5-Amino-1MQ

What 5-Amino-1MQ is

5-Amino-1MQ is a lab-made small molecule that has been tested only in cells and in mice. As of mid-2026, no human trial of it has been published. The FDA has not approved it, and neither has the EMA in Europe or the MHRA in the UK. Nothing in this guide is proof that it is safe or that it works in people. The findings are here for research and learning only.

Its full name is 5-amino-1-methylquinolinium. Many compounds on this site are peptides. This one is not. It is a quinolinium salt with a low molecular weight. In the mouse studies done so far, it was given as a shot under the skin. A 2024 study found that mice took up very little of it by mouth [18].

The compound blocks an enzyme called NNMT, short for nicotinamide N-methyltransferase. An enzyme is a protein that speeds up one chemical reaction. NNMT sits in the fluid inside cells. Liver and white fat make the most of it. 5-Amino-1MQ is selective, meaning it is aimed at NNMT, and it can cross the outer wall of a cell.

Why NNMT? Scientists turned the enzyme down in mice by acting on its gene. Those mice burned more energy and were protected from obesity caused by diet [5]. Researchers have since called NNMT a central node. It ties the methylation state of a cell to how the whole body uses energy [8]. A newer review names NNMT as a possible treatment target for metabolic syndrome. It sums up a growing set of lab studies that tie the enzyme to body fat, insulin sensitivity and the way the liver handles fat [19].

A group at the University of Texas Medical Branch made 5-Amino-1MQ and described it first, in 2018. They screened a series of quinolinium-based NNMT blockers and improved them step by step. 5-Amino-1MQ stood out for three reasons. It was selective for NNMT. It crossed cell walls well. Given as a shot, it cut body weight and fat in obese mice [11]. Since then, the same group and nearby groups have published follow-up studies on aging muscle and on wider metabolic problems.

How much research there is

A small set of cell and mouse studies, mostly from one lab, and no human data.

Question	Answer
Stage of the evidence	Cells and mice only. No human trial data for 5-Amino-1MQ had been published as of 2026
Kinds of studies	Enzyme tests and cell tests in a dish. Mice made obese by diet, and aged mice. Gene knockdown work [5] and enzyme biochemistry [12] back these up
Who was tested	Mice only: mice with diet-induced obesity and aged mice. No people
Checked by other labs	The lab that made it published the earlier quinolinium series in 2017 [10] and the first 5-Amino-1MQ paper in 2018 [11]. Its follow-up studies run to 2024 [15], [18]. A separate group backed NNMT as a target with a blocker series built in a different way [16]. That group did not use 5-Amino-1MQ
Where the work comes from	Mainly one university lab, at the University of Texas Medical Branch. Drug companies also run early NNMT blocker programs, but those are not about 5-Amino-1MQ
Approval	A research compound still under study. Not approved by the FDA, the EMA or the MHRA
Do the results agree	Yes, within one research program. The 2018 study, the 2018 abstract and the 2024 study all reported less body weight and fat in obese mice [11], [14], [18]. Only the 2024 study reported better glucose tolerance and insulin sensitivity [18]

How it might work

The idea rests on blocking one enzyme, NNMT. That enzyme sits where two basic cell supplies meet.

• SAM (S-adenosylmethionine) is the main methyl donor used all through the cell. A methyl group is a small chemical tag.
• NAD+ (nicotinamide adenine dinucleotide) is a helper molecule, or coenzyme. It is central to energy metabolism and to a wide range of enzyme reactions.

NNMT as a methyl drain

NNMT takes a methyl group off SAM and puts it on nicotinamide. That makes two products: MNA (1-methylnicotinamide) and SAH (S-adenosylhomocysteine).

In the body, this reaction does not really run backward. Some tissues also carry a lot of NNMT. So the enzyme can use up an outsized share of the SAM a cell has. Cancer metabolism researchers gave this a name, a “metabolic methylation sink”. Their work looked at how NNMT leaves fewer methyl groups for other jobs, such as tagging DNA and histones, the proteins DNA wraps around [4].

SAM is made and refilled by a loop of reactions called the methionine cycle. Biochemical work showed that NNMT physically interacts with that cycle and helps set how fast it runs. That makes NNMT a control point for methyl donors, not just a cleanup enzyme [12].

A 2017 review summed up this change in thinking. NNMT was once seen as a side enzyme that clears vitamin B3. It is now studied as a metabolic regulator in obesity, diabetes and cancer research [8].

The link to NAD+

Nicotinamide is more than the thing NNMT works on. Cells also turn it straight into NAD+ through the NAD+ salvage pathway. That pathway is one of the main ways cells keep their NAD+ levels up.

