What it is
5-Amino-1MQ is not a peptide. It is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), built on a permanently charged methylquinolinium scaffold rather than an amino acid chain. The free cation carries the formula C10H11N2+, a calculated molecular weight of 159.21 g/mol, PubChem CID 950107 and CAS 685079-15-6. It is sold in more than one salt form; the chloride salt corresponds to PubChem CID 176507677 with a calculated molecular weight of 194.66 g/mol, but no independently confirmed CAS number for the chloride salt itself could be located, and this entry does not print one. Vendor material describes an iodide salt as also circulating; that claim comes from a chloride-salt seller’s own marketing copy and is reported here only as an unverified claim about market composition, not as an established fact.
The compound is referred to under several shorthand forms in the primary literature, including 5-A-1-MQ, 5A1MQ, 5-AMQ and, in at least one paper, “5MQ,” a label that is also used elsewhere for a different, unsubstituted parent molecule. A page or product that says only “1MQ” should be read carefully, since that string alone is ambiguous between compounds.
Where it came from
The molecule was discovered and characterized by Harshini Neelakantan, Hua-Yu Leo Wang, Stanton F. McHardy and Stanley J. Watowich, working across the University of Texas Medical Branch at Galveston and the Center for Innovative Drug Discovery at the University of Texas at San Antonio, in a structure-activity screening program against NNMT (Neelakantan et al. 2017, Journal of Medicinal Chemistry). Later preclinical papers from the same author group carry an affiliation to Ridgeline Therapeutics, a company Neelakantan and Watowich went on to co-found. This entry corrects a claim that circulates about the compound’s origin: 5-Amino-1MQ was not developed at the Salk Institute. The Salk-adjacent work that is sometimes conflated with it is a separate 2014 Nature paper from a Beth Israel Deaconess Medical Center and Harvard Medical School group (Kraus et al. 2014), which used genetic antisense-oligonucleotide knockdown of the Nnmt gene in mice, not this drug, to show that lowering NNMT activity protected against diet-induced obesity. That paper established NNMT as a plausible drug target; it is the UTMB and UTSA group, later Ridgeline, that built and tested 5-Amino-1MQ itself as a small-molecule inhibitor of it.
Mechanism, and where the animal-versus-human line falls
NNMT is a cytosolic enzyme that transfers a methyl group from S-adenosylmethionine (SAM) to nicotinamide, the form of vitamin B3 that feeds the NAD+ salvage pathway, producing 1-methylnicotinamide. Because nicotinamide is a direct NAD+ precursor and SAM is the cell’s general methyl donor, a 2021 review described high NNMT activity as capable of draining both pathways at once (Ambrose review, Molecular Metabolism 2021).
The foundational demonstration that reducing NNMT activity protects against diet-induced obesity in mice used genetic knockdown, not a drug: Kraus et al. 2014 found Nnmt to be the most reciprocally regulated gene in white adipose tissue in a mouse model of altered glucose transport, that its expression rose in the adipose tissue and liver of obese, diabetic mice, and that antisense knockdown of the gene raised cellular energy expenditure and adipose SAM and NAD+ levels. Separately from that genetic work, Neelakantan and colleagues built methylquinolinium NNMT inhibitors, screened for membrane permeability and enzyme selectivity, and reported that in cultured adipocytes these inhibitors lowered intracellular 1-methylnicotinamide, raised NAD+ and SAM, and suppressed lipogenesis (Neelakantan et al. 2018, Biochemical Pharmacology). A later research line from the same UTMB group proposed a second, independent mechanism in aged skeletal muscle: that NNMT activity rises with age in muscle and is tied to muscle-stem-cell senescence through impaired NAD+ salvage and dysregulated SIRT1 activity, and that inhibiting it in aged mice reactivated senescent muscle stem cells (Neelakantan et al. 2019, Biochemical Pharmacology).
