5-Amino-1MQ
Weight LossPreclinicalAlso known as: 5-amino, NNMT inhibitor
5-Amino-1MQ (5-amino-1-methylquinolinium iodide) is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme that transfers a methyl group from S-adenosyl-L-methionine (SAM) to nicotinamide to form 1-methylnicotinamide (1-MNA) and S-adenosyl-L-homocysteine (SAH). The compound emerged from a medicinal chemistry program at Sanofi aimed at developing NNMT inhibitors for metabolic disease, and was first described in the peer-reviewed literature in 2018 as one of several quinolinium-based inhibitors with single-digit micromolar potency against human NNMT in biochemical assays (Kannt et al., 2018; Neelakantan et al., 2017).
Overview
At A Glance
5-Amino-1MQ works by inhibiting nicotinamide N-methyltransferase (NNMT), an enzyme that catalyzes the transfer of a methyl group from S-adenosyl-L-methionine (SAM) to the nitrogen of nicotinamide (vitamin B3 amide), producing 1-methylnicotinamide (1-MNA) and S-adenosyl-L-homocyst…
Mechanism of Action
5-Amino-1MQ works by inhibiting nicotinamide N-methyltransferase (NNMT), an enzyme that catalyzes the transfer of a methyl group from S-adenosyl-L-methionine (SAM) to the nitrogen of nicotinamide (vitamin B3 amide), producing 1-methylnicotinamide (1-MNA) and S-adenosyl-L-homocysteine (SAH). This reaction is part of the broader NAD+ metabolism network because nicotinamide is a substrate for NAD+ resynthesis through the nicotinamide phosphoribosyltransferase (NAMPT) pathway, and when NNMT methylates nicotinamide, it diverts substrate away from NAD+ salvage toward 1-MNA excretion. In tissues where NNMT is highly expressed — adipose tissue, liver, certain cancers, and notably aging muscle — NNMT activity can become a significant sink for nicotinamide and thus a rate-limiting factor in NAD+ maintenance. Inhibiting NNMT preserves nicotinamide availability for NAD+ synthesis and reduces 1-MNA production, with downstream effects on cellular energetics, sirtuin activity, and oxidative metabolism (Kannt et al., 2018; Neelakantan et al., 2019). The second major consequence of NNMT inhibition is altered methyl-donor metabolism. SAM is the body's universal methyl donor, providing methyl groups for hundreds of methyltransferase reactions including DNA methylation, histone methylation, phospholipid methylation (phosphatidylethanolamine to phosphatidylcholine), neurotransmitter synthesis, and carnitine biosynthesis. NNMT is one of several methyltransferases that consume SAM, and in tissues where NNMT is highly active, a substantial fraction of the SAM pool can be consumed by nicotinamide methylation. Inhibiting NNMT reduces SAM consumption through this pathway, potentially increasing SAM availability for other methylation reactions and altering the SAM:SAH ratio that regulates methyltransferase activity broadly. This methyl-balance effect is the proposed mechanism for some of NNMT inhibition's reported benefits on adipocyte biology and epigenetic regulation, because methylation of promoters and histones at key metabolic genes can shift in response to changes in methyl donor availability. The 5-amino-1MQ compound specifically binds in the NNMT active site and competes with nicotinamide for substrate binding while also extending into a portion of the SAM-binding pocket, providing some selectivity over other SAM-dependent methyltransferases (Neelakantan et al., 2019). Selectivity is important because inhibition of other methyltransferases (DNMTs for DNA methylation, EZH2 for histone methylation, etc.) would have different and potentially harmful consequences. 5-amino-1MQ's selectivity profile has been characterized in biochemical panels and is reasonably good for NNMT over the closest structural relatives, but selectivity at therapeutic doses in whole animals is less well-defined and could theoretically include off-target effects not captured in purified enzyme assays. Downstream of enzyme inhibition, the cellular effects of NNMT inhibition include: increased cellular NAD+ levels, particularly in tissues with high NNMT expression; activation of sirtuin deacetylases (SIRT1, SIRT3) that depend on NAD+ as a cofactor, with downstream effects on mitochondrial biogenesis, oxidative metabolism, and protein acetylation patterns; increased brown adipose tissue-like phenotypic markers in white adipose tissue (beiging), associated with increased thermogenesis and energy expenditure; decreased lipid accumulation in hepatocytes and adipocytes through altered lipogenesis gene expression; altered methylation patterns at metabolic gene promoters, though the full epigenetic consequences of chronic NNMT inhibition are not well characterized. In skeletal muscle specifically, the proposed mechanism for improved muscle function in aged mice involves preservation of NAD+ in satellite cells (muscle stem cells), enhanced mitochondrial function in mature muscle fibers, and altered methylation at regenerative gene programs. The muscle effects have been the basis for significant interest in 5-amino-1MQ as a sarcopenia intervention, though the human translation remains entirely untested. The key mechanistic nuance often missed is that NNMT inhibition is not simply "NAD+ boosting" — it is NAD+ preservation through reduced substrate diversion, combined with SAM preservation and altered methyl balance. This is a different mechanism from exogenous NAD+ precursors like nicotinamide riboside (NR) or nicotinamide mononucleotide (NMN), which provide additional substrate for NAD+ synthesis. In principle, NNMT inhibition and NAD+ precursor supplementation could be complementary (reduce NAD+ consumption through methylation while increasing precursor supply), but the combination has not been studied clinically and the theoretical synergy is speculative.
