5-Amino-1MQ
5-Amino-1MQ is a small permanently charged quinolinium salt, not a peptide, developed as a selective inhibitor of nicotinamide N-methyltransferase (NNMT) with an IC50 of roughly 1 microM against the enzyme. It came out of a methylquinolinium structure-activity series screened against the nicotinamide-binding site, and it has only ever been used as a laboratory probe compound in rodent and cell studies. It is supplied as the iodide salt (CAS 42464-96-0, C10H11IN2); the catalogue code HY-131042, by which two of the independent studies below identify their compound, is a registered synonym of that same salt.
Information on this page is provided for laboratory research reference. The compound is not a drug, supplement, or medical product, and is not for human or veterinary use, ingestion, or consumption.
No reviewed report has been published for this product family yet. The molecular values opposite are public reference data, not results measured on a CRX sample.
Browse published reports →NNMT transfers a methyl group from S-adenosylmethionine (SAM) onto nicotinamide, producing 1-methylnicotinamide and consuming both a methyl donor and a precursor that would otherwise re-enter the NAD+ salvage pathway. 5-Amino-1MQ occupies the nicotinamide substrate site, so blocking the enzyme lowers 1-methylnicotinamide while raising intracellular NAD+ and SAM. NNMT is over-expressed in adipose tissue and skeletal muscle in obesity and ageing, which is the rationale behind every efficacy study below. Selectivity was tested against a narrow panel of five enzymes (DNMT1, PRMT3, COMT, NAMPT, SIRT1), none of which it inhibited; a later and much broader screen did find one off-target, monoamine oxidase-A. It showed high passive and active transport with no detectable efflux in Caco-2 cells, but that in-vitro permeability did not carry over to the animal: measured oral bioavailability in mice was 3.5%, and essentially every efficacy study below delivered the compound by injection.1,2,4
Fat loss & metabolism
In diet-induced obese mice given subcutaneous injections for 11 days, 5-amino-1MQ-treated animals lost 2.0 g of body weight (about 5.1% from baseline) while saline controls gained 0.6 g (about 1.4%). Epididymal white adipose mass was roughly 35% lower, adipocyte size more than 30% smaller, and plasma total cholesterol about 30% lower than in saline controls.2
In diet-induced obese mice injected subcutaneously once daily for about 30 days, the high-dose 5A1MQ arm gained 0.9 g of body weight against 5.4 g in vehicle controls, and 1.3 g of fat mass against 4.7 g. The low-dose arm gained 5.2 g and was no different from vehicle. Lean mass showed no treatment effect in any arm.4
In the same diet-induced obese mice, fed-state plasma insulin rose 112% from baseline in vehicle controls and 46% in the low-dose arm, but fell 9% in the high-dose arm. On a day-21 oral glucose tolerance test, high-dose animals had lower glucose at 15 and 30 minutes and lower insulin at 15 minutes than both comparators. The authors note off-target MAO-A activity may explain part of that glucose effect.4
In the same diet-induced obese mice, high-dose 5A1MQ reduced terminal liver weight to 1.4 g against 2.1 g in vehicle controls and cut microvesicular steatosis by about 73%. NAFLD activity score improved dose-dependently, and serum ALT, AST and triglycerides showed dose-related decreases relative to vehicle, alongside reduced hepatic macrophage staining.4
In obese mice switched from a Western diet to a lean diet, adding injected 5-amino-1MQ produced 29.3% fat mass loss from baseline against 2.9% for the diet switch with vehicle, and cumulative body weight loss of 6.3 g against 2.9 g. Whole-body lean-mass-to-body-weight ratio rose 6.4% from baseline, while the diet switch alone did not change that ratio.3
In cultured mouse 3T3-L1 cells, 5-amino-1MQ lowered intracellular 1-methylnicotinamide in fully differentiated adipocytes with an EC50 of 2.3 microM, plateauing near 40% of untreated levels, and significantly raised intracellular NAD+ at 10 microM and SAM at 30 microM against untreated controls. In cells treated throughout differentiation, lipid accumulation was 50% lower at 30 microM and 70% lower at 60 microM than untreated.2
Longevity & anti-ageing
In mice injected from 22 to 24 months of age, sedentary treated animals had about 40% greater grip strength than sedentary saline controls, while exercised untreated animals gained about 20%; the combination reached about 60%. Intramyocellular lipid in treated sedentary mice was more than 30% lower than in sedentary controls, reaching levels seen in the exercised groups.5
In 19-month-old female mice given intraperitoneal injections, NNMT inhibition slowed the fall in grip strength index and limited the decline in lean mass index to 4.34% against 7.53% in saline controls. Quadriceps contraction force at 4V stimulation was about 2.02-fold that of saline controls, while gastrocnemius force and fat mass index did not differ. Ten mice were split across the two arms.6
In the same aged female mice and in young mice given D-galactose to induce accelerated ageing, injected NNMT inhibition raised quadriceps NAD+ content and PGC1-alpha and phosphorylated AMPK protein against saline-treated controls, matching the NAD+-sparing signature seen in cultured adipocytes.6
Recovery & repair
In 24-month-old mice given a barium chloride injury to the tibialis anterior, subcutaneously injected 5-amino-1MQ raised muscle stem cell proliferation and fusion, giving nearly 2-fold greater myofiber cross-sectional area than saline controls and a shift toward larger fibres. Peak tibialis anterior torque was about 70% higher than in saline controls.7
In a blinded study of male BALB/cJ mice with surgically induced hindlimb ischaemia, injected NNMT inhibitor begun 3 hours before surgery improved plantarflexor absolute force (p<0.0001), power (p=0.0305) and total work over a 6-minute test (p=0.0367) against placebo, but did not change limb perfusion, capillary density, muscle mass or myofibre size, and only trended toward less necrosis (p=0.08).8
What investigators recorded alongside the results above, at the rates their papers state.
