5-Amino-1MQ is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), not a peptide — a 159.21 Da quinolinium compound supplied as the iodide salt. It appears in peptide catalogs because the research questions it addresses overlap with metabolic peptide work, but chemically and analytically it belongs to a different class entirely, and treating it like a peptide will produce bad experiments. We supply research-grade 5-Amino-1MQ as lyophilized powder in sealed vials, for laboratory use only.
What is 5-Amino-1MQ, precisely
The full name is 5-amino-1-methylquinolinium. It is a methylated quinoline derivative carrying a permanent positive charge on the ring nitrogen — a quaternary cation, which is why it is supplied as a salt with an iodide counter-ion. Its target, NNMT, is a cytosolic enzyme that transfers a methyl group from S-adenosylmethionine (SAM) to nicotinamide, producing 1-methylnicotinamide. 5-Amino-1MQ is a structural mimic of that product, and it inhibits the enzyme by occupying the nicotinamide binding site.
That design logic — a product analog acting as a competitive inhibitor — explains the molecule's structure and its selectivity profile, and it is worth understanding before designing an assay around it.
Origin and structure
- Compound class. Small-molecule quinolinium, non-peptide. Not made by solid-phase synthesis and not characterised by peptide methods.
- Formula and mass. C10H11N2 as the cation, 159.21 g/mol; supplied as the iodide salt C10H11IN2 at 286.11 g/mol. Which figure you use for molar calculations depends on whether you weigh the salt or account for the counter-ion, and getting this wrong introduces a systematic 1.8-fold error.
- CAS. 42464-96-0.
- Charge. Permanently cationic, which drives its aqueous solubility and shapes how it distributes across membranes.
How 5-Amino-1MQ is thought to work
NNMT sits at a junction between two metabolic systems. It consumes nicotinamide, which is a salvage-pathway precursor for NAD+, and it consumes SAM, the cell's universal methyl donor. Inhibiting NNMT is therefore reported to have two simultaneous consequences: more nicotinamide remains available for NAD+ salvage, and less SAM is diverted into methylating nicotinamide, altering methyl-donor flux more broadly.
Published preclinical work has reported that NNMT expression is elevated in adipose tissue in obesity models, and that inhibiting the enzyme in adipocytes raises cellular NAD+ and increases sirtuin activity, with downstream effects on lipogenic gene expression and adipocyte size. In rodent studies, NNMT inhibition and knockdown have been reported to reduce adiposity in diet-induced obesity models without a change in food intake, which distinguishes the mechanism sharply from incretin agonists such as semaglutide that act on appetite circuitry.
One caveat belongs in any honest account. 1-methylnicotinamide, the product NNMT makes, is not inert — it has reported biological activity of its own, so inhibiting the enzyme removes a signalling molecule as well as conserving a substrate. Attributing an observed effect purely to NAD+ conservation is a simplification that the current literature does not fully support.
Selectivity deserves scrutiny before this compound is used as a mechanistic probe. The human genome encodes dozens of SAM-dependent methyltransferases, and an inhibitor that mimics a methylation product occupies a binding site whose architecture is not unique to NNMT. Published selectivity screens exist, but the practical implication for a laboratory is that an effect observed after treatment should not be attributed to NNMT inhibition without a supporting arm — enzyme knockdown, a structurally unrelated inhibitor, or rescue by the reaction product. Without one, the result describes what the compound did, not what the enzyme does.
What research has examined
- Enzyme and biochemical studies. Purified NNMT inhibition assays establishing potency and mode of inhibition, plus selectivity screens against other methyltransferases — an important control given how many SAM-dependent enzymes exist.
- Cell studies. Adipocyte cultures measuring NAD+ levels, sirtuin activity, lipogenic gene expression and lipid accumulation.
- Rodent studies. Diet-induced obesity models reporting reduced adiposity, plus work in muscle examining regenerative capacity and in cancer models where NNMT overexpression is a recurring observation.
- Human data. None published. There is no clinical trial programme for 5-Amino-1MQ, and no human pharmacokinetic or safety data exist in the peer-reviewed literature. Every claim about this compound rests on cell and animal work.