NNMT uses up free nicotinamide when it turns it into MNA. Researchers have proposed that a very active NNMT pulls raw material away from salvage. Blocking the enzyme is thought to do two things at once. It may leave more nicotinamide for making NAD+, and it may keep SAM free for other methylation jobs [5].

This is why 5-Amino-1MQ is studied next to NAD+ precursors, compounds the body turns into NAD+. Both are studied for a possible effect on NAD+ in cells. They act at different points:

• NAD+ precursors add raw material directly.
• Blocking NNMT is studied for how much of the nicotinamide already in the body stays in salvage and is not sent off to methylation.

Three reviews give the wider picture.

• A broad review of ways to raise NAD+ walks through this salvage logic in detail. It lists the many molecular approaches now in lab testing and early human testing [13].
• NAD+ has drawn a great deal of research as a regulator of metabolism and of aging in cells. The wider field uses that link to justify its interest in enzymes that sit upstream of NAD+, and NNMT is one of them [7].
• A 2021 review places NNMT at a crossroads between cell metabolism and epigenetic control, the system of tags that turns genes on and off. It treats blocking NNMT as a single lever that could shift both methylation and NAD+-dependent metabolism together [17].

Fat tissue and energy use

White fat and liver carry very high levels of NNMT. The first gene knockdown research used antisense oligonucleotides, short lab-made strands that turn a gene down. They lowered NNMT in just those two tissues in mice. The mice burned more energy, resisted diet-induced obesity and had better insulin sensitivity [5]. This is the work that made NNMT a metabolic target.

Human tissue research ran alongside it. It found that fat tissue is a major source of the NNMT that travels in the blood, and of products of the homocysteine pathway that follow from it. NNMT levels in human fat samples tracked with body measurements and with metabolic measures. This evidence is observational. Researchers use it to argue that NNMT in fat could matter in human metabolism too, apart from the mouse knockdown data [3].

The gene work and the tissue work together are the basic case cited for building small-molecule NNMT blockers such as 5-Amino-1MQ.

MNA as a marker

MNA, the product NNMT makes, is easy to measure in blood and urine. Researchers use it as a sign of how active the pathway is. MNA also has its own body of drug research, which is useful background:

• In rodents, MNA worked against blood clots. It did so through a pathway that depends on cyclooxygenase-2 and prostacyclin, which is separate from any effect on NNMT [1].
• In other rodent work, MNA lowered inflammation in a contact-hypersensitivity model. The authors again pointed to prostacyclin signaling [2].
• A study in rats mapped how MNA is absorbed, spread through the body and removed. Researchers draw on that data when they read MNA in the blood as a sign of NNMT activity [9].

None of this MNA research used 5-Amino-1MQ. It shows why the products of this pathway interest researchers apart from methylation and NAD+.

From early tools to a selective blocker

The first chemical tools used to probe NNMT had problems. Some were not selective enough, some crossed cell walls poorly, and some had both faults. That limited their use in cell and animal research.

A structure-activity relationship study came out in 2017. This kind of study changes a molecule piece by piece to see what each change does. It worked through a quinolinium series to improve selectivity for NNMT and drug-like traits. That work came right before the choice of 5-Amino-1MQ as a lead compound, and fed into it [10].

One year later, the same group published the first paper devoted to 5-Amino-1MQ. It reported how selective the compound was, how well it crossed cell walls, and what it did in a diet-induced-obesity model [11].

Later, an independent industry group described a tricyclic series of NNMT blockers with a different structure, made for research on metabolic disorders. The chemistry has nothing to do with the 5-Amino-1MQ series. Researchers see it as outside support for NNMT as a target a drug can hit, and for blocking NNMT as a research approach [16].

What the studies found

Every study below used cells or rodents. No human trial data for 5-Amino-1MQ had been published when this guide was last reviewed.

Mice made obese by diet

• The 2018 study. Obese mice on a high-fat diet got shots of 5-Amino-1MQ for 11 days. Obesity that was already in place went into reverse. Body weight and body fat fell, fat cells shrank, and blood cholesterol dropped. The study did not measure blood sugar or insulin. The mice did not eat less. The authors read this as an effect on energy use, not on appetite [11].
• The conference abstract. The same group also reported on building NNMT blockers that work by mouth. The abstract does not name the compounds. The aim was to cut body fat, insulin resistance and high blood sugar. The abstract repeated the main mouse results on body weight, fat and cholesterol. It added data on how rats handled the compounds [14].

