5-Amino-1MQ

5-Amino-1MQ is a small synthetic molecule that inhibits an enzyme called nicotinamide N-methyltransferase, abbreviated as NNMT. It is cataloged on this site alongside research peptides, but it is important for researchers to know that it is not a peptide: it has no amino acid sequence whatsoever. Instead, it is a quinolinium compound, a small charged ring molecule, developed in academic laboratories in the 2010s as a tool for studying what occurs in fat and muscle tissue when NNMT is inhibited.

This page summarizes the research record in research terms: what the molecule is, how the enzyme it targets became a research subject, how researchers study it, how research material is made and tested, and where the limits of evidence lie. The entire efficacy record for this compound is preclinical, established in cells and mice. 5-Amino-1MQ supplied for laboratory work is a research material only. It is not an approved medicine or supplement, and nothing on this page describes use in people.

5-Amino-1MQ, full name 5-amino-1-methylquinolinium, is a small organic cation built on a quinoline ring system, two fused rings with a nitrogen atom that carries a permanent positive charge and a methyl group. An amino group at position 5 of the ring is the feature that gives the compound its potency, and the name records both facts: the 5-amino position and the 1-methyl group on the ring nitrogen, shortened to 1MQ.

The bare cation has the molecular formula C10H11N2+ and a molecular weight of about 159.21 grams per mole. Chemical databases record it under PubChem CID 950107. Because a charged molecule cannot exist alone, it is always supplied as a salt: the iodide salt, formula C10H11IN2, weighs about 286.11 grams per mole and carries CAS number 42464-96-0, and a chloride salt form is also recorded. Catalog pages that quote different weights for this compound typically reference different salts, which is why the salt form on a certificate of analysis is important.

One crucial point of accuracy deserves emphasis because supplier material can be incorrect in both directions. Some catalogs list this compound with a formula containing oxygen and a weight near 176 grams per mole, which describes a different substance, and others describe it as a peptide or describe its production as peptide synthesis. It is neither. It is a fully synthetic small molecule of the quinolinium class, in the same broad chemical family as other charged heterocyclic enzyme inhibitors, and it is grouped with peptide products on research sites only because the metabolic questions it is used to study overlap with theirs.

The history has two threads that meet in 2014. The older thread is NNMT itself, an enzyme known for decades as part of the body's methylation machinery, clearing nicotinamide, a form of vitamin B3, by attaching a methyl group to it. The enzyme drew little metabolic attention until epigenetics and NAD+ biology made its side effects interesting: every nicotinamide molecule NNMT methylates is one the cell cannot recycle into NAD+, and every reaction consumes one of the cell's methyl donors.

The threads met in a 2014 paper in Nature from Daniel Kraus, Barbara Kahn, and colleagues at Beth Israel Deaconess Medical Center and Harvard Medical School. Comparing fat tissue from mice engineered for insulin sensitivity or resistance, the team found NNMT was the most strongly reciprocally regulated gene in white adipose tissue, with NNMT levels elevated in the fat and liver of obese and diabetic mice. Knocking the enzyme down in mice protected them against diet-induced obesity, turning NNMT from a housekeeping enzyme into a research target almost overnight.

The compound thread starts at the University of Texas Medical Branch, where Harshini Neelakantan, Stanton McHardy, Stanley Watowich, and colleagues developed small molecule inhibitors of NNMT. Their 2017 structure-activity study in the Journal of Medicinal Chemistry mapped a series of methylquinolinium compounds and identified 5-amino-1-methylquinolinium, the molecule shortened to 5-Amino-1MQ, as a potent and selective member. A 2018 paper from the same program demonstrated the inhibitor series reversing high fat diet-induced obesity in mice, and a 2019 paper extended the work to aged muscle stem cells. The compound has remained an academic research tool since: no company has carried it into human trials, and no clinical development program exists in the published record.

The mechanism is a single enzyme inhibition, and it is unusually straightforward. NNMT resides in the cytosol of fat and liver cells and catalyzes one reaction: it takes nicotinamide and, using S-adenosylmethionine, called SAM, as the methyl donor, produces 1-methylnicotinamide. 5-Amino-1MQ was designed to occupy the enzyme's substrate site and block that reaction. In the 2017 structure-activity work, it inhibited NNMT with an IC50 of about 1.2 micromolar, roughly ten times more potently than the unsubstituted parent compound 1-methylquinolinium, and testing showed it crossed cell membranes, which an intracellular enzyme inhibitor must do, and did not inhibit related methyltransferases or NAD+ salvage enzymes at the studied exposures.

Blocking the enzyme sets off three connected changes that researchers measure. First, nicotinamide that would have been methylated remains available for the NAD+ salvage pathway, and intracellular NAD+ levels rise in treated adipocytes; NAD+ is the cofactor that links the cell's redox state to energy metabolism and feeds the sirtuin enzymes, including SIRT1. Second, SAM that would have been consumed accumulates, altering methylation capacity, including histone methylation marks in fat tissue. Third, the 2014 knockdown work connected those changes to a polyamine flux program: ornithine decarboxylase and related enzymes increase, adipocytes consume more oxygen, and energy expenditure rises.

