5-Amino-1MQ: what the studies show, status and safety
Summary
5-Amino-1MQ is not a peptide. It is a small synthetic molecule with no amino acids in it, and it blocks an enzyme called NNMT that processes a breakdown product of vitamin B3. It appears in this peptide register because it is marketed as a peptide and sold beside them. Not one study in people exists. The animal work comes almost entirely from one research group and the company founded out of it, and the substance has never been through a safety programme of any kind.
Key findings at a glance
- It is not a peptide, and not by a narrow margin. The molecule is two fused rings weighing 159.21 g/mol, with no amino acids at all [1]. It was designed at a chemistry bench in 2017, not copied from anything the body makes [2].
- Zero studies in people. A search of the ClinicalTrials.gov registry on 6 September 2026 used nine search terms. It found no registered trial of 5-Amino-1MQ, and none of any other NNMT blocker either [3].
- One screening test flagged a second target. At 10 µmol/l the substance blocked the enzyme monoamine oxidase A by 67.4 percent. The company developing it names this as a problem still to be solved [4].
- In human blood-vessel cells the same enzyme block was harmful. Under chemical stress, fewer endothelial cells survived when NNMT was blocked, and the result held across three separate methods [5].
- Swallowing may waste almost all of it. Mice absorbed 3.5 percent of an oral dose [4], rats 38.4 percent [6]. Almost every study showing an effect injected the substance under the skin instead.
- No toxicology exists at all. No study of repeated-dose toxicity, genetic damage, fertility, development or cancer risk has been published for this molecule [4], [7].
- Banned in sport around the clock. Class S0 of the 2026 Prohibited List catches it through its wording rather than by naming it [8].
What it is
5-Amino-1MQ is a small synthetic molecule that blocks the enzyme nicotinamide N-methyltransferase, usually shortened to NNMT. Chemically it is a quinolinium salt, meaning two fused rings carrying a permanent positive charge. It has no biological original: nothing like it occurs in the body [1], [2].
It was first described in 2017 by an academic group at the University of Texas Medical Branch, where it appeared in a screening paper as "compound 1k" [2]. The company Ridgeline Therapeutics later grew out of that group, and nearly every animal study on the substance since then carries authors employed by or founding it [4], [9].
The papers state this themselves. The 2024 muscle study declares that its senior author founded Ridgeline Therapeutics and that two co-authors are employees of it [9]. The 2024 metabolic study lists the company as the affiliation of four of its five authors [4]. The 2018 study, published before the company existed, declared no competing interest [13].
The name it is sold under is a laboratory abbreviation. It is not an approved drug name, and at least five spellings circulate in the literature, including 5A1MQ, 5-AMQ and 5MQ [1], [2].
Quick facts
| Field | Value | Ref |
|---|---|---|
| Common name | 5-Amino-1MQ, also 5A1MQ or 5-AMQ | [1] |
| Class | Small synthetic molecule, a quinolinium salt; an enzyme blocker | [1], [2] |
| Amino acid sequence | None. It is not a peptide | [1] |
| Formula and mass | C10H11N2+, 159.21 g/mol as the cation | [1] |
| Traded salt form | Iodide, C10H11IN2, 286.11 g/mol; iodide is about 44 percent of that weight | [10] |
| Target | The enzyme NNMT (EC 2.1.1.1) | [2] |
| How long it lasts in the body | Never measured in a person; 6.3 to 13.3 hours in mice, 3.8 to 6.9 hours in rats | [4], [6] |
| Status | Research chemical, approved nowhere | [11] |
| Developer | Academic group at the University of Texas Medical Branch, then Ridgeline Therapeutics | [2], [9] |
| CAS registry number | 685079-15-6 (cation), 42464-96-0 (iodide) | [1], [10] |
| PubChem CID | 950107 (cation), 66522933 (iodide) | [1], [10] |
| UNII | PMX593N4N3 (cation), K9G33W2TTZ (iodide) | [1], [10] |
| ChEMBL | CHEMBL4116828; no clinical phase, no approval date | [11] |
The distinction from peptides is not a technicality. A small molecule is broken down by liver enzymes rather than by the enzymes that cut peptides apart. It can in principle cross the gut wall, and it slips past the laboratory methods built to find banned peptides in an athlete's sample [1].
