Evidence Grade E — Very limited evidence. 0 published studies. 0 registered clinical trials.
Medically reviewed by a licensed medical professional
5-Amino-1MQ is a small molecule enzyme inhibitor — not a peptide — that targets NNMT, an enzyme involved in cellular energy metabolism. No human clinical trials have been conducted. It is included in this database because it is commonly encountered alongside peptide compounds in unregulated channels. It is prohibited by WADA.
5-Amino-1MQ is also known by these brand and alternate names:
No published studies found on PubMed.
5-Amino-1MQ has no marketing authorisation. No human clinical trials have been conducted. The key preclinical study treated diet-induced obese mice for 11 days and reported body weight and fat mass changes. No human pharmacokinetic, safety, or efficacy data exist.
5-Amino-1MQ is not a peptide. Products available through unregulated channels lack pharmaceutical quality assurance. The absence of any human data means effects, safety, interactions, and appropriate dosing in humans are entirely unknown.
Research in animal models suggests 5-Amino-1MQ inhibits the enzyme NNMT, which plays a role in cellular energy balance by consuming a cofactor (SAM) that is important for numerous metabolic processes. The proposed downstream effects observed in obese mice have not been tested in humans. The compound is a small molecule with no peptide structure.
The evidence base is entirely preclinical, with all published data originating from a single laboratory group. The key study treated obese mice for 11 days and reported weight and fat changes. No human pharmacokinetic, safety, or efficacy data exist. No formal toxicology studies have been conducted. The absence of any human data means the compound's effects, safety, interactions, and appropriate dosing in humans are completely unknown. Products from unregulated channels lack pharmaceutical quality assurance.
PeptideTrace tracks 0 registered clinical trials for 5-Amino-1MQ sourced from ClinicalTrials.gov.
No trials registered on ClinicalTrials.gov for this compound.
5-Amino-1MQ (5-amino-1-methylquinolinium) is a quaternary quinolinium small molecule (not a peptide) that functions as a nicotinamide N-methyltransferase (NNMT) inhibitor. The free cation has a molecular formula of C10H11N2+ and molecular weight of 159.21 g/mol; the commonly supplied iodide salt (CAS: 42464-96-0) weighs 286.11 g/mol. The structure features a quinoline ring with a methyl group at nitrogen-1 and an amino group at position 5. No formal pharmacokinetic studies exist in any species. The use of three daily subcutaneous injections in mouse studies implies a short duration of action. High passive membrane permeability has been confirmed via PAMPA and Caco-2 assays, suggesting oral absorption potential. Research administration routes include subcutaneous, intraperitoneal, and oral.
5-Amino-1MQ is a nicotinamide-competitive, selective NNMT inhibitor with an IC50 of 1.2 uM. NNMT normally methylates nicotinamide using S-adenosylmethionine (SAM) as the methyl donor, producing 1-methylnicotinamide (1-MNA) and S-adenosylhomocysteine. This enzyme diverts nicotinamide away from the NAD+ salvage pathway. By blocking NNMT, the compound preserves nicotinamide for NAD+ synthesis, increasing intracellular NAD+ levels (confirmed in 3T3-L1 adipocytes at >=3 uM, p < 0.05). Elevated SAM activates histone H3K4 methylation and polyamine biosynthesis, an energy-consuming futile cycle that increases cellular energy expenditure. The NAD+/SIRT1 axis is also activated, promoting oxidative metabolism. The compound shows no inhibition of DNMT1, PRMT3, COMT, NAMPT, or SIRT1, indicating high selectivity for NNMT. The foundational target validation was published by Kraus et al. in Nature (2014), establishing that NNMT knockdown in white adipose tissue protected against diet-induced obesity.
All published data is preclinical. No branded pharmaceutical product exists. The key study by Neelakantan et al. (2018, Biochem Pharmacol) treated diet-induced obese C57Bl/6 mice (N=9/group) with 20 mg/kg SC three times daily for 11 days. Results showed approximately 7% body weight reduction, approximately 35% reduced white adipose tissue mass, approximately 30% decreased adipocyte size, and lowered plasma total cholesterol, with no impact on food intake and no observable adverse effects. A 2019 study in 24-month-old mice (N=6-7/group) demonstrated nearly 2-fold greater myofiber cross-sectional area after muscle injury (p < 0.0001) and approximately 70% increased peak torque (p = 0.033), with complete plasma chemistry panels showing no organ toxicity. A 2024 study showed approximately 25% grip strength increases in aged sedentary mice and approximately 60% increases when combined with exercise. No clinical trials are registered on ClinicalTrials.gov for any NNMT inhibitor.
The information on this page is provided for educational and research reference purposes only. This is not medical advice. Always consult a qualified healthcare professional before making any health-related decisions.
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Setmelanotide is marketed as Imcivree (Rhythm Pharmaceuticals; approved November 2020 for POMC, PCSK1, or LEPR deficiency; June 2022 for Bardet-Biedl syndrome; December 2024 expanded to patients aged 2 years and older). Genetic testing confirming an eligible mutation is required before treatment. In patients with POMC or PCSK1 deficiency, approximately 80% achieved at least 10% weight loss in clinical trials. In Bardet-Biedl syndrome, 32.3% achieved the same threshold. The most common side effects are injection-site reactions and skin darkening (due to the melanocortin pathway's connection to pigmentation). Setmelanotide exemplifies precision medicine — it is highly effective in the specific genetic populations it targets but is not indicated for common obesity.
CT-388 is in Phase II/III development (not yet approved). Phase II results (469 patients, 48 weeks) showed 22.5% placebo-adjusted weight loss at the highest dose, with low discontinuation rates due to adverse events (5.9%). Phase III trials are underway. The combination of high efficacy and low discontinuation rates in Phase II is notable — many obesity drugs achieve high weight loss but suffer from tolerability-driven dropouts. Roche's $2.7 billion acquisition of the developer signals significant confidence in the programme.
Evidence Reviews
This content is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making decisions about your health.
