Gathering the record
Relay is organizing the evidence and source boundaries.
Quaternary quinolinium small-molecule NNMT inhibitor
5-Amino-1MQ is a small-molecule inhibitor of the enzyme NNMT—not a peptide. Researchers have studied it mainly in cells and mice for body fat, glucose handling, fatty liver, aged muscle, and cancer biology. No published human treatment trial was located.
60-Second Overview
Start with what it is, why it matters, what research has shown, and what remains unknown. The science follows after the orientation.
Start here. These four answers explain why the compound matters before the page introduces the deeper science.
5-Amino-1MQ is an experimental small molecule, not a peptide. It blocks an enzyme called NNMT, which participates in cellular methylation and energy-related chemistry.
Researchers use NNMT inhibition to explore body fat, glucose handling, fatty liver, aging muscle, and tumor biology in laboratory and animal models. These are separate research questions, not one established clinical use.
Mouse studies reported changes in weight, fat mass, glucose measures, liver findings, or injured-muscle function. Results varied by model and endpoint. Human tumor datasets have measured NNMT biology, but patients were not treated with 5-Amino-1MQ. No human treatment trial was located.
Human pharmacokinetics, route, target exposure, tolerability, interactions, organ toxicity, and clinical benefit remain unknown. Intensive mouse exposures and short-term observations cannot be converted into human administration or safety conclusions.
The research depth, routes, studies, and primary sources below explain how Relay knows—and where the evidence stops.
Research context
Published research has investigated this compound using the following study designs.
These records explain what researchers did. They are not instructions, recommendations, or a transferable protocol.
Published research investigated 5-Amino-1MQ in a small controlled mouse model of diet-induced obesity, with supporting enzyme and fat-cell experiments.
Reported study administration—not a recommendation.
Research at a glance
Evidence depth, confidence, and route context explain how Relay knows—not what anyone should do.
Mouse metabolic, muscle, and cancer models plus cell studies are available, but no registered human interventional study was located.
Research depth describes how large and mature the overall record is. It does not tell you whether the results were positive.
Human pharmacokinetics, tolerability, effective exposure, interactions, and clinical benefit have not been established.
Confidence describes how reliable and consistent the conclusions are. It can be high for one outcome and low for another.
The strongest evidence type shows what the best-supported conclusions are actually based on.
Human findings are more directly relevant than animal or laboratory results, but they still apply only to the populations and outcomes studied.
Route-specific record
These are exposures used in cited research for a specific route and population—not an instruction for an individual.
Half-life describes how long it takes the measured amount in the body to fall by half. It is not a dosing recommendation.
Evidence can change by administration method. Findings from one route should not automatically be applied to another.
Evidence boundary: Only nine mice received the experimental compound, and no human administration study was identified. Mouse weight and fat changes do not establish a human route, exposure, benefit, safety profile, or product standard. Amounts shown describe cited research exposure—not a dosage recommendation.
Detailed evidence
Start with the strongest supported conclusion and its main uncertainty. Claim-level records below show how the evidence changes by question, population, route, formulation, and study design.
No direct human treatment evidence; human bladder-tumor datasets associated NNMT-positive fibroblasts with outcomes, but patients did not receive 5-Amino-1MQ
This is the strongest supported conclusion in the current human evidence—not a summary of every claim made about the compound.
Human pharmacokinetics, safety, tolerability, dose-response, interactions, and whether any mouse metabolic or muscle signal translates into clinical benefit
Keeping the main uncertainty visible prevents an early or promising finding from looking more settled than it is.
Questions people bring to the evidence
Research questions—not promises of benefit.
Its commonly studied form is 5-amino-1-methylquinolinium iodide. The quinolinium cation is the active chemical identity discussed in the research; iodide is the counterion.
NNMT transfers a methyl group from SAM to nicotinamide to form 1-MNA. In cultured adipocytes, 5-amino-1MQ lowered 1-MNA, increased NAD+ and SAM, and reduced lipid accumulation.
Two controlled mouse studies reported lower body weight or weight gain and less white-fat mass without lower food intake.
A 28-day mouse study reported better glucose tolerance and insulin sensitivity plus less liver fat, inflammation, ballooning, and abnormal serum markers.
One injury model reported larger regenerated fibers and greater injured-muscle torque; a later exercise study reported higher grip strength with 5A1MQ alone and with exercise.
The compound slowed HeLa-cell proliferation in vitro and reduced bladder-tumor growth while enhancing anti-PD-L1 effects in mice.
The traceable intervention record consists of laboratory and animal studies. Patient tumor datasets studied NNMT biology but did not expose people to 5-Amino-1MQ.
Those popular use cases are extrapolated from cells and mice rather than controlled human outcomes.
The foundational paper reported no observable adverse effects in its short mouse experiment, but there is no human adverse-event or dose-escalation dataset.
Published mouse experiments used very different subcutaneous, oral, and intravenous exposures, and one mouse PK study reported poor oral bioavailability.
In a January 2026 warning letter, FDA stated that the bulk substance was not eligible for 503B compounding because it was not on the 503B bulks list and was not tied to a shortage-list drug.
NNMT participates in nicotinamide clearance, NAD-related metabolism, methyl-donor balance, and tissue-specific signaling. Effects of inhibiting it can differ across fat, liver, muscle, and tumor biology.
Mechanisms
5-Amino-1MQ, commonly studied as 5-amino-1-methylquinolinium iodide, is a membrane-permeable substrate-site NNMT inhibitor. In cultured adipocytes it lowers the NNMT product 1-MNA, changes NAD+ and SAM pools, and suppresses lipogenesis. Diet-induced-obesity mouse studies reported less weight or fat gain, better glucose and insulin measures, and improved liver histology. Separate aged-mouse experiments reported muscle-regeneration and grip-strength signals, while cancer work remains limited to cell and mouse treatment models plus observational human tumor profiling. No registered or published human pharmacokinetic, safety, tolerability, or efficacy trial was located. FDA has not approved the compound and addressed its ineligibility for 503B compounding in a January 2026 warning letter.
