5-Amino-1MQ: NNMT Inhibitor Evidence, Dosing & Legal Status

5-Amino-1MQ (5-amino-1-methylquinolinium) is cross-listed in this peptide library only because it is sold through the same research-chemical channels and marketed to the same fat-loss and longevity audience as genuine metabolic peptides. It is, however, a small-molecule quaternary-ammonium quinolinium cation (formula C₁₀H₁₁N₂⁺, molecular weight about 159 g/mol, PubChem CID 950107) with no amino-acid chain and no peptide bond — its true home in this taxonomy is among adjacent compounds.5 This monograph holds it to the same evidence-first standard as everything else in the encyclopedia.

This article is informational and editorial content for research and educational purposes only. It is not medical advice, not a protocol to follow, and not a sourcing or buying guide. 5-Amino-1MQ is an unapproved investigational research chemical with zero published human trials; it is sold as a "research chemical not for human use" and is prohibited in sport. Dosing figures are reported strictly as seen in the published literature for completeness. Consult a licensed clinician before any health decision.

What is 5-Amino-1MQ and how does it work?

5-Amino-1MQ is a selective, membrane-permeable inhibitor of nicotinamide N-methyltransferase (NNMT), developed in academic medicinal-chemistry programs at the University of Texas Medical Branch and UT San Antonio as a tool compound and metabolic-disease drug candidate.1 Structurally it is a quaternary quinolinium cation supplied as the iodide salt, with a permanent positive charge on the N-methylated ring nitrogen and an amino group at the 5-position — a nicotinamide and methyl-substrate mimic, not a polypeptide.5 Despite its cationic nature, medicinal-chemistry optimization produced enough membrane permeability to reach the intracellular enzyme target.1

NNMT is a cytosolic phase-II enzyme that transfers a methyl group from S-adenosylmethionine (SAM) to nicotinamide, yielding 1-methylnicotinamide and S-adenosylhomocysteine. When pathologically over-expressed, NNMT acts as a methyl sink and a drain on the nicotinamide that feeds NAD+ salvage. 5-Amino-1MQ competitively occupies NNMT's nicotinamide-binding pocket — not the conserved SAM pocket shared by other methyltransferases — which underlies its selectivity.1 By blocking the reaction it is reported to preserve SAM, lower 1-methylnicotinamide, and spare nicotinamide for NAD+ resynthesis, secondarily supporting NAD+ and sirtuin signaling while suppressing adipocyte lipogenesis.1 In vitro the biochemical IC₅₀ for NNMT is roughly 1 micromolar, with a clean off-target profile: no meaningful inhibition of DNMT1, PRMT3, NAMPT, or SIRT1 across tested concentrations.1 Crucially, no published human pharmacokinetics, half-life, or oral-bioavailability data exist — all in-vivo dosing in the primary literature used subcutaneous injection in mice, and the public record of NNMT-inhibitor translation status can be reviewed in the 2026 Pharmacological Research review.8

What is the evidence by indication?

Every indication below rests on animal and/or in-vitro data only. There are no human randomized controlled trials and no human cohort or observational efficacy data for 5-Amino-1MQ in any indication, so the highest defensible grade is C.8

The foundational obesity study (Neelakantan et al., Biochemical Pharmacology 2018) treated male diet-induced obese mice with 5-Amino-1MQ at 20 mg/kg subcutaneously three times daily for 11 days against saline controls. Treated mice lost roughly 2 grams of body weight (about 5 percent from baseline) while controls gained weight; epididymal white-adipose mass fell about 35 percent, adipocyte cross-sectional area fell over 30 percent, and plasma total cholesterol dropped about 30 percent — all without any change in food intake, indicating a metabolic rather than anorectic mechanism.1 In vitro, the compound raised adipocyte NAD+ roughly 1.2- to 1.6-fold and cut lipid accumulation by 50 to 70 percent at 30 to 60 micromolar with no cytotoxicity.1 A 2021 follow-up showed NNMT inhibition combined with a low-fat-diet switch normalized whole-body adiposity faster than diet alone and reshaped the gut microbiome.4

