NNMT Inhibitor Research

5-Amino-1MQ

Dosage & Dose Escalation Guide

Experimental small-molecule NNMT inhibitor—not a peptide and not FDA approved. No established human dosage. Preclinical mouse obesity and muscle signals; oral bioavailability shown in rats, unknown in humans.

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NNMT Inhibitor
Small Molecule
Metabolic Research
Not a Peptide

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Not a peptide
Quinolinium small molecule (C10H11N2+). Commonly marketed alongside peptides but chemically distinct.
NNMT
Inhibits nicotinamide N-methyltransferase, altering NAD+ salvage and SAM-dependent metabolism in models.
No human dose
Commercial 50–150 mg/day oral protocols are anecdotal — not clinical-trial regimens.

How It Works

NNMT methylates nicotinamide using SAM. 5-Amino-1MQ blocks that enzyme in laboratory models, reducing diversion of nicotinamide from NAD+ salvage and altering methyl-donor balance. Downstream metabolic effects are preclinical and tissue-dependent — not proven human outcomes.

NNMT Inhibition

✓Competitive inhibition at nicotinamide-binding region
✓IC50 commonly summarized around 1.2 µM in assays
✓IC50 is not a human dose

NAD+ / SAM Axis

✓May leave more nicotinamide for NAD+ salvage
✓Less SAM consumed by NNMT in models
✓Effects are tissue- and context-dependent

Adipose & Muscle Models

✓Reduced lipogenic activity in experimental systems
✓Fat-mass reduction in obese mice
✓Aged-mouse muscle function signals with exercise

Result

Mouse Fat-Mass Signal

No Human Efficacy Trial

Human Safety Unknown

Expected Results Over Time

Updated August 2026

5-Amino-1MQ Dosage, Results & Safety: Complete NNMT Inhibitor Research Guide

Research status: 5-Amino-1MQ is an experimental small-molecule NNMT inhibitor, not a peptide and not an FDA-approved drug. No established human dosage, published human efficacy trial, or validated human safety profile exists. Published evidence consists of biochemical experiments, cell studies, pharmacokinetic work in rats, and mouse studies. Commercial oral protocols—often advertised as 50–150 mg/day for 6–12 weeks—are not clinical-trial protocols. In January 2026, FDA specifically stated that 5-Amino-1MQ was not eligible for the section 503B compounding exemptions involved in an enforcement case because it was not on the 503B bulks list or used for a drug on the shortage list.

5-Amino-1MQ—short for 5-amino-1-methylquinolinium—is a laboratory compound that inhibits nicotinamide N-methyltransferase (NNMT). NNMT uses nicotinamide and the methyl donor S-adenosylmethionine (SAM) to form 1-methylnicotinamide and S-adenosylhomocysteine. Researchers are testing whether inhibiting this reaction changes NAD+ salvage, methyl-donor balance, adipose metabolism, liver metabolism, and age-related muscle function.

Diet-induced obese mice lost weight and fat mass after injected 5-Amino-1MQ in early studies. Later mouse experiments reported dose-related metabolic effects, additive effects with a lower-fat diet, and improvements in muscle function in aged animals. However, none of these outcomes has been demonstrated in people. Rat pharmacokinetic data show that oral exposure is possible in that species, but human oral bioavailability is unknown.

30-Second Summary

Question	Answer
What is it?	A synthetic methylquinolinium small molecule—not a peptide
Main target	Nicotinamide N-methyltransferase (NNMT)
Proposed research mechanism	Reduces nicotinamide methylation and alters NAD+ salvage and SAM-dependent metabolism
Administration studied	Primarily subcutaneous injection in mice; oral and IV pharmacokinetics studied in rats
Human dosage	None established
Human results	No published controlled human efficacy trials identified
Main preclinical finding	Reduced body weight and adipose mass in diet-induced obese mice
Human side effects	Unknown
FDA status	Not approved for any indication
503B compounding status	Not on the 503B bulks list; FDA challenged its use by an outsourcing facility in 2026
Evidence level	Preclinical

What Is 5-Amino-1MQ?