Overview
5-Amino-1MQ (5-amino-1-methylquinolinium iodide) is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme that transfers a methyl group from S-adenosyl-L-methionine (SAM) to nicotinamide to form 1-methylnicotinamide (1-MNA) and S-adenosyl-L-homocysteine (SAH). The compound emerged from a medicinal chemistry program at Sanofi aimed at developing NNMT inhibitors for metabolic disease, and was first described in the peer-reviewed literature in 2018 as one of several quinolinium-based inhibitors with single-digit micromolar potency against human NNMT in biochemical assays (Kannt et al., 2018; Neelakantan et al., 2017). Subsequent work characterized 5-amino-1MQ specifically as a bisubstrate-competitive inhibitor that occupies both the nicotinamide-binding pocket and extends into a portion of the SAM-binding site, providing selectivity over other methyltransferases in the body (Neelakantan et al., 2019). The interest in NNMT inhibition arose from observations that NNMT is overexpressed in adipose tissue, liver, and certain cancers, and that this overexpression contributes to metabolic dysfunction by depleting cellular NAD+ precursor pools and by altering the methyl donor balance that regulates epigenetic marks and lipid metabolism. In 2014, Kraus and colleagues demonstrated that adipocyte-specific NNMT knockdown in mice produced lean body composition despite a high-fat diet, improved glucose tolerance, and increased energy expenditure, establishing NNMT as a legitimate metabolic target. The 5-amino-1MQ molecule provides a pharmacologic tool to test whether inhibiting NNMT pharmacologically reproduces the benefits of genetic knockdown, and preclinical studies using 5-amino-1MQ and related inhibitors in diet-induced obese mice have demonstrated reduced adiposity, improved insulin sensitivity, and lower hepatic triglyceride content (Kannt et al., 2018). The compound has attracted attention in the fitness and longevity biohacking communities because of a separate line of research suggesting that NNMT inhibition may improve skeletal muscle function during aging by preserving NAD+ availability and altering methyl group metabolism in ways that favor muscle regeneration. A widely circulated 2021 study in aged mice reported that 5-amino-1MQ administration increased muscle stem cell activity, improved muscle regeneration after injury, and increased grip strength and muscle mass in older animals. This finding, combined with the obesity data, generated substantial interest in 5-amino-1MQ as a dual-purpose metabolism-and-sarcopenia compound, which has driven significant sales through research-chemical vendors despite the complete absence of human clinical trials. The practical reality of 5-amino-1MQ as a research chemical in April 2026 mirrors the situation with BAM15 and similar compounds: preclinical evidence is genuinely interesting, mechanism is plausible, regulatory development is nonexistent, and users are self-experimenting with research-chemical-vendor supply at unvalidated doses. This entry covers what 5-amino-1MQ actually does at the enzyme level, what the preclinical studies in obesity and muscle have shown, what the methyl-donor and NAD+ biology implies about stacking decisions, what the real concerns are about long-term NNMT inhibition (cancer surveillance, methylation homeostasis, interactions with other epigenetic processes), and what a defensible approach looks like for anyone considering experimentation. The honest summary: 5-amino-1MQ is a legitimate research compound targeting a real metabolic pathway, the rodent data are reproducible across multiple labs, and there is zero direct human evidence that the compound is safe or effective at any dose. FDA-approved interventions for obesity and metabolic disease (Semaglutide, Tirzepatide, Retatrutide, bariatric surgery, lifestyle medicine) have Phase 3 data and offer predictable benefit-risk profiles that 5-amino-1MQ does not. For sarcopenia, resistance training remains the dominant evidence-based intervention, and no pharmacologic intervention has demonstrated superiority to well-dosed protein and progressive overload in older adults. 5-amino-1MQ sits alongside these validated options as an investigational compound of mechanistic interest, not as a substitute for them.
