The short version

Plain English first. Everything below this section is the same material with the sources, the numbers and the caveats attached.

What 5-Amino-1MQ is

Quinoline is a benzene ring fused to a pyridine ring. Methylate the ring nitrogen and you get a permanently positively charged quinolinium. Add an amino group at position 5. That is the entire molecule.

The permanent positive charge is the point. It makes the molecule a structural mimic of 1-methylnicotinamide — the methylated pyridinium that the target enzyme produces — which is why it inhibits that enzyme, and why it can never be isolated as a neutral compound. It always arrives as a salt, with a counterion attached.

This is not pedantry, and the regulator agrees. FDA's substance registry holds three separate records — one for the cation, one for the chloride, one for the iodide. The distinction is registered.

Three published errors we found in one afternoon

Worth listing, because this is exactly the class of error a certificate of analysis is supposed to catch, and because it tells you how carefully this compound is handled commercially.

• A major chemical database has a page titled “chloride” carrying the iodide's formula, weight and CAS number, with a synthesis section describing making the iodide.
• A supplier datasheet states the molecular weight as 295.12. The correct figure for that formula is 286.11. The error corresponds to no plausible alternative salt or hydrate.
• Retail listings sell “chloride powder” while printing the iodide's CAS number. Either the name is wrong or the number is, and a buyer cannot tell which.

What we could not get: no X-ray structure, melting point, pKa or logP from any primary source we could open. PubChem and FDA's registry are JavaScript applications this environment could not render, so the formula comes from page metadata and the salt weights from a single analytical supplier.

How it works

The mechanism is real, specific and well described. It is also the place where the marketing makes its cleanest substitution.

Nicotinamide N-methyltransferase — NNMT — is a cytosolic enzyme, most abundant in liver and white fat. It does exactly one thing:

It consumes nicotinamide, which is the entry substrate of the NAD⁺ salvage pathway — the route by which mammals make more than 85% of their NAD⁺. And methylation is a one-way door: 1-methylnicotinamide cannot be turned back into nicotinamide. So in theory, inhibit NNMT, spare the nicotinamide, and NAD⁺ rises.

The logic is sound. The question is whether it has been measured, and in what.

Has NNMT inhibition been shown to raise NAD⁺?

Yes, in three settings. None of them is an animal given 5-Amino-1MQ, and none is a human.

The part nobody markets: what you lose

The reaction has two products, and blocking it lowers both. One of them, 1-methylnicotinamide, is not inert — it has a published literature of its own as an anti-thrombotic and vasoprotective metabolite acting through a COX-2 / prostacyclin pathway. 5-Amino-1MQ does exactly what you would expect to it: intracellular levels fell to about 40% of untreated, with a cellular EC₅₀ of 2.3 µM.

So the honest mechanistic summary is a trade, not a free gain. You recover nicotinamide into the salvage pathway, and you suppress a vasoprotective metabolite. Nobody has characterised the net effect of that trade in a living human, and nobody has characterised it in a living animal either.

Where it genuinely does well: selectivity

Tested against a panel of related enzymes, 5-Amino-1MQ came back clean. No inhibition of DNMT1 or PRMT3 at concentrations from 10 nM up to 200 or 600 µM. No inhibition of NAMPT — which matters, because NAMPT is the rate-limiting salvage enzyme and hitting it would have confounded the entire NAD⁺ story. Only trivial effects on COMT and SIRT1, and only at 600 µM.

Selectivity at 500-fold over its own potency is respectable, and “it’s selective” is one of the few vendor claims about this compound that survives scrutiny. The weakness here is potency, not promiscuity — see the evidence section.

Pharmacokinetics

There is no human pharmacokinetic data for 5-Amino-1MQ. No absorption, no half-life, no C_max, no bioavailability, no accumulation data. Any human half-life figure you see is unsourced — we looked specifically and found none attached to any citation.

The only pharmacokinetic study of this compound in any species is a 2021 rat assay paper from the same group that discovered it. We could not open it. Every route we tried returned a paywall, a robots block, a rate limit or a challenge page. What circulates from it, via two independent secondary sources that agree:

Reported, not verified. We have not read the primary text and will not present these as established. Note also that one of the two secondary sources misattributes the paper to a different author group — whose own compound happens to have a reported oral bioavailability of about 40%, uncomfortably close to 38.4%. Two different NNMT inhibitors are being conflated in the secondary literature right now.