Our explainer on NNMT as a metabolic target covers the pathway in more depth, and the adipose tissue hub places it alongside other approaches.
Forms and sizes we supply
| Attribute | Specification |
|---|---|
| Form | Lyophilized powder, sealed glass vial |
| Sizes | 50 mg, 100 mg |
| Purity | Greater than or equal to 99% by HPLC, lot-matched COA |
| CAS | 42464-96-0 |
| Molecular weight | 159.21 g/mol (cation); 286.11 g/mol (iodide salt) |
| Formula | C10H11N2 cation, supplied as C10H11IN2 |
| Class | Small-molecule NNMT inhibitor (non-peptide) |
| Intended use | Laboratory research only |
Vial sizes are larger than for peptides because a 159 Da molecule needs far more mass to reach the same molar quantity — 50 mg of this compound is roughly 175 micromoles of cation, whereas 50 mg of a 4 kDa peptide is about 12 micromoles. Sizes are on the 5-Amino-1MQ product page, with an oral format as 5-Amino-1MQ capsules, both in the fat-loss and metabolic collection.
Reconstitution and storage in a lab context
The compound is water-soluble thanks to its permanent positive charge, and bacteriostatic water is adequate for most bench preparation; DMSO is used for concentrated stocks in cell assays, as with most small molecules. A worked calculation: 50 mg reconstituted in 5 mL gives 10 mg/mL, equal to 10,000 mcg/mL, and 0.1 mL of that solution carries 1,000 mcg. Converting that to molarity requires deciding which mass figure applies — using the salt mass of 286.11 g/mol, 10 mg/mL is approximately 35 mM.
Store the solid at minus 20 degrees Celsius, sealed and protected from light and moisture; hold solutions at 2 to 8 degrees Celsius and use within the study window. Small molecules are generally more robust than peptides to handling, but the iodide salt is light-sensitive and amber vials or foil are sensible. See our reconstitution guide and molecular weight and moles note.
Two further handling differences separate small molecules from peptides in practice. First, the permanent cationic charge means this compound does not cross membranes by passive diffusion the way a neutral lipophilic small molecule would, so cell-assay uptake is worth verifying rather than assuming — a discrepancy between enzyme-assay potency and cell-assay potency is often a transport problem, not a pharmacology one. Second, DMSO stocks carry their own constraint: the final solvent concentration reaching cells must stay low enough not to affect the readout, which caps how dilute a working solution can be prepared from a given stock. Both points are routine for small-molecule work and routinely overlooked by laboratories whose habits were formed on peptides.
Purity, COA and how to read it
A certificate for a small molecule looks different from a peptide certificate, and expectations should adjust accordingly. HPLC purity remains the headline figure, but there is no net peptide content to consider — instead, salt form and counter-ion content are the equivalent concern, since they determine how much active cation a weighed sample actually contains. Identity is normally confirmed by mass spectrometry and, for a well-characterised small molecule, ideally by NMR, which resolves structure in a way mass alone cannot. Residual solvent testing is relevant here in a way it is not for peptides. See how to read a COA.
Tissue context is worth keeping in view when interpreting results. NNMT expression varies widely between tissues and is reported to be elevated in adipose tissue in obesity models and in several tumour types, so the consequence of inhibiting the enzyme depends heavily on how much of it a given tissue expresses in the first place. A cell line with low baseline NNMT will show little response regardless of inhibitor potency, and that is a property of the model rather than a finding about the compound. Confirming baseline expression before treating a null result as informative is standard practice here.
Regulatory status
5-Amino-1MQ is not an approved medicine in any jurisdiction and has no clinical development programme. It is not a peptide, not a dietary ingredient with established regulatory standing, and not authorised for human or veterinary administration. It is supplied as a laboratory reference chemical, research use only. Its appearance in consumer-facing capsule products elsewhere does not change that status — see research use only, explained.
Related compounds and comparisons
The closest comparison in our range is 5-Amino-1MQ vs SLU-PP-332, another small molecule addressing metabolic questions by a different route. For NAD-focused work see NAD+.