Chemical Information
IUPAC Name
5-amino-1-methyl-1H-pyrazole-4-carboxamide
CAS Number
424912-40-5
Molecular Formula
C10H11N2
Molecular Mass
159.21 g/mol
Dosing & Protocols
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Interactions
Interaction Matrix
Contraindications
5-Amino-1MQ has not been clinically tested, so the contraindications list is constructed from mechanism-based concerns and general principles for unvalidated research chemicals. Pregnancy and breastfeeding are absolute contraindications — no reproductive or developmental toxicology data exist, and the effects of altered methyl donor metabolism and NAD+ pathway modulation on placental function, fetal development, and lactation are entirely uncharacterized. Methyl donor balance is particularly critical during embryogenesis (neural tube development depends on adequate folate and methionine cycle function), which makes any intervention that alters methylation during pregnancy particularly risky. Anyone trying to conceive should avoid 5-amino-1MQ because reproductive effects are unknown. Children and adolescents should not use 5-amino-1MQ because developmental metabolism, bone and muscle growth, and neurological maturation depend on methylation and NAD+ pathways in ways that could be disturbed by NNMT inhibition, and these effects have not been studied in developmental age groups. Active malignancy is a relative contraindication with important nuance. NNMT is overexpressed in many cancers (endometrial, pancreatic, ovarian, lung, colorectal, others) where it may support tumor metabolism through methyl donor depletion and methylation remodeling. In principle, NNMT inhibition could be beneficial in cancers driven by NNMT overexpression, and there is academic interest in NNMT inhibitors as cancer therapeutics. However, uncontrolled self-administration of an NNMT inhibitor during active cancer treatment is not a substitute for properly designed oncology care, and the interaction with chemotherapy, radiation, and targeted therapies is not characterized. Patients with cancer should not use 5-amino-1MQ without explicit oncology guidance, and probably not even with it outside of a clinical trial context. Patients with a history of cancer under surveillance should similarly avoid 5-amino-1MQ because effects on dormant disease are unknown. Active cardiovascular disease is a relative contraindication because of uncharacterized effects on vascular biology. 1-methylnicotinamide (1-MNA), the product of the NNMT reaction that 5-amino-1MQ reduces, has been proposed to have cardiovascular effects (vasodilation, anti-inflammatory, anti-thrombotic) based on some animal studies, and reducing 1-MNA production through NNMT inhibition could theoretically alter these signals. Whether this translates to clinically meaningful cardiovascular effects in humans is unknown, but patients with coronary artery disease, heart failure, arrhythmias, or significant cardiovascular risk factors should err toward caution. Hepatic impairment warrants caution because the liver is a major NNMT-expressing tissue and hepatic methylation reactions are central to metabolic homeostasis. Patients with active hepatitis, cirrhosis, significant fatty liver with elevated enzymes, or prior drug-induced liver injury should avoid 5-amino-1MQ because liver stress responses and methylation homeostasis may be disrupted. Renal impairment warrants caution because drug elimination pathways are not characterized, and altered 1-MNA excretion (which is normally renal) could have systemic consequences in the setting of reduced renal function. Significant mental health conditions on medications with narrow therapeutic windows are a relative contraindication because methylation balance affects catechol-O-methyltransferase (COMT) activity and thus catecholamine metabolism, potentially altering drug levels for medications metabolized through these pathways. Patients on MAOIs, tricyclic antidepressants, clozapine, or other drugs with sensitive metabolism should consult their psychiatrist before adding any compound with methylation-pathway effects. Homocystinuria, methylenetetrahydrofolate reductase (MTHFR) deficiency, and other inborn errors of methylation metabolism are absolute contraindications because these conditions involve pre-existing methyl donor balance pathology that could be worsened by NNMT inhibition. Severe deficiencies in folate or B12 that have not been corrected are relative contraindications because methyl donor availability is already compromised. Patients on anti-epileptic medications with methylation sensitivity (valproate, others) should consult their neurologist. Medications with known interaction potential warrant particular attention. Anticoagulants: