The Longevity Desk
11 min readMitochondria

5-Amino-1MQ: Every Study I Could Find Is a Dish or a Rodent

It is sold as a peptide and it is not one. I could not find a published human study, and the NAD+ rise and the fat loss were never measured in the same organism.


What it is, and why it is not a peptide

5-Amino-1MQ is sold on peptide sites and shelved with peptides, and it is not a peptide. The active species is 5-amino-1-methylquinolinium, a small permanently charged organic cation: PubChem CID 950107, formula C10H11N2+, molecular weight 159.21, CAS 685079-15-6. A cation carries a positive electrical charge. No amino acids, no peptide bonds. The powder is the iodide salt, 5-amino-1-methylquinolinium iodide, PubChem CID 66522933, molecular weight 286.11, which is also the name FDA used in writing about it, and any listing quoting 159 is quoting the cation rather than the material.

Go and run the search yourself

Go to PubMed and search "5-amino-1MQ" or "5-amino-1-methylquinolinium". I ran it and got three records, a bladder cancer fibroblast paper, a HeLa cell proliferation paper and a mouse microbiome paper, none of them a human study (PMID 39067875, PMID 33645410, PMID 35013352). Add the Clinical Trial and Randomized Controlled Trial filters and nothing comes back at all. ClinicalTrials.gov has no record of the compound either, an intervention search returning zero studies. The EU Clinical Trials Register answered my query with the line "Query did not match any clinical trials". Europe PMC reads full text rather than titles and abstracts, and returns 26 documents mentioning the compound anywhere in their pages: preclinical work, reviews and preprints.

Now read the seller pages. RealPeptides.co describes a twelve week randomised placebo controlled study at the University of Copenhagen published in 2024, a Phase 1 safety study in the Journal of Clinical Endocrinology and Metabolism in 2024, and a 90 day rat toxicology study in Toxicology and Applied Pharmacology in 2021, quotes participant level side effect percentages, and cites no PMID, DOI or NCT for any of it. I searched PubMed restricted to those two journals and got three papers, from 2003, 2015 and 2020, none of them the studies described.

What the trials found

There are no human trials. Everything below is a rodent.

"Shrinks fat cells by over 30 percent" is real, and it is a mouse finding. Histology means the fat pad was cut out and looked at under a microscope. Neelakantan 2018 took histology of epididymal white fat from treated diet-induced obese mice, 17 week old male C57BL/6 on a 45 percent fat diet, nine per cohort, and reported more than a 30 percent decrease in fat cell size and more than a 40 percent decrease in fat cell volume. (PMID 29155147) The dosing is where it parts company with the product: three separate subcutaneous injections a day at 20 mg/kg each, about 34 mg/kg/day, for eleven days. Subcutaneous means under the skin. The retail item is a capsule swallowed once. Weight change in that experiment, the number marketing skips, was 2.0 grams, about 5.1 percent of baseline. Food intake did not differ between treated and control animals, which is the basis for calling the effect metabolic rather than appetite driven.

The largest fat loss figure in the literature is Sampson 2021, about 29.3 percent fat mass loss over seven weeks in 22 week old male diet-induced obese mice, six to eight per arm, at 40 mg/kg/day by daily injection. (PMID 33707534) Check the comparator: both arms were also switched to a lean diet, so it is diet plus drug against diet alone, and diet alone gave 2.9 percent. Babula 2024 gave 10 and 32 mg/kg/day by once daily subcutaneous injection for 30 days to roughly 18 week old male diet-induced obese mice, eight per group, with dose dependent limits on weight and fat gain. (PMID 39161060) All male, all obese, all injected.

Strike off Kraus and colleagues, Nature 2014, which vendor pages routinely offer as evidence here. It knocked the Nnmt gene down in mouse white fat and liver with an antisense oligonucleotide, which is not the same intervention as inhibiting the protein with a small molecule. (PMID 24717514)

The NAD+ number was measured in a dish

NNMT is nicotinamide N-methyltransferase, the enzyme this compound blocks, and adipocytes are fat cells. NAD+ is nicotinamide adenine dinucleotide, which has its own entry here.

NNMT methylates nicotinamide using S-adenosylmethionine as the methyl donor, spending an NAD+ precursor and the cell's universal methyl donor in one reaction, so blocking it drops 1-methylnicotinamide and raises NAD+ and SAM. All of that was measured in cultured mouse 3T3-L1 adipocytes with the compound added to the medium. (PMID 29155147) The figure sitting under the marketing is a concentration dependent NAD+ rise of roughly 1.2 to 1.6 fold, across 1 to 60 micromolar, over 24 hours. That is the whole of the published NAD+ evidence. The SAM half is weaker even in the dish, significant only at 30 micromolar, with the p value at 60 micromolar coming in at 0.06.

Then the part that matters more than either number. I could not find any published measurement of NAD+ or SAM in an animal given this compound. The readouts in the 2018 mouse experiment were body weight, food intake, white fat mass, fat cell size and a plasma lipid panel. I went through the full texts of Neelakantan 2018, Sampson 2021 and Babula 2024 looking for metabolite data in treated animals and found none. The mechanism has been shown in cells, the fat loss has been shown in mice, and never in the same organism. A boiler tested in one house, a warm radiator noted in another, and nobody has checked the pipe between them.

How it compares

It is shelved with the peptides and sold beside the NAD+ drips, so read across.

