An experimental compound often discussed for fat loss. It is a small molecule, not a peptide.
6-minute readFull profile reviewed July 25, 2026
Evidence is explained by question. Dosing references show their own check dates.
60-second overview
5-Amino-1MQ at a glance
Why people look into it, what studies found, and what is still unknown.
Why people look into it
Whether changing an enzyme involved in cell metabolism affects weight or metabolic health.
What studies found
Mouse studies reported changes in weight, fat, and blood sugar, with results varying by model. No human treatment trial was located.
What is still unclear
Human benefits, absorption, interactions, organ effects, and safety are unknown. Mouse amounts cannot establish a human dose.
About the evidence and review date
Educational information only. Evidence reviewed through July 25, 2026. Published studies, sponsor announcements, and trials without results are labeled separately. Evidence gaps apply to the specific finding beside them.
Research questions
Why people research it
Each label shows how much evidence supports that question.
Weight and fat lossAnimal or lab research
Insulin sensitivity and glucose handlingAnimal or lab research
Fatty liver and liver metabolismAnimal or lab research
Muscle strength and injury recoveryAnimal or lab research
Exercise performanceAnimal or lab research
Cancer and immunotherapy biologyAnimal or lab research
Human weight loss or body recompositionNot demonstrated
Human anti-aging or longevityNot demonstrated
What studies show
What the evidence supports
The research behind the answer
No direct human treatment evidence; human bladder-tumor datasets associated NNMT-positive fibroblasts with outcomes, but patients did not receive 5-Amino-1MQ
See each finding and its sources (12)
Mechanistic rationale
5-Amino-1MQ is a synthetic small-molecule NNMT inhibitor, not a peptide.
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.
Names such as 5A1MQ, 5-amino-1MQ, 5MQ, and the iodide salt are used inconsistently online, so product identity cannot be assumed from a shorthand label.
Peer reviewedChemical identity and inhibitor characterization
Laboratory study
5-Amino-1MQ inhibits nicotinamide N-methyltransferase and changes connected metabolic pools in laboratory models.
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.
Cell-metabolite changes do not establish a whole-body human effect, and NNMT biology differs by tissue and disease context.
Peer reviewedAdipocyte metabolite and lipogenesis experiments
Animal study
5-Amino-1MQ reduced body weight or fat-related measures in diet-induced-obese mice.
Two controlled mouse studies reported lower body weight or weight gain and less white-fat mass without lower food intake.
Mouse weight and fat findings do not demonstrate human weight loss, appetite effects, body recomposition, or durability.
5-Amino-1MQ improved glucose, insulin, and fatty-liver measures in obese mice.
A 28-day mouse study reported better glucose tolerance and insulin sensitivity plus less liver fat, inflammation, ballooning, and abnormal serum markers.
The study cannot establish human diabetes, insulin-resistance, MASLD/MASH, or liver-disease treatment.
Aged-mouse studies reported muscle-regeneration and grip-strength signals with NNMT inhibition.
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.
These specialized aged-mouse models do not establish human muscle recovery, sarcopenia treatment, workout performance, or anti-aging benefit.
No published human pharmacokinetic, safety, tolerability, or efficacy trial of 5-Amino-1MQ was located.
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.
Registry and literature searches can miss unpublished or newly posted work and should be repeated as the evidence changes.
Peer reviewedHuman biomarker versus mouse intervention boundary
No direct evidence located
5-Amino-1MQ has not been demonstrated in humans to cause weight loss, suppress appetite, improve fatty liver, increase strength, speed recovery, or slow aging.
Those popular use cases are extrapolated from cells and mice rather than controlled human outcomes.
Absence of demonstrated benefit is not proof that an effect is impossible; it means the human question is unanswered.
Animal reports of no observable adverse effects do not establish human safety.
The foundational paper reported no observable adverse effects in its short mouse experiment, but there is no human adverse-event or dose-escalation dataset.