Wider metabolic problems

• A 2024 study took this line further. Obese mice got 5-Amino-1MQ once a day for 28 days. They gained less weight and fat than untreated mice. Glucose tolerance and insulin sensitivity got better, and signs of fatty liver eased. These were new measures on top of the earlier body fat results [18].
• A review from about the same time set these results within the wider research on NNMT and metabolic syndrome. It summed up the lab case for blocking NNMT across body fat, blood sugar control and fat metabolism. It called this an active area of ongoing study [19].

Muscle and aging

• A 2019 study from the same group tested 5-Amino-1MQ in aged mice. The paper calls it only an NNMT inhibitor in its title. It woke up senescent muscle stem cells, also called satellite cells. Senescent cells are cells that have stopped dividing. Aged muscle also regrew better after injury. This moved NNMT blocker research past body fat and into the biology of aging muscle [15].
• Later reviews often cite this result as a sign that NNMT matters in tissues other than liver and fat. It is one study in aged mice. It has not been repeated, and it is not a human finding.

Liver and mechanism

• Sirt1. In mice, NNMT controlled how the liver handles nutrients by keeping the Sirt1 protein stable. Sirt1 is a deacetylase that depends on NAD+, and it is closely tied to metabolic and longevity research. This gives a specific route from NNMT activity to NAD+-dependent signaling in the liver [6].
• Methionine cycle. Biochemical work mapped the physical contacts between NNMT and the enzymes of the methionine cycle. It made clearer how NNMT controls methyl donors at the level of molecules, which supports the model described above [12].
• The 2021 review pulled the liver and epigenetic threads together. It described the crossroads position of NNMT, between cell metabolism and epigenetic control, as the shared reason behind the research program on NNMT blockers in metabolic disease [17].

Safety

In mice

• The diet-induced-obesity studies reported no significant harmful findings at the doses used. Food intake stayed the same. The authors said this argued against general toxicity or sickness as the cause of the weight changes [11].
• The aged-mouse muscle study also used 5-Amino-1MQ. A blood chemistry panel in treated mice showed no signs of toxicity [15].
• This guide’s review of the published research found no dedicated study of toxicity, gene damage or long-term cancer risk for 5-Amino-1MQ.

What is not known

• There is no human data on safety, tolerability or how the body handles 5-Amino-1MQ. All data on dose, exposure and effect come from mice and may not carry over to people.
• Nobody has described effects past the lengths of the published mouse studies.
• No formal drug interaction studies were found.
• Few labs other than the one that made it have repeated the work.
• The first medicinal chemistry work checked selectivity against other methyltransferases and metabolic enzymes. It did not profile every related enzyme family in full [10].

Legal status in the US

• Not FDA approved. 5-Amino-1MQ has no approval for any medical use from the FDA. The same is true of the EMA in Europe and the MHRA in the UK.
• Not named by WADA. As of 2026, the World Anti-Doping Agency does not list it by name on its Prohibited List.
• Research use. It is a small-molecule research compound with no approved human use. It is supplied strictly for laboratory research, not for human use, whatever its WADA status.

Limits of the research

1. No human data. Every result in this guide comes from cells or mice. If it is ever studied in people, the size of the effects, the safety record and the way the body handles it could be very different.
2. One main lab. Most of the primary research on 5-Amino-1MQ comes from a single university group. No independent lab has yet published a repeat using this exact compound.
3. Short studies. The published mouse studies gave the compound for fairly short periods. Effects and tolerability over longer times have not been described.
4. Cause is not pinned down. The biochemistry of NNMT in methylation and NAD+ metabolism is well described. It is less clear how much of the whole-animal result comes from blocking NNMT and how much from other possible off-target effects of 5-Amino-1MQ.
5. Narrow models. The research so far used diet-induced-obesity mice and aged mice. The results should not be stretched to other species, settings or diseases.
6. Possible bias in what gets published. This cannot be ruled out. It applies to any early research field that sits in a small number of labs.

In mice, blocking NNMT with 5-Amino-1MQ cut body fat and improved blood sugar. Nobody has yet tested it in people.

References

Selected peer-reviewed references, each verified against the CrossRef API before inclusion. Ordered by date of publication.

