5-Amino-1MQ

5-Amino-1MQ Research Overview

5-Amino-1MQ is a small molecule, not a peptide, that blocks the enzyme NNMT in fat cells. Mouse studies show reduced fat mass and improved metabolic markers; there are no human trials of any kind.

Also known as: 5-amino-1-methylquinolinium, 5-A-1MQ, 5-AMQ, NNMT inhibitor

Background

5-Amino-1MQ is not a peptide. It is a small, positively charged molecule developed at the University of Texas Medical Branch as a selective inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme that is unusually active in the fat and liver tissue of obese animals and people. It came out of a medicinal chemistry program that was specifically trying to build NNMT inhibitors able to cross cell membranes, since earlier compounds could hit the enzyme in a test tube but not inside a cell.

The evidence base is entirely rodent and cell culture. In diet-induced obese mice, about 11 days of twice-daily injections cut body weight by roughly 5 to 7 percent, reduced white fat mass by around 12 percent and shrank fat cells, with lower cholesterol and no change in food intake. A later study in aged mice reported improved muscle stem cell activity and faster muscle regeneration after injury. That is the whole picture. No human safety, pharmacokinetic or efficacy study has been published.

Despite that, 5-Amino-1MQ is widely sold as oral capsules and marketed for fat loss, with administration parameters numbers that appear to be loose extrapolations from mouse experiments. The oral route itself is an open question, since the animal work used injections and oral absorption has not been characterized. It sits in the category of plausible mechanism, real animal data, and zero human evidence. Anyone taking it is running an uncontrolled experiment on themselves.

Mechanistic Profile

NNMT takes a methyl group from SAM (S-adenosylmethionine) and attaches it to nicotinamide, producing 1-methylnicotinamide. In fat cells this consumes both an NAD+ precursor and the cell's main methyl donor. Blocking the enzyme leaves more nicotinamide available for NAD+ synthesis and raises SAM levels, which together increase cellular energy expenditure and shift adipocytes away from storing lipid. In mouse fat this shows up as smaller adipocytes, higher fatty acid oxidation and less new fat synthesis. The muscle regeneration findings are thought to run through the same NAD+ and methylation changes acting on muscle stem cells. Whether any of this happens at oral doses in clinical literature has not been measured.

Reported Research Findings

• Diet-induced obese mice lost about 5 to 7 percent of body weight and 12 percent of white fat mass over 11 days without eating less. (rodent)

• Fat cell size and plasma cholesterol dropped in treated mice. (rodent)

• Improved muscle stem cell proliferation and regeneration after injury in aged mice. (rodent)

• Selective for NNMT over related methyltransferases in enzyme assays, and membrane permeable in cell studies. (in vitro)

• Genetic knockdown of NNMT protected mice against diet-induced obesity, the finding that motivated inhibitor development. (rodent)

Analytical Validation, Formulation and Storage

• Purity: 99% or higher as verified by HPLC, with a third-party certificate of analysis available per batch.

• Formulation: lyophilised (freeze-dried) powder in a sterile sealed glass vial, to be reconstituted with an appropriate solvent for laboratory use.

• Reported half-life: Not established in clinical literature. Short in rodents based on the twice-daily administration parameters used in studies..

• Storage: keep lyophilised material cool, dark and dry (long-term at or below -20 °C). Store reconstituted solutions refrigerated, avoid repeated freeze-thaw cycles and use within laboratory-defined windows.

Selected Literature

• Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochemical Pharmacology, 2018.

• Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. Biochemical Pharmacology, 2019.

• Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature, 2014.

Cloud Aminos supplies 5-Amino-1MQ as a high-purity research material intended strictly for controlled laboratory use in vitro or in established animal models. This compound is not approved as a drug, diagnostic or dietary ingredient and is not manufactured, packaged or marketed for human consumption, self-experimentation, clinical application or any use outside properly designed and ethically approved research protocols.