How it works
The proposed mechanism starts with one enzyme. NNMT takes a methyl group from a carrier molecule called SAM and attaches it to nicotinamide, a form of vitamin B3, producing a substance called 1-methylnicotinamide. Blocking that step is the whole idea [2], [12].
- It docks where the vitamin normally sits. Calculations and enzyme measurements place the molecule in the nicotinamide pocket of the enzyme rather than at the methyl-carrier site. This is a model drawn from computation, not a solved structure of this molecule bound to the enzyme [2].
- Two budgets shift at once. If the methylation step stalls, less SAM is consumed and less nicotinamide is drained away. Both the methyl-group pool and the cell's NAD+ supply may therefore rise. In fat cells the substance lowered 1-methylnicotinamide and raised both [13].
- Energy turnover rather than appetite. The founding idea came from a 2014 paper in which switching off the Nnmt gene in mice protected them against diet-induced obesity. That paper used gene-silencing molecules, not this substance, which did not yet exist [12].
- Muscle stem cells may wake up. For the ageing-muscle results, the authors propose that a restored NAD+ balance reactivates muscle stem cells that had gone dormant. The evidence is from mice and from a muscle cell line [14].
- The direction is not the same in every tissue. In human blood-vessel cells, blocking the very same enzyme reduced survival under stress. That was shown with this substance, with a second blocker and with genetic silencing, so it is a property of the enzyme block rather than of the molecule [5].
There is no mechanistic measurement in a person for any of this. Nor is it settled how much of any given result belongs to the enzyme block itself, given the second target found in screening [4].
What the studies found
Every result below comes from a rodent or from cells in a dish. Nobody has run a study of this substance in a person, of any size, for any purpose [3].
Body weight and fat in obese mice
Animal data In the central efficacy paper, obese mice on a high-fat diet received injections under the skin for 11 days. They lost weight progressively against salt-water controls, with less fat tissue, smaller fat cells and lower total cholesterol. Food intake did not change, so the authors read the effect as energy turnover rather than appetite [13].
Animal data A later study combined the substance with a switch to a reduced-calorie diet. Cumulative weight loss reached 6.3 grams against 4.3 grams on the diet change alone, in groups of 6 to 8 mice. The regain seen after about three and a half weeks in the diet-only group did not appear [15].
That comparison is the important one. The control mice lost weight on the diet change by itself, and the substance added to that.
Blood sugar and liver
Animal data Obese mice were given one injection a day for 28 days at either of two dose levels, 8 animals per group. Weight and fat gain rose less, glucose tolerance and insulin sensitivity improved, and the liver showed less fat and fewer inflammatory cells, with liver enzyme values normalised. Proof that the substance had reached its target was only obtained in the higher-dose group [4].
Muscle in old mice
Animal data In 24-month-old mice with an injured leg muscle, treatment produced 60 to 75 percent more dividing muscle stem cells. Repaired fibres rose by 40 to 48 percent, depending on dose, with 10 to 13 animals per group. At the higher dose the average fibre cross-section was about 1.8 times larger and peak torque roughly 70 percent higher [14].
Animal data In a second study, 35 old female mice were split into four groups over two months: sedentary, treated, running-wheel exercise, and exercise plus treatment. Grip strength ran about 40 percent above sedentary controls on the substance alone, 20 percent on exercise alone and about 60 percent in combination [9].
35 female mice aged 22 to 24 months, four groups of 7 to 10 animals, two months of treatment. These are mouse results and do not transfer to people. Source [9].
Cells in a dish
In vitro Against a standard panel the molecule looked clean. It blocked none of three similar methyl-transferring enzymes, and neither of the two enzymes that regenerate NAD+, tested up to high concentrations [13]. An independent Turkish group found that it slowed the division of cervical cancer cells in a dish, with signs of programmed cell death [16].