1. Chlopicki S, Swies J, Mogielnicki A, Buczko W, et al. (2007). 1-Methylnicotinamide (MNA), a primary metabolite of nicotinamide, exerts anti-thrombotic activity mediated by a cyclooxygenase-2/prostacyclin pathway. British Journal of Pharmacology, 152(2), 230–239. DOI: 10.1038/sj.bjp.0707383
2. Bryniarski K, Biedron R, Jakubowski A, Chlopicki S, et al. (2008). Anti-inflammatory effect of 1-methylnicotinamide in contact hypersensitivity to oxazolone in mice; involvement of prostacyclin. European Journal of Pharmacology, 578(2-3), 332–338. DOI: 10.1016/j.ejphar.2007.09.011
3. Riederer M, Erwa W, Zimmermann R, Frank S, et al. (2009). Adipose tissue as a source of nicotinamide N-methyltransferase and homocysteine. Atherosclerosis, 204(2), 412–417. DOI: 10.1016/j.atherosclerosis.2008.09.015
4. Ulanovskaya O, Zuhl A, Cravatt B (2013). NNMT promotes epigenetic remodeling in cancer by creating a metabolic methylation sink. Nature Chemical Biology, 9(5), 300–306. DOI: 10.1038/nchembio.1204
5. Kraus D, Yang Q, Kong D, Banks A, et al. (2014). Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature, 508(7495), 258–262. DOI: 10.1038/nature13198
6. Hong S, Moreno-Navarrete J, Wei X, Kikukawa Y, et al. (2015). Nicotinamide N-methyltransferase regulates hepatic nutrient metabolism through Sirt1 protein stabilization. Nature Medicine, 21(8), 887–894. DOI: 10.1038/nm.3882
7. Verdin E (2015). NAD+ in aging, metabolism, and neurodegeneration. Science, 350(6265), 1208–1213. DOI: 10.1126/science.aac4854
8. Pissios P (2017). Nicotinamide N-Methyltransferase: More Than a Vitamin B3 Clearance Enzyme. Trends in Endocrinology & Metabolism, 28(5), 340–353. DOI: 10.1016/j.tem.2017.02.004
9. Szafarz M, Kus K, Walczak M, Zakrzewska A, et al. (2017). Pharmacokinetic Profile of 1-Methylnicotinamide Nitrate in Rats. Journal of Pharmaceutical Sciences, 106(5), 1412–1418. DOI: 10.1016/j.xphs.2017.01.022
10. Neelakantan H, Wang H, Vance V, Hommel J, et al. (2017). Structure-Activity Relationship for Small Molecule Inhibitors of Nicotinamide N-Methyltransferase. Journal of Medicinal Chemistry, 60(12), 5015–5028. DOI: 10.1021/acs.jmedchem.7b00389
11. Neelakantan H, Vance V, Wetzel M, Wang H, et al. (2018). Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochemical Pharmacology, 147, 141–152. DOI: 10.1016/j.bcp.2017.11.007
12. Hong S, Zhai B, Pissios P (2018). Nicotinamide N-Methyltransferase Interacts with Enzymes of the Methionine Cycle and Regulates Methyl Donor Metabolism. Biochemistry, 57(40), 5775–5779. DOI: 10.1021/acs.biochem.8b00561
13. Rajman L, Chwalek K, Sinclair D (2018). Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence. Cell Metabolism, 27(3), 529–547. DOI: 10.1016/j.cmet.2018.02.011
14. Neelakantan H, Watowich S (2018). Development of Oral Bioavailable Nicotinamide N-Methyltransferase Inhibitors to Reduce Adiposity, Insulin Resistance, and Hyperglycemia. Diabetes, 67(Supplement_1). DOI: 10.2337/db18-115-lb
15. Neelakantan H, Brightwell C, Graber T, Maroto R, et al. (2019). Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. Biochemical Pharmacology, 163, 481–492. DOI: 10.1016/j.bcp.2019.02.008
16. Kannt A, Rajagopal S, Hallur M, Swamy I, et al. (2021). Novel Inhibitors of Nicotinamide-N-Methyltransferase for the Treatment of Metabolic Disorders. Molecules, 26(4), 991. DOI: 10.3390/molecules26040991
17. Roberti A, Fernández A, Fraga M (2021). Nicotinamide N-methyltransferase: At the crossroads between cellular metabolism and epigenetic regulation. Molecular Metabolism, 45, 101165. DOI: 10.1016/j.molmet.2021.101165
18. Babula J, Bui D, Stevenson H, Watowich S, et al. (2024). Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction. Diabetes, Obesity and Metabolism, 26(11), 5272–5282. DOI: 10.1111/dom.15879
19. Sun W, Zhu X, Li J, Mei Y, et al. (2024). Nicotinamide N-methyltransferase (NNMT): a novel therapeutic target for metabolic syndrome. Frontiers in Pharmacology, 15. DOI: 10.3389/fphar.2024.1410479