Small mouse studies are not designed to detect human organ toxicity, drug interactions, reproductive risk, rare events, or long-term effects.
There is no approved human dose, route, reconstitution procedure, cycle, or storage standard for 5-Amino-1MQ.
Published mouse experiments used very different subcutaneous, oral, and intravenous exposures, and one mouse PK study reported poor oral bioavailability.
Animal mg/kg schedules cannot be converted into human instructions. Seller directions and community protocols are not regulator-approved product information.
Peer reviewedMouse route and pharmacokinetic comparisons
No direct evidence located
5-Amino-1MQ is not FDA approved, and FDA has specifically addressed its 503B compounding eligibility.
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.
The warning letter concerns one facility and the legal conditions for 503B outsourcing facilities; it is not a clinical safety or efficacy trial.
NNMT is a context-dependent metabolic enzyme, not a universally harmful switch.
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.
A favorable effect in one cell type or mouse disease model cannot be assumed in another tissue or in a healthy human.
Peer reviewedNNMT pathway and selectivity experiments
Missing reports do not establish safety. Findings apply to the product, route, amounts, population, comparison, and follow-up studied.
Side-effect frequency, study withdrawals, and gaps
How often side effects occurred
The available information does not reliably show how often particular side effects occur.
Evidence boundary
Under-detected or under-reported events must not be described as rare.
Why people stopped in studies
Relay has not verified which side effects led people to stop treatment in studies.
Evidence boundary
This is an evidence gap, not proof that discontinuations did not occur.
Warning information
Relay has not verified a compound-specific warning summary for this profile.
Evidence boundary
Not 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
Emergency instructions
This profile does not contain verified, product-specific emergency instructions.
Evidence boundary
Relay does not infer emergency guidance from study discontinuations, mechanism, or incomplete adverse-event reporting.
Dosing references
Dosing & preparation
Each table labels its source and applies only to the named route, product, or study. An online example or community report is not an approved dose.
Route: Route unverified · No exact human administration route established in this review
Evidence gap · Route unverified
No verified administered-human regimen
The reviewed NNMT-inhibition evidence is preclinical. Animal doses do not establish an oral or injectable human schedule.
What would fill this gap: A verified human trial of 5-amino-1MQ with defined formulation and exposure.
Dosing review checked Oct 20, 2026. Additional sources are available below.
Formulation & handling · Route unverified
No route-specific preparation instructions were verified. A different route or product does not supply them.
Starting dose, maintenance, and trial targets explained
Starting dose: the amount used at the beginning of the named label schedule or trial.
Maintenance: the ongoing amount described by that product label.
Trial target: the amount assigned to a study group. Different groups may stop increasing at different targets.
Other source records, populations, and limits · all routes
Preclinical evidence only
5-Amino-1MQ diet-induced-obesity mouse study material
Amount in this source
A complete human regimen was not verified in this source record. See the dosing status above.
Frequency
Repeated exposure during an eleven-day animal protocol
Route
Subcutaneous administration in mice and laboratory cell exposure
Duration
11 days
Population, study design, and limitations
Published research investigated 5-Amino-1MQ in a small controlled mouse model of diet-induced obesity, with supporting enzyme and fat-cell experiments.
Population: 18 diet-induced-obese mice; nine per treatment group
Design: Controlled diet-induced-obesity mouse experiment with supporting adipocyte and enzyme-selectivity assays
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.
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.
Why this matters
A plausible mechanism can explain why a study was attempted. It does not prove that the compound improves a human outcome.
Signals and targets
NNMT enzyme — primary molecular targetNo established receptor agonist or antagonist mechanismNAD+, SAM, 1-MNA, and SIRT1-linked pathways — downstream context
Proposed biological steps
Nicotinamide N-methyltransferase inhibition
Reduced formation of 1-methylnicotinamide in models
Altered nicotinamide and NAD+ salvage-pathway pools
Altered SAM/SAH methyl-donor balance
Reduced adipocyte lipogenesis in vitro
Context-dependent effects across metabolic and tumor tissues
Research reference
How mature is the evidence?