Approved?Human trials behind itWhat that evidence covers
5-Amino-1MQNo, and not eligible for compounding under section 503BNone I could find, across four databasesMouse fat cells in a dish, and injected rodents
NAD+Not an approved drug in the United States for any indicationOne pharmacokinetic study in eight men, one randomised trial in 180 adultsPlasma levels, and ejection fraction in damaged hearts at 10 mg a day into a vein
SemaglutideYes, including as a pillPast 25,000 people in outcome trials aloneWeight, heart attacks, strokes and failing kidneys, on manufactured product

The last column is the one that matters. The middle row is the molecule this compound is supposed to raise, and even that record is a hospital dose into a vein for a heart condition. None of it transfers to a swallowed capsule of this.

Where the dose came from

Pharmacokinetics is what a dose does after it goes in, and intravenous means into a vein. The only dedicated pharmacokinetics and oral bioavailability paper is in rats: 38.4 percent oral bioavailability, terminal half-life about 3.8 hours intravenously and 6.9 hours orally. (PMID 34304009) Babula 2024 also ran mouse pharmacokinetic arms at three routes, intravenous 5 mg/kg, oral 30 mg/kg and subcutaneous 25 mg/kg. I could not find any published human pharmacokinetic data, so nobody has published what a swallowed capsule does to a person's blood levels.

The dose that circulates is 50 to 150 mg a day by mouth, usually 50 mg for one to two weeks then 100 mg, in blocks of 8 to 12 weeks with 4 to 8 weeks off. Convention, not evidence, and the pages publishing it say so in the same breath, with peptides.org stating that the compound has not been clinically tested and that any dosing suggestion is speculative. I found no derivation for the number. Meanwhile retail listings sell capsules at 500 micrograms, half a milligram, one hundredth to one three hundredth of the protocol dose, under the same name, and it is compounded as an injectable besides. Two jars on one shelf wearing the same label, one holding a pinch and the other a heaped spoon.

What could go wrong

The only published tolerability statement is one line in the 2018 mouse paper, no observable adverse effects over eleven days with nine animals per group, and no formal toxicology in that paper. I found no human safety data, no peer reviewed case report of harm, and no independent analysis of what is in grey market product; the purity numbers in circulation are vendor commissioned certificates. A 2026 review of the NNMT inhibitor class describes the safety profiles of these compounds as unknown.

The regulatory file is not much longer. A bulks list is what a compounding pharmacy may make medicines from. FDA has named this compound once that I could find. On 20 January 2026 the Office of Compounding Quality and Compliance at CDER wrote to GenoGenix LLC of Boca Raton, Florida, Warning Letter 718739, stating that 5-amino-1-methylquinolinium iodide is not eligible for compounding under section 503B because it does not appear on the 503B bulks list. A full text search of FDA's warning letter database for the term returns "Showing 1 to 1 of 1 entries". The compound was not on the agenda of the Pharmacy Compounding Advisory Committee meeting of 23 and 24 July 2026 that considered peptides for the 503A bulks list, I could not find it in the Dietary Supplement Ingredient Directory, and I found no GRAS notice or new dietary ingredient notification. It is not named on the WADA 2026 Prohibited List and I found no anti-doping document naming it. I found no approval from the American, European, British, Australian or Canadian medicines regulators anywhere.

What nobody knows

What it does in a person. There is no published human study to read, by any route, so everything attached to the capsule comes from a plate or a rodent.

Whether the NAD+ rise happens in a living animal. I could not find the mechanism and the fat loss joined in one organism.

What it does over time. Nothing in the record runs beyond a few weeks in a rodent.

My take

Two things bother me here and they are not the same thing.

The first is the gap between the mechanism and the effect. The claim is about an organism and the data behind it are from cultured cells.

The second is the route. Every efficacy result came out of a needle in a rodent, mostly under the skin, at milligrams per kilogram per day, one of them at three injections daily. The product is a capsule taken once. The nearest thing to a bridge anybody has published is 38.4 percent oral bioavailability in a rat, and a rat is not a person.

If you have run this, which product were you actually holding, the 500 microgram capsules or the 100 mg protocol? A two hundredfold gap on identical labelling, and I would like to know which one your source was describing.

Frequently asked

Are there any human studies of 5-Amino-1MQ?

I could not find one, by any route. A PubMed search returned three records, none of them human. ClinicalTrials.gov returned zero studies and the EU register matched none.

Does 5-Amino-1MQ shrink fat cells?

In mice. Treated obese male mice showed more than a 30 percent decrease in fat cell size, nine animals per cohort, after eleven days of injections under the skin at 20 mg/kg three times a day, a mouse dose and not a recommendation.

Does 5-Amino-1MQ raise NAD+ in people?

I could not find any published measurement in a person, or in any animal given the compound. What exists is cultured mouse fat cells, roughly 1.2 to 1.6 fold across 1 to 60 micromolar over 24 hours.

Why do 5-Amino-1MQ capsules come in such different strengths?

Because nothing anchors the number. The figure that circulates is 50 to 150 mg a day by mouth, convention rather than evidence, and I found no derivation for it. Retail capsules are sold at 500 micrograms under the same name.

Is 5-Amino-1MQ approved, and what is known about its safety?

It is not approved. I found no authorisation from the American, European, British, Australian or Canadian medicines regulators. The only published tolerability statement I could find is one line in a 2018 mouse paper, and a 2026 review of the class calls the safety profiles unknown.


This content is for educational and informational purposes only and is not medical advice. Peptides discussed are research compounds and may not be approved for human use. Nothing here should be used to diagnose, treat, cure, or prevent any disease. Always consult a qualified healthcare professional before starting any peptide, supplement, or protocol. Individual responses vary. Do not self-administer compounds without proper medical supervision.

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