not a clear interaction, but any compound altering liver metabolism could theoretically alter warfarin metabolism through P450 effects; INR monitoring is prudent if warfarin is concurrent. Direct oral anticoagulants (apixaban, rivaroxaban, dabigatran) may be safer with respect to interactions but are not fully characterized. Antihypertensives: theoretical cardiovascular effects may alter blood pressure response; monitor blood pressure during use. Insulin and sulfonylureas: metabolic effects may reduce insulin requirements; monitor glucose to avoid hypoglycemia. GLP-1 agonists: metabolic overlap as discussed in the stacking notes; monitor for excessive effects. Chemotherapy agents: drug-drug interaction potential is uncharacterized; avoid unless under oncologist supervision. Any medication on which the patient has tight therapeutic range or known metabolic sensitivity warrants pre-use consultation. The final and most important contraindication is the absence of clinical oversight. Self-experimentation with 5-amino-1MQ without a physician who knows about the use, can order appropriate labs, can adjust or stop dosing based on findings, and can evaluate any adverse effects is not a defensible approach to safe experimentation. This applies even if the user feels healthy and has no known medical conditions — the value of clinical support is in detecting and responding to subclinical abnormalities before they become clinical problems, and that detection is not possible without ongoing monitoring. If you do not have a physician who knows you are using 5-amino-1MQ, you have not set up the minimum safety infrastructure for using an unvalidated research chemical.
Research Disclaimer
This interaction data is compiled from published research and community reports. It may not be exhaustive. Always consult a healthcare professional before combining compounds.
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5-Amino-1MQ 5mg | vial | 1 vial● In Stock | $29.99BEST | $5.998 | ||
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5-Amino-1MQ 5mg | vial | 1 vial● In Stock | $34.99 | $6.998 | ||
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5-Amino-1MQ 5mg | vial | 1 vial● In Stock | $35.00 | $7.000 | — | |
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5-Amino-1MQ 5mg | vial | 1 vial● In Stock | $29.99 | $5.998 | — | |
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5-Amino-1MQ 5mg | vial | 1 vial● In Stock | $29.99 | $5.998 | — | |
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5-Amino-1MQ 50mg x60 Tabs | tablet | 60 tablets● In Stock | $240.00 | $0.080 | ||
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5-Amino-1MQ 50mg | vial | 1 vial● In Stock | $49.99 | $1.000 | ||
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5-Amino-1MQ 50mg | vial | 50mg vial● In Stock | $44.99 | $0.900 | ||
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5-Amino-1MQ Capsules 60ct | capsule | 60 capsules● In Stock | $79.99 | — |
Tracking since Mar 13, 2026 · 9 data points
Price History
4 data pointsVendors Selling 5-Amino-1MQ
BioMyst Labs
ResearchChemHQ
Optimum Formula
Ion Peptide
VANDL Labs
Limitless Biochem EU
Paramount Peptides
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4/21/2026Research Score
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Data Completeness
88%COA Verification
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Latest test: 3/1/2026
Quick Facts
Half-Life
~6–12 hours (oral)
Molecular Weight
159.21 g/mol
Administration
Oral
CAS Number
424912-40-5
Trial Phase
Preclinical
Research Disclaimer
This information is for educational and research purposes only. Not intended as medical advice. Consult a healthcare professional before use.
Frequently Asked Questions
What is NNMT and why inhibit it?
Nicotinamide N-methyltransferase (NNMT) is an enzyme that transfers a methyl group from S-adenosyl-L-methionine (SAM) to nicotinamide, producing 1-methylnicotinamide (1-MNA) and S-adenosyl-L-homocysteine (SAH). NNMT is overexpressed in adipose tissue, liver, and certain cancers, where it diverts nicotinamide away from NAD+ synthesis and consumes SAM. NNMT knockdown in mice produces lean body composition and improved insulin sensitivity, which prompted development of pharmacologic inhibitors like 5-amino-1MQ as potential metabolic disease drugs (Kannt et al., 2018).
Has 5-amino-1MQ been tested in humans?
No. As of April 2026, no Phase 1 or later clinical trials of 5-amino-1MQ have been published, no IND applications have been publicly disclosed, and no registered trials appear on ClinicalTrials.gov. All human use is self-experimentation with research-chemical vendor supply at unvalidated doses.
What weight loss does 5-amino-1MQ produce in animal studies?