A distinct and separate body of literature exists on NNMT biology in actual human tissue: NNMT expression in human adipose tissue has been reported to rise with obesity, type 2 diabetes and insulin resistance, and to fall after exercise or bariatric surgery (Kannt et al. 2015, Diabetologia). That is human evidence that the enzyme NNMT is biologically relevant to human metabolic disease. It is not evidence that this drug, 5-Amino-1MQ, does anything at all in a living person, and the two should never be read as the same claim. No paper located for this entry demonstrated brown-fat-style “browning,” such as UCP1 induction, following 5-Amino-1MQ treatment; the sourced mechanism is suppressed lipogenesis and altered NAD+/SAM availability, and a browning claim should not be taken as established.
What has been studied, and in what species
Every quantitative efficacy finding for 5-Amino-1MQ itself comes from mice, and every pharmacokinetic finding comes from rats. In diet-induced obese mice, systemic treatment with an NNMT inhibitor was reported to reduce body weight and white adipose mass, decrease adipocyte size and lower plasma total cholesterol, without affecting total food intake or producing observable adverse effects in that efficacy-focused paper (Neelakantan et al. 2018). A later 28-day, dose-ranging study in diet-induced obese mice, run once daily and comparing intravenous, oral and subcutaneous dosing, reported that treatment dose-dependently limited body weight and fat mass gains, improved oral glucose tolerance and insulin sensitivity, suppressed elevated insulin levels, and attenuated hepatic steatosis, with reduced liver weight, size, triglyceride content and circulating ALT and AST that moved toward normal (Babula et al. 2024, Diabetes, Obesity and Metabolism). The exact milligram-per-kilogram doses used in these two obesity papers were not confirmed for this entry and are not stated as numbers here.
In a separate muscle-injury study in 24-month-old mice, a barium-chloride tibialis anterior injury model, animals treated with 5 or 10 mg per kilogram of an NNMT inhibitor for one week, or 10 mg per kilogram for three weeks, were reported to show roughly a two-fold increase in myofiber cross-sectional area and about a 70 percent increase in peak torque of the injured muscle compared with saline-treated controls (Neelakantan et al. 2019). A later study in aged mice, comparing the same inhibitor against exercise and the combination, reported roughly 40 percent greater grip strength in sedentary treated mice than sedentary controls, about 20 percent in exercised mice, and roughly 60 percent in the combined group, an additive pattern (Dimet-Wiley et al. 2024, Scientific Reports).
A rat pharmacokinetic study developed and validated a liquid chromatography-tandem mass spectrometry assay and reported an oral bioavailability of 38.4 percent, a mean oral peak plasma concentration of 2,252 ng/mL, and a terminal elimination half-life of about 3.8 hours after intravenous dosing and 6.9 hours after oral dosing (Awosemo et al. 2021, Journal of Pharmaceutical and Biomedical Analysis). This is a rodent pharmacokinetic finding; no comparable human pharmacokinetic data exists.
The only study located that touched human-derived material at all was a cultured human cervical cancer cell line, HeLa, in which the compound reduced proliferation and produced apoptotic changes and reduced phospho-Akt and SIRT1 protein levels, while not affecting proliferation of a separate human embryonic kidney cell line used as a comparison (Akar et al. 2021). That paper cited the mouse obesity and muscle literature as background context; it did not itself test weight, fat mass or muscle outcomes, and it is a fully in-vitro cancer-cell experiment, not a study of a person.
The human evidence: there is none
As of this writing, no interventional human trial, no observational human study and no published case report of 5-Amino-1MQ being administered to a human being, at any dose, for any purpose, has been located. This is stated plainly rather than softened, because the accurate description is that human data does not exist, not merely that it is limited. Searches of ClinicalTrials.gov for “5-Amino-1MQ,” “NNMT inhibitor,” and the condition “NNMT,” and a search by sponsor for Ridgeline Therapeutics, each returned zero registered trials. Every claim about weight, fat mass, muscle strength or metabolic improvement attributed to this compound anywhere rests on mouse studies, with pharmacokinetics coming from rats.