The second pillar is aged muscle. Neelakantan et al. (2019) reported that aged mouse muscle has elevated NNMT, and that inhibiting it with 5-Amino-1MQ reactivated senescent muscle stem cells and improved regenerative capacity and contractile recovery after injury in aged mice — the authors called it the first clear evidence that NNMT inhibitors are a viable pharmacological approach to enhancing aged-muscle regeneration.23 The popular NAD+-booster and longevity framing is mechanistic extrapolation: in-vitro NAD+ rises are real, but no study has measured intracellular NAD+ after 5-Amino-1MQ in humans, and clinical longevity claims remain unproven marketing.8 Separately, because NNMT is tumor-promoting in many cancers, NNMT inhibitors are studied as anti-cancer tools — preclinical research interest that is the opposite of a wellness indication and a reminder that NNMT biology is context-dependent.67

What doses appear in the literature, and what are the risks?

Reported strictly as information, not a protocol. The only controlled dosing is preclinical: 20 mg/kg subcutaneously, three times daily (about 60 mg/kg/day) for 11 days reversed adiposity in diet-induced obese mice, with a tolerability arm finding that dose well tolerated.1 Naive milligram-per-kilogram scaling from mouse to human is not clinically validated and should not be used to infer a human dose. Consumer and research-chemical channels market the compound predominantly as oral capsules, commonly cited around 50 mg per day and sometimes 50 to 150 mg per day, often cycled — figures that originate from vendor copy, not from any pharmacokinetic or efficacy study, for a cationic molecule whose only in-vivo evidence used injection.8

On safety, there is simply no published human safety, tolerability, or pharmacokinetic study, so the human adverse-effect profile is genuinely unknown.8 The short rodent studies showed no overt toxicity at effective doses, but they were never designed to detect chronic, carcinogenic, reproductive, or methylation-related harm.1 The dominant theoretical concerns are mechanistic: the compound by design alters SAM and NAD+-precursor flux, so chronic perturbation of one-carbon and epigenetic methylation is uncharacterized, and because NNMT is over-expressed in many tumors with context-dependent effects, individuals with active or prior cancer are commonly advised to avoid it.6 No formal human drug-interaction or CYP studies exist; pregnancy and lactation are precautionary contraindications for a methyl-donor-modulating agent; and as an unregulated research chemical, products carry real risks of mislabeling, under- or over-dosing, and contamination.8

What is the FDA and WADA status in 2026?

5-Amino-1MQ has no FDA-approved indication and no investigational new drug application on the public record. It is sold as an unapproved research chemical — and, dubiously, as a dietary or energy-expenditure product — which does not require FDA pre-market approval but is also not a lawfully marketed dietary ingredient or an approved drug, and it is not an established 503A-compoundable or 503B bulk substance for human therapeutic use.8 No 5-Amino-1MQ trial is listed as registered or completed on ClinicalTrials.gov as of 2026. The underlying quinoline-derived NNMT-inhibitor chemotype is covered by issued US patents, including US 11,401,243 and US 12,071,409.910

For athletes the picture is clear despite the compound not being named on the list. Under the 2026 WADA Prohibited List (in force 1 January 2026), a non-approved substance like 5-Amino-1MQ is prohibited at all times under category S0 (Non-Approved Substances), and its metabolic-modulator profile may additionally implicate category S4 (Hormone and Metabolic Modulators).11 Any WADA-tested athlete should treat it as banned regardless of efficacy.11

Bottom line. 5-Amino-1MQ is a genuinely interesting, well-characterized small-molecule NNMT inhibitor — not a peptide — with a clean in-vitro selectivity profile and reproducible rodent data: in obese mice it cut fat mass, adipocyte size, and cholesterol without suppressing appetite, and in aged mice it rejuvenated muscle stem cells.12 From a root-cause metabolic standpoint, targeting an over-expressed methyl-sink enzyme is a more upstream strategy than stimulant thermogenics. But the honest evidence grade is C across the board: not a single registered, completed, or published human trial, no human pharmacokinetics or oral-bioavailability data, and a validated route (subcutaneous injection) that no consumer uses. The gap between the confident fat-loss, NAD+, and longevity marketing and the entirely preclinical data is large — treat consumer products as experimental with an unknown safety floor.