In the animal experiments themselves, the measured outcomes were reduced body weight and white fat mass, smaller adipocytes, and lower plasma cholesterol in diet-induced obese mice, with no change in food intake reported, which is why researchers describe the effect as expenditure-driven rather than appetite-driven. In aged muscle, the same inhibition was reported to affect stem cell senescence rather than fat. All of these findings are in cells and mice. The mechanism is well defined chemically; whether it produces any particular effect in a person is a question that no published study has tested.

Since 5-Amino-1MQ is a small molecule and not a peptide, its manufacture is ordinary organic synthesis, not solid-phase peptide synthesis. This section describes the peptide platform briefly for contrast, as this site's readers encounter it on every other page, and then describes how a compound of this class is actually produced.

Research peptides are built by SPPS: one amino acid at a time on a resin bead, through repeated coupling and deprotection cycles, followed by cleavage, HPLC purification, mass spectrometry identity checks, and lyophilization. None of that sequence applies here, since there is no chain to build. A quinolinium compound is instead made by classical solution chemistry: the quinoline ring system is assembled or taken from a commercial quinoline starting material, the amino group is positioned at 5, and the ring nitrogen is methylated in a quaternization step, which installs the permanent positive charge and creates the salt with whichever counterion the methylation reagent carries, commonly iodide. The product is then isolated, typically by precipitation and recrystallization, and dried.

Verification follows the small molecule version of the same discipline used for peptides. Purity is measured by analytical HPLC, which separates the compound from synthesis impurities and reports its share of the chromatogram. Identity is confirmed by mass spectrometry, which for this compound must show the cation at about 159 grams per mole, and by the salt form stated on the documentation: a certificate quoting the iodide salt should account for a formula weight near 286 grams per mole, and one quoting the free cation near 159. Nuclear magnetic resonance spectroscopy is also standard for small molecules and can confirm the ring substitution pattern that mass alone cannot. Research material of this compound is supplied as a dry powder, commonly after freeze drying of a purified solution, for the same stability reasons as peptides. Each batch is documented with a certificate of analysis, and third-party testing is how a buyer verifies a specific lot. Given that catalog listings for this exact name have been documented with incorrect formulas, the identity checks on the certificate are not a formality.

Metabolic research in fat tissue is the founding area. Researchers use NNMT inhibition, by genetic knockdown or by this compound series, to study how adipocytes balance NAD+ salvage, methylation, and energy expenditure, measuring adipocyte size, fat pad mass, oxygen consumption, and lipid profiles in diet-induced obesity models. The cultured-cell arm of the same work measures intracellular NAD+ and SAM levels and fat cell formation itself, since the inhibitors were reported to reduce adipogenesis in culture.

Aged muscle is the second area. NNMT is overexpressed in aging skeletal muscle, and researchers study whether inhibiting it rescues the function of senescent muscle stem cells, the cells that rebuild muscle after injury. The 2019 study in this site's database measured stem cell proliferation and fusion, fiber size, and contractile force in injured aged mouse muscle. This line connects the compound to sarcopenia research, the study of age-related muscle loss, rather than to obesity research.

A third, younger area is cancer biology. NNMT is overexpressed in several tumor types and in the stromal cells surrounding tumors, and researchers have used NNMT inhibitors as tools to study how the enzyme shapes the tumor environment and cancer cell metabolism. This site's database does not hold those records under this compound, and the area is mentioned here only to indicate the field's direction: it is enzyme biology studied with a tool compound, in cells and animals.

What the research does not include is equally clear. There are no published human trials of 5-Amino-1MQ for any purpose, no human pharmacokinetic record, and no dose-ranging work in humans in the literature. Every efficacy statement in the field traces to the University of Texas program's cell and mouse experiments or to the genetic knockdown work that inspired them.

The evidence base for 5-Amino-1MQ consists of three database records and is entirely preclinical. Two come from a single university research program, and the third, the field's founding paper, tested genetic knockdown rather than this molecule. There are no human trials, no human safety or pharmacokinetic data, and no independent replication program of the mouse findings in the published record this page draws on. In the taxonomy this site applies to other compounds, this is an early, thin record, thinner than BPC-157's and not comparable to the incretin compounds' trial programs at all.

Authorship concentration is total rather than partial: every compound-specific efficacy claim traces to one laboratory group. That does not invalidate the work; the chemistry is sound and the target is real. It means the findings have not yet survived the most critical test in preclinical science, which is repetition by groups with no stake in the outcome.

A marketplace issue compounds the scientific one. This compound is sold in consumer channels with identity errors documented in its own catalog ecosystem, including listings that give it a peptide identity or a formula it does not have. Nothing in the mouse record supports any use in people, and research material should be judged by its certificate of analysis: correct cation mass, stated salt form, and HPLC purity, verified by third-party testing. For these reasons, 5-Amino-1MQ is supplied and discussed here strictly as a research material: not an approved drug or supplement, not for human or animal use outside controlled research settings, and no statement on this page makes a medical claim.