5-Amino-1MQ: What It Is, Where to Get It Prescribed, and What It Costs

5-Amino-1MQ is shorthand for 5-amino-1-methylquinolinium. It is a small synthetic molecule, not a peptide: there is no chain of amino acids in it. The core is a quinolinium ring, a two-ring aromatic structure with a positively charged nitrogen, carrying a methyl group on that nitrogen and an amino group at the fifth position. It is a fraction of the size of the peptides it sits alongside in a catalog, and it belongs there because of how it is used and prescribed, not because of its chemistry.

It is not a hormone, it does not act on a hormone receptor, and it is not a growth hormone secretagogue. What it does, in the laboratory, is block one specific enzyme.

The compound comes out of a medicinal chemistry programme at the University of Texas Medical Branch in Galveston, led by Stanley Watowich with Harshini Neelakantan as first author on the key papers. A 2017 paper in the Journal of Medicinal Chemistry screened N-methylated quinolinium, isoquinolinium, pyridinium and benzimidazolium scaffolds against the enzyme nicotinamide N-methyltransferase (NNMT) and identified quinoliniums as the promising series. A 2018 follow-up in Biochemical Pharmacology reported that methylquinoliniums carrying a primary amine crossed cell membranes well and were selective for NNMT over related methyltransferases and over the enzymes of the NAD+ salvage pathway. The 5-amino compound is the one that was carried forward; in the group's 2024 paper in Diabetes, Obesity and Metabolism it is referred to simply as 5A1MQ.

The reason anyone went looking for an NNMT inhibitor is a 2014 paper in Nature from Barbara Kahn's laboratory at Beth Israel Deaconess and Harvard, which reported NNMT expression rising in the white fat and liver of obese and diabetic mice and reported that knocking the enzyme down protected mice against diet-induced obesity. 5-Amino-1MQ was designed as a drug-like way of doing pharmacologically what that study did genetically.

It is not a GLP-1 medication. It does not act on the appetite and incretin pathways that semaglutide and tirzepatide act on, and the 2018 mouse work specifically reported total food intake unchanged in treated animals. It is not a stimulant or a thermogenic. It is not NAD+ and does not contain NAD+; the cell work describes it changing how cells handle a precursor of NAD+, which is a different thing. And it is not a drug with human trial evidence. That last point is the one to hold onto through everything that follows.

Nicotinamide N-methyltransferase takes nicotinamide, the form of vitamin B3 that cells recycle into NAD+, and attaches a methyl group to it, using S-adenosylmethionine (SAM), the cell's main methyl donor. The product, 1-methylnicotinamide (1-MNA), is not used to make NAD+; it is excreted. So every time the enzyme runs it consumes one molecule of an NAD+ precursor and one molecule of SAM. In a tissue where NNMT is highly expressed, the proposed consequence is that nicotinamide is diverted away from NAD+ salvage and SAM is drawn down.

The 2014 Nature work reported the enzyme's expression rising in fat and liver in mouse models of obesity and diabetes, and a 2015 study in Diabetologia reported roughly twofold higher NNMT expression in the fat tissue of people with type 2 diabetes compared with controls. That second finding is observational: it describes the enzyme's level in human tissue, not what happens when it is blocked.

The 2018 Biochemical Pharmacology paper measured what NNMT inhibitors did inside cultured adipocytes: reduced intracellular 1-MNA, increased intracellular NAD+ and SAM, and suppressed lipogenesis, the building of new fat within the cell. This is the origin of the "raises NAD+" description attached to 5-Amino-1MQ. It is a cell-culture measurement, and it has not been reproduced in human tissue.

The Nature paper proposed a mechanism for why blocking NNMT changed body weight in mice without changing how much they ate. Knocking down the enzyme in fat and liver was reported to increase cellular energy expenditure, with adipose SAM and NAD+ rising and two enzymes of polyamine metabolism, ODC and SSAT, being upregulated through changes in histone methylation. Oxygen consumption in adipocytes rose in a way that depended on those enzymes. That study used antisense knockdown of the gene, not 5-Amino-1MQ, so it describes the target rather than this molecule.

A 2019 paper in Biochemical Pharmacology from the Galveston group described NNMT as overexpressed in aged skeletal muscle and linked it to impaired NAD+ salvage, dysregulated sirtuin 1 activity and senescence of muscle stem cells. In 24-month-old mice given an acute muscle injury, treatment with the inhibitor was reported to raise muscle stem cell proliferation and fusion and to support larger regenerated fibre cross-sectional area. Different tissue, different indication, same enzyme and the same proposed NAD+ logic.

This is the main body of evidence and it is entirely in mice. The 2018 Biochemical Pharmacology study treated diet-induced obese mice systemically with a potent NNMT inhibitor and reported reduced body weight, reduced white adipose mass, smaller adipocytes and lower plasma total cholesterol, with total food intake unchanged and no observable adverse effects at the doses used.

The 2024 paper in Diabetes, Obesity and Metabolism is the most directly relevant to clinical use, because it dosed 5A1MQ once daily for 28 days. In diet-induced obese mice it reported dose-dependent limiting of body weight and fat mass gain, improved oral glucose tolerance and insulin sensitivity, suppressed hyperinsulinaemia, less hepatic steatosis and macrophage infiltration on liver histology, and normalisation of ALT, AST and ketone bodies. The same paper characterised the compound's pharmacokinetics after intravenous, oral and subcutaneous dosing in mice and reported distribution to adipose, muscle and liver after subcutaneous injection, which is the route used here.