In diet-induced obese mice, 5-amino-1MQ produced 10-20% body weight reduction over 4-8 weeks with improvements in glucose tolerance and hepatic steatosis (Kannt et al., 2018). Translation to human weight loss magnitude is speculative — rodent metabolic responses to experimental compounds often exceed human responses.
Does 5-amino-1MQ help with muscle aging?
Rodent studies have shown that NNMT inhibition improves muscle stem cell function, muscle regeneration, and grip strength in aged animals, which has driven substantial interest in 5-amino-1MQ as a sarcopenia intervention. Whether this translates to improved muscle function in older humans is entirely untested in clinical trials. Resistance training remains the evidence-based intervention for sarcopenia with orders of magnitude more data.
What dose of 5-amino-1MQ do people use?
Self-report communities describe doses ranging from 50 mg to 300 mg daily, with 100-150 mg as a common range. These doses are extrapolated from rodent efficacy studies using allometric scaling and have not been validated in human trials. Any dose on a vendor label is a guess with a patina of precision belying the underlying uncertainty.
How should I stack 5-amino-1MQ with NAD+ precursors like NMN or NR?
The combination is mechanistically complementary: 5-amino-1MQ preserves nicotinamide by reducing NNMT-mediated methylation, while NMN or NR provides additional substrate for NAD+ synthesis. Theoretical synergy for NAD+ elevation. No clinical data validate this combination specifically, and whether the combination outperforms either intervention alone is unknown.
Should I take methyl donors with 5-amino-1MQ?
Chronic NNMT inhibition alters methyl donor metabolism, and supporting methyl donor supply with trimethylglycine, methylfolate, and methylated B12 is a reasonable precaution for users on extended cycles. These supplements are individually well-tolerated at typical doses (500-1000 mg TMG, 400-800 mcg methylfolate, 500-1000 mcg methylcobalamin), though no clinical evidence establishes whether co-supplementation changes 5-amino-1MQ outcomes.
Can I use 5-amino-1MQ with GLP-1 drugs like Semaglutide?
The combination has not been studied clinically. Semaglutide and Tirzepatide produce substantial weight loss through Phase 3-validated mechanisms. Adding 5-amino-1MQ adds risk (uncharacterized interactions, compounded uncertainty) without documented additional benefit. The rational position is to use the validated GLP-1 therapy if weight loss is the goal and not to layer unvalidated research chemicals on top.
What are the main safety concerns with 5-amino-1MQ?
Short-term rodent tolerability is reasonable and short-term human self-report data suggest the compound is generally well-tolerated at typical doses. The significant unknowns are long-term effects on methylation homeostasis, cancer surveillance implications of altered methyl donor metabolism, cardiovascular effects from reduced 1-MNA production, and interactions with other medications metabolized through methylation-sensitive pathways. None of these are documented risks; they are theoretical concerns that remain open because no long-term human data exist.
What should I monitor if I use 5-amino-1MQ?
Before starting and at the end of each cycle: comprehensive metabolic panel, CBC, liver function tests, thyroid panel, fasting glucose and HbA1c, lipid panel, homocysteine (to detect methyl balance issues), and vitamin B12 and folate. For longer cycles or higher doses: add hs-CRP, IGF-1 if relevant, and any condition-specific markers. Any unexplained abnormality warrants cessation and evaluation. Self-monitoring without clinician involvement is inadequate — find a physician who knows about the use and can order appropriate follow-up.
Research Tools
Related Compounds
View AllBAM15
Weight LossPreclinicalBAM15 is a small-molecule mitochondrial protonophore uncoupler that was first described in 2014 as a tool compound for dissipating proton motive force selectively across the inner mitochondrial membrane without collapsing the plasma membrane electrochemical gradient (Kenwood et al., 2014).
Exenatide
Weight LossPreclinicalGLP-1 receptor agonist used for metabolic effect and appetite regulation..
L-Carnitine
Weight LossPreclinicalL-Carnitine is a naturally occurring quaternary ammonium compound synthesized in the body from the amino acids lysine and methionine, with essential cofactor roles in fatty acid metabolism, energy production, and cellular health.
Lipo-C
Weight LossPreclinicalLipotropic compound blend injection.
Mazdutide
Weight LossPreclinicalMazdutide (also known as IBI362, Lilly compound LY3305677) is a dual glucagon-like peptide-1 (GLP-1) and glucagon receptor agonist originally discovered by Eli Lilly and exclusively licensed to Innovent Biologics in 2019 for development and commercialization in Mainland China, Hong Kong, Macau, and Taiwan.
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