Safety
No human safety data exists, because no human has been studied. The efficacy-focused diet-induced-obesity paper noted, as part of its results rather than as a dedicated toxicology finding, that treated mice showed no change in total food intake and no observable adverse effects; a separate paper reported liver enzyme values improving toward normal in treated obese mice as part of its efficacy analysis. Neither is a dedicated safety or toxicology study, and no repeat-dose toxicology, genotoxicity or reproductive toxicology study for 5-Amino-1MQ was located. Anyone taking this compound is doing so with no established human dose, no documented human side-effect profile and no data on drug interactions, long-term organ effects, or use in pregnancy or lactation.
Regulatory status
5-Amino-1MQ has never been submitted as an investigational new drug application in the United States and has no approved label anywhere. Author affiliations show Ridgeline Therapeutics continuing preclinical NNMT-inhibitor publications into 2024 and beyond, including into a chronic kidney disease research line, which indicates ongoing industry and academic interest in the mechanism, but no evidence that any of it has reached a registered human trial. This entry does not state a position on whether 5-Amino-1MQ appears on the FDA’s list of bulk substances used in compounding, or whether an FDA warning letter has ever named it, because that could not be independently confirmed; it also does not assert a World Anti-Doping Agency status beyond noting that no reference to the compound was found in the anti-doping literature searched here, which is not the same as a verified clearance.
What circulates, and why the route is different here
Unlike most entries on this site, which circulate as injectable peptides, 5-Amino-1MQ is typically sold and used as an oral capsule product. That fits its identity as a small, drug-like molecule rather than a peptide that would be broken down if swallowed, and it is directionally consistent with the rat pharmacokinetic finding above showing meaningful oral exposure, though that is a rodent figure and not a justification for a human dose. Market material commonly describes 50 mg capsules taken once to three times daily, roughly 50 to 150 mg per day, sometimes with a cycling pattern of about three to four weeks on and one to two weeks off. These figures were not independently verified against current vendor listings this session, are drawn from enthusiast and product material already on hand rather than a live market survey, and are reported only as a pattern, never as a recommendation.
The comparison this site’s policy requires is unusually stark for this compound: a specific milligram figure and a cycling schedule circulate for a molecule that, as described above, has never been given to a human being in any published study of any kind. There is no dose in the clinical literature to compare the circulating figure against, favorably or unfavorably, because none exists. The circulating number did not come from a human trial arm being repackaged, the way it does for many other entries on this site; it has no known relationship to anything measured in a person at all.
What is not known
The largest unknown, and the one this entry leads and closes on, is everything about this compound in a human being. Whether it has any effect at all in a person, whether it is safe at any dose, and whether the mouse findings on weight, fat mass, glucose handling or muscle strength would translate to humans in any degree, are all unanswered questions with no published data bearing on them.
There is no established human dose, no human maximum tolerated dose, and no basis in the literature for converting the mouse milligram-per-kilogram figures that do exist, such as the 5 and 10 mg/kg used in the muscle-injury study, into a human-equivalent figure for any purpose. There is no human pharmacokinetic data, meaning the oral bioavailability and half-life figures above are rat values only. The longest reported dosing period located for this compound is 28 days for the metabolic mouse study, or roughly two months for the aged-mouse grip-strength study; no chronic animal study beyond that, and certainly no long-term human study, was found. Whether NNMT inhibition produces true thermogenic “browning” of fat, as opposed to the sourced finding of suppressed lipogenesis and altered NAD+/SAM handling, has not been demonstrated in the papers located here. The chloride salt’s CAS number remains unconfirmed, and a vendor claim that most product sold is actually the iodide salt, not the chloride, has not been independently checked.
5-Amino-1MQ is, on the record assembled here, a mouse and rat finding, not a human one. Every downstream claim about what it does for a person’s weight, muscle or metabolism is an extrapolation from that animal record, made in the absence of a single published human study.