5-Amino-1MQ 50mg

▎ 5-Amino-1MQ Structure

▎5-Amino-1MQ Research

Molecular Background

5-Amino-1-methylquinolinium (5-Amino-1MQ or 5A1MQ) is a small-molecule quinolinium compound studied as an inhibitor of nicotinamide N-methyltransferase (NNMT). PubChem lists the parent 5-amino-1-methylquinolinium cation under CID 950107, with the molecular formula C10H11N2+ and a molecular weight of 159.21 g/mol. The iodide salt is listed separately in PubChem, so the chemical form used in an experiment should be identified from the corresponding study or analytical documentation.[7]

Research Progress

JoAnne J. Babula and colleagues administered vehicle or 5A1MQ once daily to diet-induced obese (DIO) mice for 28 days. Longitudinal measurements included body composition, blood glucose, and plasma insulin, while liver histopathology, circulating biomarkers, plasma pharmacokinetics, and tissue distribution were evaluated at study endpoints. The authors reported dose-dependent differences in body-weight and fat-mass gain, oral glucose tolerance, insulin sensitivity, hyperinsulinemia, hepatic steatosis, macrophage infiltration, liver triglycerides, and selected circulating biomarkers in the 5A1MQ groups. Separate pharmacokinetic experiments examined intravenous, oral, and subcutaneous exposure and tissue distribution in age- and strain-matched mice.[2]

Andrea L. Dimet-Wiley and colleagues studied 22- to 24-month-old mice assigned to sedentary or progressive weighted-wheel-running groups, with vehicle or 5A1MQ exposure. The investigators assessed grip strength, running performance, plantar-flexor torque, fatigue, muscle mass, fiber characteristics, cross-sectional area, intramyocellular lipid content, and skeletal-muscle proteomic and metabolomic profiles. At the reported study time point, sedentary 5A1MQ-treated mice showed approximately 40% greater grip strength than sedentary controls, exercised mice showed approximately 20% greater grip strength than sedentary controls, and the combined exercise-plus-5A1MQ group showed approximately 60% greater grip strength than sedentary controls. The authors also reported differences in intramyocellular lipid content, gastrocnemius fiber cross-sectional area, and molecular profiles across the study groups.[3]

Fig1. Grip-strength, body-weight, and running-performance measurements reported in aged mice assigned to sedentary or progressive weighted-wheel-running groups with vehicle or 5A1MQ exposure.[3]

Twenty-two-month-old mice were randomized to progressive weighted-wheel running (PoWeR) or sedentary (Sed) groups, with 5A1MQ or vehicle control [A]. Longitudinal body-weight measurements, grip-strength testing, body-weight-normalized grip strength, and running-distance data were analyzed using the statistical methods described in the source publication [B-E]. Mean +/- SEM and the reported significance testing are shown in the original figure.[3]
Catherine M. Sampson and colleagues examined 5A1MQ together with a reduced-calorie diet substitution in diet-induced obese mice. Compared with diet substitution alone, the combined group showed greater changes in body weight and fat mass, a higher lean-mass-to-body-weight ratio, lower liver and epididymal white-adipose-tissue weights, and differences in hepatic fat accumulation. The authors reported that several body-composition and liver-adiposity measurements in the combined group approached values observed in age-matched lean-diet controls. Adipose-tissue metabolomic analysis also identified changes in ketogenic amino acids and metabolites associated with energy-metabolism pathways.[4]

Ololade Awosemo and colleagues developed and validated an LC-MS/MS method for quantifying 5A1MQ in rat plasma and urine. Chromatographic separation used an ACE Excel C18 column and multiple-reaction monitoring in positive-ion mode. Calibration curves were linear from 10 to 2500 ng/mL, and the authors reported that intra-day and inter-day precision and accuracy met the +/-15% bioanalytical validation criterion used in the study. Extraction recovery, matrix effects, dilution integrity, and sample stability were also evaluated. The method was then applied to rat pharmacokinetic experiments following intravenous and oral administration. The authors reported a mean terminal elimination half-life of 3.80 +/- 1.10 h after intravenous administration and 6.90 +/- 1.20 h after oral administration, with an oral bioavailability estimate of 38.4% under the conditions of the study.[5]