A reference for the studies, populations, and routes behind this profile.
Research depthMultiple preclinical programs
Mouse metabolic, muscle, and cancer models plus cell studies are available, but no registered human interventional study was located.
Why this matters
Research depth describes how large and mature the overall record is. It does not tell you whether the results were positive.
Evidence confidenceVery low for human outcomes
Human pharmacokinetics, tolerability, effective exposure, interactions, and clinical benefit have not been established.
Why this matters
Confidence describes how reliable and consistent the conclusions are. It can be high for one outcome and low for another.
Strongest evidenceControlled mouse metabolic and muscle experimentsWhy this matters
The strongest evidence type shows what the best-supported conclusions are actually based on.
Human evidenceNo direct human administration study locatedWhy this matters
Human findings are more directly relevant than animal or laboratory results, but they still apply only to the populations and outcomes studied.
Route studiedSubcutaneous administration in mice and laboratory cell exposure
Schedules studiedRepeated exposure during an eleven-day animal protocol; 11 days
Amounts studiedWithheld: this record provides research context without a transferable amountWhy this matters
These are exposures used in cited research for a specific route and population—not an instruction for an individual.
Half-lifeNot established for this exact editorial recordWhy this matters
Half-life describes how long it takes the measured amount in the body to fall by half. It is not a dosing recommendation.
Route evidencePublished research investigated 5-Amino-1MQ in a small controlled mouse model of diet-induced obesity, with supporting enzyme and fat-cell experiments.Why this matters
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.
Studies
Study-by-study record
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.
Why this matters
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
Outcomes measured
Body weight, fat mass, lean mass, and food intake
Glucose tolerance, insulin sensitivity, and plasma insulin
Liver weight, triglycerides, steatosis, inflammation, and ballooning
Serum ALT, AST, ketone bodies, CK, and LDH
Mouse plasma pharmacokinetics and tissue distribution
What was reported
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 and important limits
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.
Animal studyPeer reviewed
NAD+ metabolism enzyme NNMT in cancer-associated fibroblasts drives tumor progression and resistance to immunotherapy by modulating macrophages in urothelial bladder cancer
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
Outcomes measured
Tumor volume and weight
Tumor-cell apoptosis
Macrophage infiltration
Response to anti-PD-L1
NNMT-positive fibroblasts in human tumor datasets
What was reported
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 and important limits
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.
Animal studyPeer reviewed
Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice
Four-group aged-female-mouse experiment comparing sedentary or progressive exercise conditions with 5A1MQ or vehicle
35 female mice aged 22 to 24 months
Outcomes measured
Grip strength and running capacity
Plantarflexor torque and fatigue
Muscle mass, fiber size, and fiber type
Intramyocellular lipid
Muscle proteomics and metabolomics
What was reported
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 and important limits
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.
Laboratory studyPeer reviewed
Small molecule inhibitor of nicotinamide N-methyltransferase shows anti-proliferative activity in HeLa cells
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
Outcomes measured
Muscle stem-cell proliferation and fusion
Myofiber cross-sectional area and size distribution
Injured-muscle peak torque
Myoblast differentiation and NAD+/NADH state in vitro
What was reported
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 and important limits
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.
Animal studyPeer reviewed
Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice
Controlled diet-induced-obesity mouse experiment with supporting adipocyte and enzyme-selectivity assays
18 diet-induced-obese mice; nine per treatment group
Outcomes measured
Body weight and food intake
White-adipose mass and adipocyte size
Plasma total cholesterol
Adipocyte 1-MNA, NAD+, SAM, and lipogenesis
Observed adverse effects in the model
What was reported
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 and important limits
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.
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NAD+ metabolism enzyme NNMT in cancer-associated fibroblasts drives tumor progression and resistance to immunotherapy by modulating macrophages in urothelial bladder cancer
2024-07-27 · PMID 39067875 · DOI 10.1136/jitc-2024-009281