength in aged mice beyond exercise alone.
- Biochemical Pharmacology (Neelakantan et al., 2024): Further characterisation of NNMT inhibition and obesity-related metabolic dysfunction in diet-induced obese mice.
- Supplier technical data and chemical databases: Identity, CAS number, salt forms and the iodide-salt to free-base conversion, plus enzyme inhibition and cell-assay potency figures.
- ClinicalTrials.gov: No registered human clinical trials of 5-Amino-1MQ as of this writing.
- World Anti-Doping Agency: Prohibited List, section S0, covering pharmacological substances without approval by any governmental health authority for human therapeutic use.