“Membrane-permeable” means less than it sounds

The 2018 paper's title advertises membrane permeability, and it was measured — by artificial membrane assays and cultured cell monolayers. The paper contains no plasma concentrations, no half-life and no bioavailability estimate. Membrane-permeable in that title means the molecule crosses a lipid bilayer in a dish, which is what you check before you dose an animal, not what you know afterwards.

What the mouse doses scale to

Using the standard body-surface-area conversion, purely to show where the market's numbers sit:

Our arithmetic, not published figures, and offered only to show that the circulating 50 to 150 mg/day oral protocol lands somewhere inside the allometric range of the mouse work. That is not validation. Allometric scaling is how you choose a starting dose for a supervised phase 1 trial. It is not a dosing recommendation, and it says nothing about whether the oral route delivers the exposure the injected mice received.

What the evidence shows

Everything known about this compound in a living organism comes from four mouse studies and one rat assay paper. Here they are, with the conditions that constrain every number taken from them.

The pivotal study, stated in full

Every fat-loss percentage in circulation traces to one experiment. Its conditions were:

Nine male mice, seventeen weeks old, made obese on a 45%-fat diet, injected under the skin three times a day — at half nine, half one and half five — for eleven days.

The controls gained 0.6 g. The treated mice lost 2.0 g. On a 38 g mouse that is a 5.1% loss against a 1.4% gain: a divergence of about six and a half percentage points, and an absolute difference of two grams. One fat pad shrank about 35%; fat cells shrank about 30%. Total cholesterol was about 30% lower.

One detail worth recording because it gets cited: triglycerides were excluded from analysis in that study due to haemolysis interference. Pages claiming the compound “improves lipids” on the strength of this paper are citing data that does not exist.

The field's own verdict on it

5-Amino-1MQ inhibits NNMT with an IC₅₀ of about 1.2 µM. Set that in context:

How we know there is no human data

Because this is the claim the whole page rests on, here is how it was established rather than assumed.

The strongest evidence is affirmative, not the absence of a search result. A 2024 peer-reviewed review dedicated to NNMT as a therapeutic target states, in print: “As of yet, clinical trials focusing on NNMT have not been documented.” That is a statement about the whole target class, from authors with access to the databases.

Corroboration comes from an unexpected direction. The sellers agree. One vendor's own product page states that no human clinical trials of 5-Amino-1MQ in obesity, sarcopenia or any other indication have been published. Another guide states that as of April 2026 no human trials have been published and that all reported effects come from mouse studies. When the marketing channel concedes the point unprompted, the point is not in dispute.

Our own searching was hampered: the trial registry's programming interface and three bibliographic databases were all blocked from this environment, and the main literature database served challenge pages. So our enumeration rests on domain-restricted search, the review statement above, and vendor concession. We consider the conclusion secure and the method incomplete, and we would rather say both than only the first.

Reconstitution

Read this knowing that we could not find an aqueous solubility figure for this compound from any source. Not one.

The analytical supplier gives a single solubility number: 2 mg/mL in DMSO. No water figure, no saline figure, nothing. Retail vendors instruct reconstitution in bacteriostatic water, and a common protocol puts 50 mg into 3 mL — which requires roughly 17 mg/mL aqueous solubility, eight times higher than the only published figure, in a far gentler solvent.

The colour rule is inverted here, and it matters

Three independent suppliers describe this material identically: red-brown powder, or in the analytical supplier's words, “faint red to dark brown.”

Most research peptides are white lyophilised cakes, and colour in a peptide vial is a red flag. For this compound the opposite is true. Reconstituted 5-Amino-1MQ should be expected to give a coloured solution, and a pure white powder sold under this name does not look like the analytical standard. Our general reconstitution guidance is written for peptides and would tell you to discard a vial that isn't clear and colourless. Here, that guidance is wrong.

A related unverified point: vendors describe a “lyophilised cake” while the analytical supplier describes a powder. Small crystalline salts generally are not lyophilised; they are crystallised, dried and weighed. Which of the two a retail vial actually contains we could not establish, and it changes how the material behaves when you add water.

Reported protocols

None of this descends from a human trial, because there is no human trial. It is recorded as market intelligence and as a safety problem.

This is the clearest harm we can point to from shelving a small molecule next to peptides — including, to be plain about it, on our own shelf. A person who reads one protocol and applies it to the other format makes a two-order-of-magnitude error, and because there is no human pharmacokinetic data, nobody can tell them what either end of that range does.