Negative and unwelcome findings
In vitro A screening panel of major receptors, enzymes and transporters found one hit: 67.4 percent inhibition of monoamine oxidase A at 10 µmol/l. In people, blocking that enzyme is linked to blood-pressure crises after eating aged cheese or drinking red wine, and to dangerous interactions with several common medicines [4].
In vitro In three lines of human blood-vessel cells under chemical stress, blocking NNMT significantly lowered survival. The authors conclude that this enzyme protects the vessel lining [5]. A substance given by injection reaches the vessel lining as surely as it reaches fat tissue.
Animal data The only independent animal use of the molecule is in cancer research. There it slowed bladder tumour growth in mice and strengthened the effect of an immunotherapy antibody [17]. That is an oncology finding and has nothing to do with what the substance is marketed for.
What is still unknown
- Whether anything seen in mice happens in a person. There is no human study of this substance, by any route [3].
- What a safe amount would be. No toxicology programme exists, so there is no dose from which safety could be argued [7].
- How much of a swallowed dose reaches the blood in a person. The two animal measurements differ more than tenfold [4], [6].
- Whether the second target found in screening matters at achievable levels. Nobody has measured blood levels in a person [4].
- Whether what is sold is what the label says. There is no pharmacopoeia standard for identity or purity, and no published analysis of market samples [7].
Side effects and safety
There is no side-effect profile for 5-Amino-1MQ, because there is no documented human use to build one from. Silence in the databases is not a clean bill of health.
- No reports of harm anywhere. The FDA adverse-event database returned "No matches found" for every search term on 6 September 2026 [18]. Substances traded outside the regulated medicines system rarely generate reports at all, and a user could hardly attribute a symptom to this one.
- A second target, named by the developers themselves. The 67.4 percent block of monoamine oxidase A at 10 µmol/l is the only concrete safety signal in the literature. The paper reporting it lists fixing that property as ongoing work [4].
- The enzyme block is not helpful everywhere. Blood-vessel cells survived stress less well when NNMT was blocked, by three separate methods [5].
- Nothing has been tested for toxicity. No repeated-dose study, no test for genetic damage, no fertility or development study, no cancer study. The longest exposure in the entire literature is two months, in mice [7], [9].
- Interactions are unstudied and plausible. Blocking monoamine oxidase A points towards interactions with antidepressants, migraine medicines, some painkillers and tyramine-rich foods. None of these has been examined [4].
- The traded form carries iodide. The salt sold commercially is roughly 44 percent iodide by weight, and nobody has assessed what that intake would mean for the thyroid [10].
One point deserves particular care. 5-Amino-1MQ does not appear on the FDA lists of substances that may pose a serious safety risk in compounding [19]. That is not a clearance. Those lists cover substances somebody nominated, which the agency then had to assess. This one was never nominated and therefore never assessed.
Chemistry adds a further open question rather than an answer. Quinoline and several of its relatives are described as mutagenic and liver-damaging, and Australia lists quinoline and its salts in a scheduled category. Whether that applies to this methylated, amino-substituted variant has never been tested [7], [20].
Doses used in studies
These are the doses used in the cited studies, listed for reference. They are not a recommendation.
Every line comes from a mouse, a rat or cells in a dish. The route matters more here than in most entries in this register, because almost everything that showed an effect was injected under the skin.