5-Amino-1MQ is a positively charged quinolinium-derived small molecule developed as an inhibitor of NNMT. It is often placed in online “peptide” catalogs because it is marketed to the same research and wellness audience, but chemically it is not an amino-acid chain.

Property	Description
Full name	5-amino-1-methylquinolinium
Common abbreviations	5-Amino-1MQ, 5A-1MQ, 5-AMQ, 5MQ
Compound class	Quinolinium small molecule
Free-cation formula	C10H11N2+
Free-cation molecular mass	Approximately 159.21 Da
Common research forms	Chloride, iodide, or other salt forms
Primary research target	NNMT

Salt form matters. The active cation is permanently charged and must be paired with a counterion. The cation, chloride salt, and iodide salt have different total molecular weights. A study reporting milligrams of active pharmaceutical ingredient is not necessarily equivalent to a vendor reporting milligrams of a complete salt.

Salt forms and active-cation fraction

Form	Approximate molecular mass	Active-cation fraction by mass	Why it matters
5-amino-1-methylquinolinium cation	159.21 g/mol	100% reference basis	The pharmacologically relevant ion, but not an isolable neutral “free base”
Chloride salt	194.67 g/mol	81.8%	100 mg of chloride salt is not 100 mg of active cation
Iodide salt	286.11 g/mol	55.6%	The heavy iodide counterion creates the largest mass difference

Product labels and certificates of analysis should identify the salt and whether the stated quantity refers to total salt or active cation. This is chemistry and quality-control context—not a consumer dose-conversion tool.

Claim-versus-evidence checker

Marketing language vs published evidence

“Orally bioavailable”

Rats only

Demonstrated in rats (~38.4% F). Poor oral bioavailability reported in mice in at least one study. Unknown in humans.

Orally bioavailableRats only
Burns fat without reducing appetiteMice only
Preserves muscleNot tested in humans
Boosts NAD+Preclinical / tissue-dependent
Improves exercise recoveryAged-mouse data only
FDA-approved peptideFalse

5-Amino-1MQ Dosage

There is no established human dosage. No FDA-approved dose, phase 1 dose-escalation study, maximum tolerated human dose, or peer-reviewed human pharmacokinetic study has established how much 5-Amino-1MQ a person can safely take.

Online protocols commonly describe oral amounts and treatment “cycles,” but those numbers are not supported by controlled human trials. They should be labeled anecdotal commercial protocols, not recommended dosage.

Doses used in published animal research

Animal research exposures — not human instructions

Study context	Species	Route	Experimental exposure	Duration	What it can establish
Early diet-induced obesity study	Mice	Subcutaneous injection	20 mg/kg, three times daily in a key experiment	11 days	Short-term efficacy in obese mice
Diet-switch and microbiome study	Mice	Subcutaneous injection	32 mg/kg active pharmaceutical ingredient once daily	Approximately 7 weeks	Effects of drug plus a lower-fat diet in mice
2024 metabolic/liver study	Mice	Subcutaneous injection	10 or 32 mg/kg once daily	28 days	Dose-response effects on body composition, glucose/insulin measures, and liver pathology
Pharmacokinetic assay study	Rats	Oral and intravenous	Study-specific rat doses	Short PK sampling period	Rat exposure, bioavailability, and analytical measurement
Aged-mouse exercise study	22-month-old female mice	Subcutaneous injection	10 mg/kg once daily	8 weeks	Muscle-function effects alone and with progressive weighted-wheel exercise
Aged-mouse injury/regeneration study	Aged mice	Subcutaneous injection	5 or 10 mg/kg daily around injury	2 weeks	Muscle stem-cell activation and regeneration after experimental injury

These are animal doses, not human-equivalent instructions. Even body-surface-area conversion would only generate a starting estimate for formal toxicology and phase 1 research; it would not establish a safe consumer dose.