The oral protocol as circulated

Typically: 50 mg daily for two weeks, then 100 mg daily, sometimes 150; taken with food; cycled 8 to 12 weeks on, 4 to 6 weeks off.

Two observations. The cycle length exceeds the longest animal study ever conducted — eight weeks — and vastly exceeds the pivotal efficacy study, which ran eleven days. And the “time off” has no rationale in any literature we found: there is no accumulation data, no receptor to desensitise, and no toxicology to space out. It appears to be a bodybuilding convention applied by default.

Where the circulating numbers actually come from

Storage

Our storage guide covers the general conventions, and this is one of the few compounds where they need adjusting.

The analytical suppliers store the solid at −20 °C. Retail vendors describe the same material as room-temperature stable for weeks. We found no stability data for this compound at any temperature, in any state. No degradation study, no shelf-life determination, nothing on the reconstituted solution. Both recommendations are assertions.

What is known that bears on it:

• There is no peptide bond to hydrolyse. That is the dominant degradation route for everything else on this shelf, and it does not apply. Small aromatic quaternary salts are generally far more robust than peptides.
• Iodide salts are commonly light-sensitive and can oxidise toward iodine — which is consistent with a described colour range running from faint red to dark brown. That range may itself reflect varying oxidation across lots.

Reported effects

There is no published toxicology programme for 5-Amino-1MQ. No acute toxicity study, no repeat-dose study, no genotoxicity battery, no reproductive toxicology, no safety pharmacology, no no-adverse-effect level in any species.

What exists is incidental observation inside efficacy experiments. The 2018 study reports that administration “did not impact total food intake nor produce any observable adverse effects” — over eleven days, in nine mice. A dose-escalation arm found 60 mg/kg/day “well tolerated with no observable adverse effects” — in two animals.

Adverse events and case reports: none found

No case report. No emergency department series. No poison centre data. No pharmacovigilance signal. We searched specifically and every result was a vendor page or a marketing article headed “side effects” describing theoretical effects with no source.

This is genuine absence of evidence, and it is not reassurance. Compare Melanotan II, where a similarly unregulated market has produced case reports of rhabdomyolysis, encephalopathy and melanoma, plus two regulator-conducted product analyses. 5-Amino-1MQ has produced none of that — but it has also been on the market for far less time, is taken orally by most buyers (a route less likely to produce a dramatic acute presentation), and causes no visible change that would send anyone to a specialist. Silence here carries less weight than silence would elsewhere.

Nobody has opened a vial

We found no independent analysis of retail 5-Amino-1MQ by any party — no regulator, no academic group, no consumer laboratory. All purity data in this market is vendor-generated, typically clustering at 99% or above with no chromatogram published anywhere.

Given the salt-form problem, the label-versus-contents question here is arguably sharper than for peptides: the counterion alone accounts for a 47% swing before you reach any question of actual purity, and no certificate we saw states which salt was assayed, or whether the purity figure refers to the mass of the salt or of the active cation.

Three predictable concerns, none of them measured

These are mechanism-derived hypotheses, explicitly not reported harms.

• Losing 1-methylnicotinamide. The compound's best-demonstrated cellular effect is cutting MNA to about 40% of baseline, and MNA has published vasoprotective and anti-thrombotic activity. Nobody has evaluated what chronic suppression does.
• Shifting the cell's methylation potential. SAM rose in treated cells, and the 2014 genetic work ties the fat phenotype to histone methylation. Chronically modulating a methyltransferase in a healthy person is a different proposition from an eleven-day mouse experiment.
• Liver. NNMT is most abundant in liver. Every efficacy claim concerns fat and muscle. No study has looked at hepatic consequences of inhibiting it long-term.

Regulatory status

Not approved as a medicine anywhere, for anything. It has never been in a human trial, so there has never been anything for a regulator to approve.

The organising fact for everything below is the one this page opened with: it is not a peptide, and essentially every regulatory action in this space over the past two years has been about peptides.

Canada — not listed, and that is not a clean bill

We checked both advisories, verbatim. Health Canada's 9 April 2026 advisory names fourteen peptides; 5-Amino-1MQ is not among them. The 1 August 2025 Canada Peptide seizure advisory names about fifty; 5-Amino-1MQ is not among those either.