Fig2. Mean plasma concentration-time profile reported for 5A1MQ following single intravenous and oral administration in rats in the cited pharmacokinetic study.[5]
Serra Akar and colleagues tested 5A1MQ at concentrations from 0.1 to 500 uM in HeLa cervical carcinoma cells. Cell viability was assessed by MTT assay, while qRT-PCR and Western blotting were used to examine selected gene and protein-expression endpoints. The authors reported concentration- and time-dependent reductions in HeLa cell proliferation, morphological changes consistent with apoptosis, increased ZEB1, SIRT1, and CD16 mRNA, decreased TWIST and SERPIN1 mRNA, and lower phospho-Akt and SIRT1 protein expression. In the same study, the authors reported no significant effect on HEK-293 cell proliferation under the tested conditions.[6]

Research Limitations

The research summarized above is predominantly preclinical and includes diet-induced obese mice, aged mice, rats used for pharmacokinetic analysis, and cultured HeLa and HEK-293 cells. Differences in species, model design, route of exposure, study duration, diet or exercise conditions, and measured endpoints limit direct comparison across these studies and do not establish safety or efficacy in humans.[2-6]
Chemical form is another consideration. PubChem distinguishes the 5-amino-1-methylquinolinium parent cation (CID 950107) from its iodide and chloride salts. Literature and commercial descriptions may use the name 5A1MQ for different forms, so experimental comparisons should consider the exact counterion, material identity, and analytical characterization used in each study.[7]

CCOCER Peptides presents 5A1MQ solely for laboratory research and analytical use. It is not intended for human or veterinary use. The research described above summarizes findings reported in third-party publications and is not a statement of clinical efficacy, safety, diagnosis, treatment, prevention, or an instruction for use.

▎Relevant Citations

References

[1] Puleo N, Allega M F, Niemann C U, et al. Emerging opportunities for nicotinamide N-methyltransferase (NNMT) inhibitor clinical translation[J]. Trends in Pharmacological Sciences, 2026,47(6):638-654.

DOI:10.1016/j.tips.2026.04.002.

[2] Babula J J, Bui D, Stevenson H L, et al. Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction[J]. Diabetes, Obesity and Diabetes, 2024,26(11):5272-5282.

DOI:10.1111/dom.15879.

[3] Dimet-Wiley A L, Latham C M, Brightwell C R, et al. Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice[J]. Scientific Reports, 2024,14:15554.

DOI:10.1038/s41598-024-66034-9.

[4] Sampson C M, Dimet A L, Neelakantan H, et al. Combined nicotinamide N-methyltransferase inhibition and reduced-calorie diet normalizes body composition and enhances metabolic benefits in obese mice[J]. Scientific Reports, 2021,11:5637.

DOI:10.1038/s41598-021-85051-6.

[5] Awosemo O, Neelakantan H, Watowich S, et al. Development & validation of LC-MS/MS assay for 5-amino-1-methyl quinolinium in rat plasma: Application to pharmacokinetic and oral bioavailability studies[J]. Journal of Pharmaceutical and Biomedical Analysis, 2021,204:114255.

DOI:10.1016/j.jpba.2021.114255.

[6] Akar S, Duran T, Azzawri A A, et al. Small molecule inhibitor of nicotinamide N-methyltransferase shows anti-proliferative activity in HeLa cells[J]. Journal of Obstetrics and Gynaecology, 2021,41(8):1240-1245.

DOI:10.1080/01443615.2020.1854696.

[7] PubChem. 5-Amino-1-methylquinolinium. PubChem CID 950107. National Center for Biotechnology Information.

Related PubChem record: 5-amino-1-methylquinolinium iodide, CID 66522933.

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