| Study | Model | Dose | Route | Duration | Ref |
|---|---|---|---|---|---|
| Neelakantan 2018, diet-induced obesity | Mouse, 17 weeks old, high-fat diet | 20 mg/kg at each of three daily injections, about 34 mg/kg a day | Under the skin | 11 days | [13] |
| Neelakantan 2019, muscle repair | Mouse, 24 months old | 5 mg/kg and 10 mg/kg, twice a day | Under the skin | 1 week, and 3 weeks in a second run | [14] |
| Sampson 2021, with reduced-calorie diet | Mouse | 32 mg/kg a day of active substance | Under the skin | To the end of the study | [15] |
| Dimet-Wiley 2022, gut bacteria | Mouse | 32 mg/kg a day of active substance | Under the skin | Throughout the diet change | [21] |
| Dimet-Wiley 2024, muscle in old age | Mouse, 22 to 24 months old, female | 10 mg/kg | Under the skin | 2 months | [9] |
| Babula 2024, efficacy | Mouse, diet-induced obesity | 10 mg/kg and 32 mg/kg a day, 8 animals per group | Under the skin | 28 days | [4] |
| Babula 2024, uptake and breakdown | Mouse | 5 mg/kg into a vein and 30 mg/kg by mouth, 3 animals each; 25 mg/kg under the skin, 6 animals single and 12 repeated | Vein, mouth, under the skin | Single doses, and 5 days repeated | [4] |
| Awosemo 2021, uptake and breakdown | Rat | Single doses into a vein and by mouth, amounts not given in the abstract | Vein and mouth | Single | [6] |
| Neelakantan 2018, selectivity testing | Enzymes in a dish | Concentration series up to 600 µmol/l | Laboratory assay | Single exposure | [13] |
| Babula 2024, screening panel | Receptors and enzymes in a dish | 10 µmol/l | Laboratory assay | Single exposure | [4] |
| Akar 2021, cancer cells | HeLa and HEK-293 cells | 0.1 to 500 µmol/l | Cells in a dish | Read over time | [16] |
Three things make it impossible to carry these numbers over to a person. Almost every result came from injection under the skin, while the product is sold as a capsule to swallow.
How much of a swallowed dose gets absorbed also differs more than tenfold between the two species measured. And no safety study exists for any of these amounts [4], [6], [7].
Two measurements in two species, made by different groups. No measurement in a person exists. Sources [4], [6].
Development and approval status
From the founding paper to the 2026 registry search
- 2014Nature paper switches off the Nnmt gene in miceGene-silencing molecules, not this substance, ref [12]
- 2017First description of the molecule as compound 1kScreening study at a chemistry bench, ref [2]
- 2018Obese mice lose weight on injections under the skin11 days, high-fat diet maintained, ref [13]
- 2021Muscle work continues; a counter-finding appears in vessel cellsRefs [14], [5]
- 2024Fullest study to date reports a second target and poor oral uptakeMonoamine oxidase A blocked 67.4 percent, ref [4]
- 2026Registry search finds no trial in people, for this or any NNMT blockerNine search terms on 6 September 2026, refs [3], [22]
- 2014 — a paper in Nature reports that silencing the Nnmt gene protects mice against diet-induced obesity, and the field begins [12].
- 2017 — the molecule is described for the first time, in a screening study of related chemical scaffolds [2].
- 2018 — the first efficacy study in obese mice appears [13].
- 2019 to 2024 — the muscle work is published, alongside studies on gut bacteria and on blood sugar [9], [14], [21].
- 2021 — an independent group reports that blocking the enzyme harms human blood-vessel cells under stress [5].
- 2024 — the fullest study to date reports both the effects and the second target [4].
- 2026 — a review of the whole class describes the move into the clinic as still ahead, and names unknown safety profiles as a limiting factor [22].
| Market | Status | Note | Ref |
|---|---|---|---|
| United States | Not approved | Never nominated for compounding, so never assessed | [11], [19] |
| European Union | Not approved | No pharmacopoeia entry; not a permitted food ingredient | [11] |
| Germany | Not approved | Not named in any substance-specific rule | [11] |
| United Kingdom | Not approved | Not separately checked | [11] |
| Australia | Not classified | Not named in the Poisons Standard | [20] |
| Canada | Not approved | Not separately checked | [11] |
| Switzerland | Not approved | Not separately checked | [11] |
| Japan | Not approved | Not separately checked | [11] |
All of this was checked on 6 September 2026. Where the table says not separately checked, that rests on the worldwide absence of any approval rather than on a search of that national register [11]. The field itself has moved on: the most recent high-profile work uses newly designed blockers instead of this one [23].
Anti-doping
5-Amino-1MQ is banned in sport at all times, in and out of competition. It is not printed on the 2026 Prohibited List by name. It falls under class S0. That class 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", and it names drugs in preclinical development as an example [8].
One consequence deserves stating plainly. Because this is not a peptide, the laboratory methods built to screen for banned peptides do not look for it [1]. The list of the American college sports association does not name it either, and states that its list is neither complete nor exhaustive [24]. Further detail sits under peptides banned in sport.