United States

We found no FDA warning letter naming this compound. On whether it is a lawful dietary supplement ingredient, the honest answer takes three steps, and two of them are our own reading of the statute rather than an FDA statement:

• The statutory test. A dietary ingredient must be a vitamin, mineral, botanical, amino acid, or a dietary substance, concentrate, metabolite, constituent or extract of one. 5-Amino-1MQ is none of these — a synthetic quaternary quinolinium salt with no natural dietary occurrence. On the face of the statute it does not qualify.
• The drug-preclusion clause, which excludes articles authorised for investigation as a new drug, almost certainly does not bite — precisely because there has never been an investigational application or a clinical trial. That is the irony: the total absence of research means the exclusion that catches many peptides misses this one entirely. The disqualification is at the first step, not the second.
• The 2026 environment. FDA held a public meeting in March 2026 on whether peptides might be included in oral supplements, and its compounding committee recommended six of seven peptides for the compounding list in July. 5-Amino-1MQ was on none of those lists — not the seven heard, not the twelve removed from Category 2 in April. It has not been considered, because every one of these processes is about peptides.

The statutory reading above is ours. We could not locate any FDA statement addressing this compound specifically.

Sport

Section S0 of the 2026 Prohibited List covers “any pharmacological substance which is not addressed by any of the subsequent sections of the List and with no current approval by any governmental regulatory health authority for human therapeutic use.” 5-Amino-1MQ has no approval anywhere and is addressed by no other section. It is captured by S0 and prohibited at all times.

Two honest qualifications: it is not named as an example on the List — the application above is ours, using the List's own definition, which we read verbatim in the 2026 edition. And S4's metabolic modulators cover specific named agents that do not include it, so S0 rather than S4 is the right home. An athlete should treat it as prohibited.

Australia

We could not determine it. No TGA action, scheduling decision or safety alert naming this compound was found, and we did not consult the Poisons Standard directly. Australian vendors do sell it. We are not going to make a claim about Australian legal status on the strength of a search that came back empty.

Sentient Biogenix supplies 5-Amino-1MQ for laboratory research use only. It is not for human or veterinary use.

Questions we actually get

Is it a peptide?

No. It is a small molecule — a methylated quinoline with an amino group, sold as a salt. Its active part weighs 159 daltons; a typical research peptide weighs a thousand to five thousand. It has no amino acids and no peptide bonds. It sits next to peptides because it is bought by the same people, not because it is related to them.

Is there any human research?

None. Not one clinical trial, not one pharmacokinetic study, not one case report, in any country, for any purpose. The 2024 review literature confirms this for the entire NNMT inhibitor class. Several vendors say so on their own product pages.

Where do the fat-loss numbers come from?

One experiment. Nine male mice, made obese on a 45%-fat diet, injected under the skin three times a day for eleven days. They lost about two grams while controls gained; one fat pad shrank by about a third. Every percentage in circulation traces to that study or to two follow-ups in aged mice.

Does it boost NAD+?

It raises NAD⁺ by 20 to 60% in cultured mouse fat cells. It has never been shown to raise NAD⁺ in a living animal that received the drug, and never in a person. The strongest whole-animal evidence for the idea comes from silencing the NNMT gene in mice, which is a different intervention.

Capsule or injection?

Every efficacy study used subcutaneous injection. Most of the market sells capsules. The only route-comparison data is one rat study we could not read. So the injected route has the evidence, the oral route has the market, and nothing bridges them in humans.

Why do the dosing recommendations differ so wildly?

Because two conventions circulate that differ by 100 to 200 times — an oral one at 50 to 150 mg a day and a subcutaneous one at 150 to 500 mcg a day. The microgram convention looks like peptide dosing logic misapplied to a molecule that is not a peptide. Neither has been validated in a human.

What's the difference between the iodide and the chloride?

The active part is identical. What differs is the counterion riding along with it. Iodide is heavy: in a 10 mg vial of the iodide, only about 5.6 mg is the compound. In the chloride, about 8.2 mg is. Same label, 47% more drug. Most vendors do not say which they sell, and some print the iodide's CAS number on chloride product.

Has anyone tested what's actually in the vials?

Not that we could find. No regulator, no academic group, no independent laboratory has published an analysis of retail 5-Amino-1MQ. Every purity figure in this market comes from the vendor or a lab the vendor chose.

Are there reported side effects?

There are no published case reports, no adverse event literature, and no poison centre data. There is also no toxicology programme — the only safety observations are “no observable adverse effects” in nine mice over eleven days. Absence of reports is not a safety record.

Is it the best NNMT inhibitor?

No. It is roughly 320 times weaker than the best published one, and only about ten times better than the molecule the enzyme naturally makes. It is the compound that proved the target works in a mouse, not the compound the field is developing.