No human data of any kind. No clinical trial of 5-amino-1MQ has been published, and the 2026 review literature describes the earlier generation of NNMT inhibitors, which includes this one, as held back by insufficient target engagement, reduced bioavailability and unknown safety profiles. Every result on this page is from mice or cultured cells.8,9
not established; no human exposure reported
Oral exposure is very poor in the one species where it was measured. In mice, oral bioavailability was 3.5%, with a low peak concentration, delayed absorption and evidence of heavy first-pass metabolism. Every efficacy study on this page dosed by subcutaneous or intraperitoneal injection; no efficacy study tested an oral route.4
3.5% oral bioavailability in mice; peak plasma concentration 14.5 ng/mL after oral dosing
Off-target inhibition of monoamine oxidase-A. Screened at 10 microM against a broad receptor, enzyme and transporter panel, 5A1MQ showed no significant activity at any target except MAO-A. The authors list reducing this MAO-A activity as an ongoing optimisation goal, and suggest it may itself account for part of the glucose-tolerance benefit attributed to NNMT inhibition.4
67.4% inhibition of MAO-A at 10 microM in vitro
Cytotoxicity in cultured cells at the top of the tested range. 3T3-L1 cell viability was significantly reduced at 60 microM, the highest concentration tested, and concentrations above 60 microM were not tested because of known cytotoxic effects in these cells. The largest reported reduction in lipid accumulation was measured at that same concentration.2
significant but slight loss of viability at 60 microM; higher concentrations untested
A muscle-performance measure moved the wrong way. In aged mice, treated animals performed significantly less cumulative work than matched saline controls during a plantarflexor fatigue task, which the authors attribute to lower peak torque on each contraction. Peak plantarflexor torque itself was not significantly changed by treatment, so the grip-strength benefit did not appear on every muscle measure.5
significantly reduced cumulative work; the separate fatigue-resistance measure was only a trend, p=0.098
What tolerability evidence exists is limited to mice and is reassuring as far as it goes. No overt toxicity or adverse behavioural effects were reported in treated diet-induced obese mice, and weight loss was not driven by appetite suppression: cumulative food intake over 11 days was 26.2 g in treated animals against 28.1 g in saline controls, not significantly different. In aged mice, a full plasma chemistry panel after chronic dosing was comparable to saline controls.2,7
no adverse events reported in an 11-day and a 2-week mouse study; no human tolerability data
- 1.Structure-Activity Relationship for Small Molecule Inhibitors of Nicotinamide N-Methyltransferase. · Journal of medicinal chemistry · 2017 · PMID 28548833
- 2.Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. · Biochemical pharmacology · 2018 · PMID 29155147
- 3.Combined nicotinamide N-methyltransferase inhibition and reduced-calorie diet normalizes body composition and enhances metabolic benefits in obese mice. · Scientific reports · 2021 · PMID 33707534
- 4.Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction. · Diabetes, obesity & metabolism · 2024 · PMID 39161060
- 5.Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice. · Scientific reports · 2024 · PMID 38969654
- 6.Identification of nicotinamide N-methyltransferase as a promising therapeutic target for sarcopenia. · Aging cell · 2024 · PMID 38838088
- 7.Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. · Biochemical pharmacology · 2019 · PMID 30753815
- 8.Nicotinamide N-methyltransferase inhibition improves limb function in experimental peripheral artery disease. · Physiological reports · 2025 · PMID 41108586
- 9.Emerging opportunities for nicotinamide N-methyltransferase (NNMT) inhibitor clinical translation. · Trends in pharmacological sciences · 2026 · PMID 42067476