A plausible mechanism can explain why a study was attempted. It does not prove that the compound improves a human outcome.
Studies
Study arms are reported for transparency. They describe what researchers did in a defined record and do not transfer across identities, routes, formulations, or populations.
A later trial phase can ask a more mature question, but it does not guarantee a positive result, regulatory approval, or relevance outside the studied population.
Three-group controlled diet-induced-obesity mouse study with separate mouse pharmacokinetic and tissue-distribution experiments
24 diet-induced-obese mice in the efficacy study; eight each in vehicle, low-dose, and high-dose groups
5A1MQ dose-dependently limited weight and fat-mass gain without changing food intake or lean mass, improved glucose and insulin measures, and reduced several fatty-liver findings. Mouse testing found poor oral bioavailability and greater exposure after non-oral routes.
Study administration: Once-daily 5A1MQ at 10 or 25 mg/kg or vehicle in mice; separate IV, oral, and subcutaneous mouse PK experiments
Limitations: All treatment and PK data were from mice. The study does not establish human weight loss, fatty-liver treatment, insulin-sensitivity benefit, route, dose, or safety. Several authors had company affiliations.
Four-group bladder-cancer mouse-model experiment supported by human tumor profiling and cell-mechanism studies
24 mice bearing experimental bladder tumors; six per group
5-Amino-1MQ reduced tumor growth and strengthened the anti-PD-L1 effect in the mouse model. Separate patient-tumor analyses linked NNMT-positive fibroblasts with worse response and prognosis.
Study administration: 5-Amino-1-methylquinolinium iodide 10 mg/kg twice daily, anti-PD-L1 every three days, both treatments, or control in mice
Limitations: The human data observed NNMT expression; patients did not receive 5-Amino-1MQ. The treatment result therefore remains preclinical and does not establish cancer efficacy, safety, or compatibility with immunotherapy in people.
Four-group aged-female-mouse experiment comparing sedentary or progressive exercise conditions with 5A1MQ or vehicle
35 female mice aged 22 to 24 months
Treated sedentary mice had about 40% higher grip strength than sedentary controls, and treatment plus exercise produced an approximately 60% difference. Some muscle-composition measures improved, but peak torque and fatigue endpoints did not show the same broad effect.
Study administration: Daily subcutaneous 5A1MQ 10 mg/kg or vehicle, with or without progressive weighted-wheel running
Limitations: This was an aged-female-mouse study, not a human performance or recovery trial. Several authors had company affiliations, and not every functional endpoint improved.
In-vitro concentration- and time-response experiment
HeLa cervical-cancer cells with HEK-293 comparator cells
5MQ reduced HeLa-cell proliferation in a concentration- and time-dependent pattern and changed several signaling markers.
Study administration: 5-amino-1-methylquinolinium at laboratory concentrations from 0.1 to 500 micromolar
Limitations: A cancer-cell-line experiment cannot establish cancer treatment, selectivity in a human body, safe exposure, or clinical benefit.
Aged-mouse acute muscle-injury experiment with one- and three-week treatment cohorts plus C2C12 myoblast assays
24-month-old mice after experimental tibialis-anterior injury
NNMT inhibition increased muscle-stem-cell activity, regenerated-fiber size, and injured-muscle peak torque in aged mice; related differentiation signals were also seen in cultured myoblasts.
Study administration: NNMT inhibitor 5 or 10 mg/kg or saline in mice following barium-chloride muscle injury
Limitations: The model used very old mice with chemically injured muscle. It does not demonstrate human recovery, strength, sarcopenia treatment, a safe route, or an effective human exposure.
Controlled diet-induced-obesity mouse experiment with supporting adipocyte and enzyme-selectivity assays
18 diet-induced-obese mice; nine per treatment group
Treated mice lost more body weight and white-fat mass, had smaller adipocytes and lower cholesterol, and did not eat less. In cultured adipocytes, 5-amino-1MQ lowered 1-MNA, increased NAD+ and SAM, and reduced lipogenesis.
Study administration: Subcutaneous 5-amino-1MQ 20 mg/kg three times daily or saline; this is an animal experiment, not human dosing guidance
Limitations: This was a short mouse study with laboratory support. 'No observable adverse effects' in nine treated mice does not establish human safety, and the intensive animal schedule must not be translated into a human protocol.
Safety snapshot
No published human pharmacokinetic, safety, tolerability, or efficacy trial of 5-Amino-1MQ was located.
No direct evidenceRegistry and literature searches can miss unpublished or newly posted work and should be repeated as the evidence changes.
Open sourceThe current record does not support a reliable common-versus-uncommon frequency split.
Evidence boundaryUnder-detected or under-reported events must not be described as rare.
No source-qualified compound-specific warning or contraindication is encoded in the current record.
Evidence boundaryNot FDA approved; FDA stated in January 2026 that the bulk substance was not eligible for 503B compounding Human pharmacokinetics, safety, tolerability, dose-response, interactions, and whether any mouse metabolic or muscle signal translates into clinical benefit
The current record does not identify a reliable compound-specific pattern of events that caused study discontinuation.
Evidence boundaryThis is an evidence gap, not proof that discontinuations did not occur.
No compound-specific patient-facing urgent-action threshold is established in the current Relay record.
Evidence boundaryRelay does not infer emergency guidance from study discontinuations, mechanism, or incomplete adverse-event reporting.
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