References

1. Neelakantan H, Vance V, Wetzel MD, et al. Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochemical Pharmacology 2018;147:141–152. PMID 29155147. DOI 10.1016/j.bcp.2017.11.007. pmc.ncbi.nlm.nih.gov — the pivotal study. Full text read. Source of the potency table, the cell-culture NAD⁺ figures, the selectivity panel and every parameter of the mouse experiment.
2. Li J-H, et al. Nicotinamide N-methyltransferase (NNMT): a novel therapeutic target for metabolic syndrome. Frontiers in Pharmacology 2024;15:1410479. DOI 10.3389/fphar.2024.1410479. frontiersin.org — the statement that clinical trials of NNMT inhibitors have not been documented. Read in full.
3. Kraus D, Yang Q, Kong D, et al. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature 2014;508(7495):258–262. DOI 10.1038/nature13198. nature.com — the genetic knockdown work, and the only in-vivo NAD⁺ evidence in the field. Abstract read; full text not opened.
4. Gao Y, van Haren MJ, Buijs N, et al. Potent inhibition of nicotinamide N-methyltransferase by alkene-linked bisubstrate mimics bearing electron deficient aromatics. Journal of Medicinal Chemistry 2021;64(17):12938–12963. DOI 10.1021/acs.jmedchem.1c01094. universiteitleiden.nl — the 3.7 nM comparator. Read via the institutional repository.
5. Dimet-Wiley A, et al. Reduced calorie diet combined with NNMT inhibition establishes a distinct microbiome in DIO mice. Scientific Reports 2022;12:484. DOI 10.1038/s41598-021-03670-5. nature.com — the seven-week study. Two conflicting PMIDs circulate for this paper; cite the DOI.
6. Dimet-Wiley AL, et al. Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice. Scientific Reports 2024;14:15554. DOI 10.1038/s41598-024-66034-9. nature.com — the eight-week study, and the authors' own statement that the NAD⁺ mechanism remains unquantified. Abstract and results read; methods not obtained.
7. Neelakantan H, Brightwell CR, Graber TG, et al. Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. Biochemical Pharmacology 2019;163:481–492. PMID 30753815. pubmed.ncbi.nlm.nih.gov — abstract read. Route of administration not established; we could not open the methods and will not infer it.
8. Awosemo O, Neelakantan H, Watowich S, et al. Development and validation of an LC-MS/MS assay for 5-amino-1-methyl quinolinium in rat plasma: application to pharmacokinetic and oral bioavailability studies. Journal of Pharmaceutical and Biomedical Analysis 2021;205:114255. DOI 10.1016/j.jpba.2021.114255. — the only pharmacokinetic study in any species. We could not open it. The 38.4% figure comes from two secondary sources, one of which misattributes the paper.
9. Sigma-Aldrich, product SML2832 — 5-amino-1-methylquinolinium iodide, ≥98% HPLC. sigmaaldrich.com — CAS, salt weight, DMSO solubility, storage temperature, physical description, and the IC₅₀ with its assay conditions.
10. World Anti-Doping Agency. Prohibited List 2026, section S0, effective 1 January 2026. — wording read verbatim from a published official copy. The application to this compound is ours.
11. Health Canada. Think twice before injecting peptides bought online. Public advisory, 9 April 2026. recalls-rappels.canada.ca — fourteen peptides. Read verbatim; 5-Amino-1MQ is not among them.
12. Health Canada. Unauthorized injectable peptide drugs seized and sold by Canada Peptide. Advisory, 1 August 2025. recalls-rappels.canada.ca — about fifty products. Read verbatim; 5-Amino-1MQ is not among them either.

Listed rather than hidden, what we could not check. The rat pharmacokinetic paper was unreachable through every route we tried, so the bioavailability and half-life figures are second-hand. Two of the four mouse studies did not yield their methods, so we do not know the route of administration for either. No aqueous solubility figure exists from any source. No stability data exists at any temperature. No independent purity analysis of retail product exists. The trial registry and three bibliographic databases were blocked from this environment, so our “no human data” conclusion rests on domain-restricted search plus an affirmative statement in the review literature plus vendor concession — secure, we think, but not exhaustively demonstrated. The dietary-supplement statutory reading is ours, not FDA's. The iodide-load calculation in the safety section is entirely ours and corroborated by nobody. And we could not determine Australian scheduling status at all, so we have made no claim about it.