Compared with related peptides
| Substance | What it is | Point of attack | Human studies | Status |
|---|---|---|---|---|
| 5-Amino-1MQ | Small synthetic molecule, 159.21 g/mol [1] | Blocks the enzyme NNMT [2] | None at all [3] | Approved nowhere; caught by class S0 [8], [11] |
| MOTS-c | Peptide of 16 amino acids, encoded in mitochondria | Not the same target; NNMT sits in the cell fluid, not in mitochondria [2] | Not assessed on this page | Named on the FDA list of substances that may pose a serious safety risk [19] |
| Semaglutide | Peptide medicine, licensed and prescription-only [25] | GLP-1 receptor [25] | Large licensing trials behind it [25] | Approved in the United States since December 2017 [25] |
| Nicotinamide and 1-MNA | A form of vitamin B3 and the product NNMT makes from it [12] | Substrate and product of the enzyme, not blockers of it [4] | Studied as a biomarker in 314 people [26] | Not the same substance class at all |
Semaglutide is the useful contrast, because it shows what a finished evidence base looks like: a licensed medicine with trials in tens of thousands of people behind it [25]. 5-Amino-1MQ sits at the opposite end, with rodent data from one group.
MOTS-c is the neighbour it is most often filed beside, and the two have almost nothing in common beyond a shopping basket. One is a peptide the body encodes; the other is a bench chemical. Their regulatory footing differs too: MOTS-c is named on the FDA list of substances that may pose a serious safety risk in compounding, and 5-Amino-1MQ is on no list at all [19].
The vitamin comparison is the one that trips people up most. Nicotinamide is the raw material of the enzyme and 1-MNA is its product, so a blocker pushes in the opposite direction from either of them [4], [12].
Common misconceptions
- "5-Amino-1MQ is a peptide." It has no amino acids and no sequence. It is a two-ring molecule of 159.21 g/mol that ended up in peptide catalogues because it is sold through the same channels [1].
- "It is basically 1-MNA, or a vitamin B3 product." The opposite. NNMT makes 1-MNA out of nicotinamide, and this substance blocks that step, lowering 1-MNA. In the animal studies that fall was used as proof the substance had reached its target [4], [13].
- "It is a fat burner." That is a claim, not a finding. What was found is that obese mice on injections gained less fat or lost weight, without eating less. In the combination study the comparison group lost weight on the diet change alone [13], [15].
- "A capsule does the same thing as the studies did." Almost every study injected the substance under the skin. The two oral measurements that exist disagree more than tenfold, and neither was made in a person [4], [6], [13].
- "The 2014 Nature paper proves it works." That paper silenced a gene with a different class of molecule, three years before this substance was described. It supports the idea of the target, not the effect of this molecule [2], [12].
- "NNMT blockers are in clinical trials." None is. Nine registry searches on 6 September 2026 returned no trial of any NNMT blocker, and a 2026 review calls the move into the clinic an open task [3], [22].
- "It is not on any FDA risk list, so it is safer than BPC-157 or KPV." Those lists cover substances somebody put forward for assessment. This one was never put forward, so the status is "never examined" rather than "examined and cleared" [19].
Frequently asked questions
Is 5-Amino-1MQ a peptide?
No. A peptide is a chain of amino acids, and 5-Amino-1MQ contains none. It is a small synthetic molecule of two fused rings weighing 159.21 g/mol, and it is sold beside peptides because it moves through the same shops and catalogues. That difference matters, because a small molecule is broken down by liver enzymes rather than by the enzymes that chop up peptides.
Has 5-Amino-1MQ ever been tested in humans?
No. A search of the ClinicalTrials.gov registry on 6 September 2026 using nine different search terms found no registered study, either of 5-Amino-1MQ or of any other NNMT blocker. There are no published case reports either, and no measurement of what the substance does in a human body.
What does 5-Amino-1MQ actually do in the body?
