5-Amino-1MQ

5-Amino-1MQ (5-amino-1-methylquinolinium) is a selective, membrane-permeable small-molecule inhibitor of nicotinamide N-methyltransferase, or NNMT (Neelakantan et al., Biochem Pharmacol 2018). Evidence tier: preclinical.

Two facts frame everything else on this page. The animal data are genuinely interesting — this is real pharmacology from a named academic group, not a vendor invention. And a search of ClinicalTrials.gov for 5-amino-1MQ returns no registered study, so every claim about what it does in a person is an extrapolation from mice.

NNMT transfers a methyl group from S-adenosylmethionine (SAM) onto nicotinamide. That single reaction sits at a junction: nicotinamide is the precursor cells recycle into NAD+, and SAM is the cell's universal methyl donor. Consuming both to make an excreted metabolite is a metabolic drain, and NNMT is over-expressed in white adipose tissue and liver of obese and diabetic mice.

The concept was validated genetically before any inhibitor existed. Knocking down Nnmt in fat and liver with antisense oligonucleotides protected mice from diet-induced obesity by increasing cellular energy expenditure, raising adipose SAM and NAD+ and increasing polyamine flux — implicating NNMT as a regulator of histone methylation and NAD+-dependent SIRT1 signalling (Kraus et al., Nature 2014).

5-Amino-1MQ was then developed as a chemical way to do the same thing. The distinction matters when reading marketing copy: this is not an NAD+ precursor like NMN or NR, which add substrate. It blocks a route by which nicotinamide is lost.

5-Amino-1MQ has no approved indication in any country, no orphan or investigational designation that has produced a public trial record, and no place in any clinical guideline. It is not a drug in the regulatory sense; it is a research compound sold to consumers.

The uses it is discussed for — fat loss, insulin sensitivity, muscle preservation with age — map onto endpoints that have been measured in rodents and nowhere else.

The obesity study reported no observable adverse effects in mice over its 11-day dosing period (Neelakantan et al., 2018). Eleven days in mice is not a safety profile — it is the shortest window in which the primary endpoint could be measured.

The theoretical concerns follow from the mechanism rather than from reports. Blocking NNMT alters SAM availability, and SAM is the methyl donor for DNA and histone methylation across every tissue, not only fat. NNMT expression is also elevated in several cancers, where its role is debated. None of this is evidence of harm; it is a description of what has not been ruled out.

The published exposures are all injected and weight-based:

• 20 mg/kg subcutaneously, three times daily for 11 days in diet-induced obese C57BL/6 mice (Neelakantan et al., 2018).

• 10 mg/kg subcutaneously, once daily for eight weeks in mice aged 22 to 24 months (Dimet-Wiley et al., Sci Rep 2024).

No human pharmacokinetic study exists — no absorption figure, no half-life, no plasma concentration data. Oral bioavailability in humans has never been characterised, which is the gap that matters most, because the compound is sold almost exclusively as an oral capsule.

5-Amino-1MQ is a quinolinium salt supplied as an oral capsule or bulk powder. That form is the central mismatch with its evidence base: every published efficacy experiment bypassed the gut entirely by injecting the compound subcutaneously.

It is a standalone small molecule with no studied combination product. It is frequently stacked in consumer protocols with NAD+ precursors or with GLP-1 agonists; no published study has tested any such combination, in animals or people. Because it is not a peptide, it also does not share the storage, reconstitution, or injection considerations of the compounds it is sold alongside.

• Target validation (Nature 2014). Nnmt knockdown in white adipose tissue and liver protected mice against diet-induced obesity via increased energy expenditure, with higher adipose SAM and NAD+ (Kraus et al.).

• Lead compound in obese mice (Biochem Pharmacol 2018). 5-Amino-1MQ at 20 mg/kg subcutaneously three times daily for 11 days reduced body weight and white adipose mass, shrank adipocytes, and lowered plasma total cholesterol versus saline — and, notably, "did not impact total food intake," meaning the effect was not simple appetite suppression (Neelakantan et al.).

• Aged muscle (Sci Rep 2024). In mice treated from 22 to 24 months, 5-amino-1MQ produced roughly 40% greater grip strength than sedentary controls, while exercise alone gave about 20%; the two were additive, reaching about 60% combined (Dimet-Wiley et al.).

What is absent is as informative as what is present: no human trial, no registered study, no toxicology package, and no independent replication outside the originating research network. This is a compound with a credible target and an empty clinical record.

For deeper dives on this compound, see:

• 5-Amino-1MQ benefits and areas of interest
• 5-Amino-1MQ side effects and safety context
• 5-Amino-1MQ dosing concepts (educational)
• 5-Amino-1MQ research and evidence overview

Is 5-Amino-1MQ a peptide? No. It is a synthetic small-molecule quinolinium salt that inhibits an enzyme. It is sold beside peptides but belongs to a different chemical class entirely.

Does 5-Amino-1MQ cause weight loss? In mice, yes. An 11-day study reported reduced body weight and adipose mass without any reduction in food intake (Biochem Pharmacol 2018). In humans it is unknown, because no clinical trial has been conducted.

Is 5-Amino-1MQ related to NAD+? Indirectly. NNMT consumes nicotinamide, which cells otherwise recycle into NAD+; suppressing NNMT raised NAD+ in mouse adipose tissue (Nature 2014). That is a different approach from supplying precursors such as NMN or NR.

Is it FDA-approved or in clinical trials? Neither. A search of ClinicalTrials.gov returns no registered study under this name, and it is sold "for research use only" without pharmaceutical quality controls.

Why do capsule doses look nothing like the research doses? Because they are unrelated to them. The mouse work injected 20 mg/kg three times daily, or 10 mg/kg once daily in the ageing study; the 50–150 mg oral range is a retail convention with no published human pharmacokinetics behind it.