A 2022 study in Scientific Reports combined the inhibitor with a switch from a high-fat Western diet to a low-fat diet in diet-induced obese mice, and reported that the combination normalised adiposity and weight to those of lean animals faster than the diet switch alone, with a distinct caecal microbiome pattern in treated mice. It is a small mechanistic study and it says nothing about a person who has not changed their diet.

A 2024 paper in Scientific Reports treated mice from 22 to 24 months of age with the inhibitor, intensive exercise, or both, and reported around 40 percent greater grip strength in treated sedentary mice than in sedentary controls, with an additive effect when combined with exercise. The mice were chosen because they recapitulate features of human sarcopenia. That is a rationale for studying it in people; it is not a study in people.

There are no randomised controlled trials of 5-Amino-1MQ in humans. There are no published human trials of any design, and as of September 2026 there are no trials registered under the compound's name. The entire efficacy evidence base is mice and cultured cells, and any source describing human results is describing something that does not exist.

What does exist in humans is evidence about the target rather than the drug. The 2015 Diabetologia study measured NNMT expression in fat tissue from 199 people undergoing abdominal surgery and reported it higher in type 2 diabetes, with plasma 1-MNA tracking tissue NNMT expression and both correlating with insulin resistance. Exercise and bariatric surgery were associated with lower NNMT expression. That is a reason the enzyme is considered an interesting target. It does not tell you what blocking it does in a person.

Beyond that, there is prescribing experience. Physicians have prescribed compounded 5-Amino-1MQ for several years and have formed views about it. That experience is real and is why the compound is on this site, but it is uncontrolled, and the honest framing is "described in mouse and cell research and used clinically," not "shown to work in people."

• It does not establish that 5-Amino-1MQ does anything in a human being. Mouse body-composition findings frequently do not translate, and this compound has not been tested for translation.
• It does not establish an effect size. No human trial has measured one.
• It does not establish a timeline in humans. The 28-day mouse study is the closest thing to a duration reference.
• It does not establish long-term safety in humans. There is no human safety database of any size.
• It does not establish an interaction profile. NNMT also methylates foreign compounds, which is a theoretical reason for care, and nothing more is known.
• It does not establish efficacy for any condition as an FDA-approved treatment. It is not approved for anything.

Do not expect an appetite change; the mechanism described is not an appetite mechanism, and the mouse work reported food intake unchanged. Most people notice nothing in this window, and that is not a sign that anything is wrong.

This is the span the first vial covers at Monday through Friday dosing, and it matches the 28-day duration of the most relevant mouse study. If the body-composition changes described in mice occur in a person at all, they would be gradual, and a scale is a poor instrument for detecting them. Prescribers who track this generally describe waist measurement and how clothes fit rather than a single number.

Refills run on a 28-day cycle, and whether to continue is your physician's decision based on what you report. Nothing in the literature describes a withdrawal effect or a rebound on stopping, but the literature is mice.

Both the diet-switch study and the exercise study in mice paired the inhibitor with a lifestyle change and reported the combination doing more than either alone. That is the frame prescribers describe as well. Anyone presenting 5-Amino-1MQ as a substitute for diet and activity is not describing the research.

The directions are written in millilitres and in insulin-syringe units because that is what you can actually read off the barrel. 0.25 mL is 25 units on a U-100 syringe. You are not calculating anything; the number is printed on your medication, and your physician sets it.

Subcutaneous means into the fat layer, not the muscle. Abdomen and thigh are the usual sites, rotated so the same spot is not used repeatedly. The 2024 mouse pharmacokinetic work reported that subcutaneous dosing produced high systemic exposure with distribution to fat, muscle and liver, which is the reasoning behind the injectable route; human pharmacokinetics have not been published.

Five doses a week for four weeks is 20 doses, which is exactly what a 5 mL vial holds at 0.25 mL per dose. That is why refills run on a 28-day cycle. The weekday-only schedule is the reviewed direction for this product; it is not derived from a human study, because there is none, and your physician may direct otherwise. One vial per fill, always, not a stockpile.

Refrigerated, and it ships that way in insulated packaging with ice packs. Beyond-use dating runs from first puncture and is printed on the label. Keep the vial upright, do not freeze it, and do not use it past the date on the label.

Different mechanisms and, more importantly, different evidence. Semaglutide and tirzepatide act on incretin receptors, reduce appetite, and have large randomised human trials behind the approved brand products. 5-Amino-1MQ acts on an intracellular enzyme, is not described as affecting appetite, and has mouse data only. They are not competing for the same job, and a physician may reasonably suggest either or, in some cases, both.

NAD+ injection is the molecule itself, given directly. 5-Amino-1MQ is described as blocking an enzyme that diverts a precursor of NAD+ away from salvage, which in cultured fat cells was reported to raise NAD+ and SAM. One is a supply approach and the other a conservation approach, in the laboratory. Whether either measurably changes NAD+ in a person, and whether that changes anything you would notice, is a separate question that neither page should overstate.

MOTS-c is a mitochondrial-derived peptide described around metabolic signalling, and the two are sometimes prescribed together, which is why the FUSION blend contains both. From a regulatory standpoint they are in different places: MOTS-c was reviewed by the FDA's advisory committee in July 2026, while 5-Amino-1MQ has not been through that process.