In mice and in cells it blocks an enzyme called NNMT, which normally attaches a methyl group to nicotinamide, a form of vitamin B3, and turns it into 1-methylnicotinamide. Blocking that step shifts two household budgets of the cell at once, the NAD+ supply and the pool of methyl groups. None of this has been measured in a person.
What did the animal studies of 5-Amino-1MQ find?
In obese mice, injections under the skin slowed or reversed weight and fat gain and improved blood sugar handling. In old mice, the same substance raised grip strength and improved muscle repair after injury. Every one of those results comes from rodents, and most come from a single research group.
Is 5-Amino-1MQ safe?
Nobody knows, because the work needed to answer that has never been done. There is no study of repeated-dose toxicity, of genetic damage, of fertility or of cancer risk. One screening test did find that the substance blocked the enzyme monoamine oxidase A by 67.4 percent, which in people is a property linked to food and drug interactions.
Why is 5-Amino-1MQ sold as a capsule when the studies injected it?
That gap is the sharpest problem with the product. Almost every study that reported an effect injected the substance under the skin of a mouse. The only two measurements of how much survives swallowing disagree wildly, at 3.5 percent in mice and 38.4 percent in rats, and neither was made in a person.
Is 5-Amino-1MQ the same as 1-MNA or nicotinamide?
No, and it works in the opposite direction. Nicotinamide is a form of vitamin B3, and 1-methylnicotinamide is what the enzyme NNMT makes out of it. 5-Amino-1MQ blocks that conversion and therefore lowers 1-methylnicotinamide. Taking both at once would work against itself.
Is 5-Amino-1MQ approved anywhere?
No. As of 6 September 2026 no medicines authority anywhere has approved it, and the ChEMBL database records neither a clinical phase ever reached nor a first approval date. It is traded as a laboratory reagent under catalogue numbers, which is a research supply route rather than a medical one.
Is 5-Amino-1MQ banned in sport?
Yes, at all times. Class S0 of the 2026 Prohibited List covers any drug-like substance that no health authority currently approves for human use, and names substances in preclinical development as an example. 5-Amino-1MQ is caught by that wording rather than printed on the list by name.
Are NNMT blockers like 5-Amino-1MQ in clinical trials?
No. As of September 2026 not a single NNMT blocker of any kind has a registered trial in people. A review published in 2026 describes the move into the clinic as still ahead of the field, and names unknown safety profiles as one of the reasons.
Sources
- PubChem. Compound CID 950107, 1-methylquinolin-1-ium-5-amine. Formula C10H11N2+, 159.21 g/mol, CAS 685079-15-6, UNII PMX593N4N3, InChIKey ZMJBCEIHNOWCMC-UHFFFAOYSA-O. Retrieved 6 September 2026. https://pubchem.ncbi.nlm.nih.gov/compound/950107
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- NCAA. Banned Substances 2026-27. Full text searched for "1MQ", "quinolin" and "NNMT" with no match; the list states that it is neither complete nor exhaustive. Retrieved 6 September 2026.
- Drugs@FDA. Semaglutide injection, application NDA 209637, sponsor Novo Nordisk, original approval 5 December 2017. Verified through the openFDA drugsfda endpoint on 6 September 2026. https://www.accessdata.fda.gov/scripts/cder/daf/
- Kannt A, Pfenninger A, Teichert L, Tönjes A et al. (2015). Association of nicotinamide-N-methyltransferase mRNA expression in human adipose tissue and the plasma concentration of its product, 1-methylnicotinamide, with insulin resistance. Diabetologia 58(4):799-808. PMID 25596852. DOI 10.1007/s00125-014-3490-7
Cite this page
The facts on this page were checked on 6 September 2026, and every register search behind the status table was run on that date. This is a substance with no human data at all, so the date of the check matters as much as the text.
myPeptides Research & Editing. (2026). 5-Amino-1MQ: what the studies show, status and safety. Version 1.0, 6 September 2026. myPeptides Peptide Register. Retrieved from https://mypep.app/peptides/5-amino-1mq
How pages in this register are compiled and graded is described under methodology; the full register is at peptides.
| Version | Date | Note |
|---|---|---|
| 1.0 | 6 September 2026 | Initial publication |