Animal-study protocol comparison

Species, route, dose, and duration — no human conversion

Species / model: Mice · Diet-induced obesity
Route: Subcutaneous
Salt / API reporting: API as reported
Dose: 20 mg/kg
Frequency: Three times daily
Duration: 11 days

Outcome: Weight ↓, WAT ↓, adipocyte size ↓, cholesterol ↓; food intake unchanged

These are animal doses, not human-equivalent instructions. No human-dose conversion control is provided.

Is 5-Amino-1MQ Oral?

5-Amino-1MQ can produce measurable plasma exposure after oral administration in rats. A validated LC-MS/MS pharmacokinetic study reported an oral bioavailability of 38.4%, a mean maximum plasma concentration of about 2,252 ng/mL, and mean terminal half-lives of 6.90 ± 1.20 hours orally and 3.80 ± 1.10 hours intravenously under its rat study conditions.

That finding supports the statement “orally bioavailable in rats.” It does not support the stronger claims “effective oral therapy in humans” or “proven oral fat-loss compound.”

A later mouse study explicitly selected subcutaneous injection because oral bioavailability was poor in mice.
The same paper noted that this poor oral bioavailability was not observed in rats.
No published human oral bioavailability, food-effect, dose-proportionality, or steady-state study was identified.

Any page calling 5-Amino-1MQ “a uniquely oral peptide” without these qualifications overstates the evidence twice: it is not a peptide, and human oral performance has not been established.

Why No Dose-Escalation Chart Is Provided

A titration chart would imply a human protocol that does not exist. There are no verified human starting-dose groups, escalation intervals, maintenance doses, or stopping rules. MyPepFinder does not convert vendor schedules into a clinical-looking timeline.

The legitimate dose-response information belongs in the preclinical study tables, with species, route, salt form, and duration visible.

5-Amino-1MQ Results

Secondary summaries often quote roughly 5% body-weight reduction, approximately 35% lower white-fat mass, more than 30% smaller adipocytes, and around 30% lower cholesterol from early obese-mouse work. Those estimates describe small mouse cohorts and should not be presented as expected human results.

Preclinical results chart

Foundational obese-mouse study — approximate reported changes

Mouse study, not human results — small cohorts; secondary-summary percentages

Key regimen: 20 mg/kg subcutaneously three times daily for 11 days. Food intake was not meaningfully reduced. Do not present these as expected human outcomes.

Early diet-induced obesity study

Neelakantan and colleagues first characterized 5-Amino-1MQ as a selective, cell-permeable NNMT inhibitor and tested it in diet-induced obese mice.

Study feature	Finding
Model	Diet-induced obese mice
Key regimen	20 mg/kg subcutaneously three times daily
Duration	11 days
Body weight	Treated mice lost weight while vehicle animals gained weight
White adipose tissue	Reduced adipose mass and smaller adipocytes
Food intake	No meaningful reduction reported
Lean mass	Not reported as the driver of weight change
Plasma cholesterol	Reduced in the experimental model

The absence of reduced food intake suggests the effect was not simply appetite suppression in that model. It does not prove that 5-Amino-1MQ “burns fat without dieting” in humans.

Diet-switch and microbiome study

Dimet-Wiley and colleagues studied obese mice moved from a Western diet to a lower-fat diet. One group received vehicle; another received 32 mg/kg 5-Amino-1MQ subcutaneously each day for about seven weeks.

Outcome	Lower-fat diet + vehicle	Lower-fat diet + 5-Amino-1MQ
Body weight	Fell relative to Western-diet control	Fell further and became statistically indistinguishable from lean controls at study completion
Fat mass	Reduced	Reduced further and approached lean-control values
Microbiome	Diet-associated changes	Distinct profile, including higher Lactobacillus and lower Erysipelatoclostridium than diet-switch vehicle animals

This study cannot isolate every drug effect because the treated group also underwent a major diet change. Microbiome findings were exploratory and do not establish a probiotic-like mechanism in people.

2024 metabolic-dysfunction study

Evidence question	Answer
Was there a dose response?	The study reported dose-dependent effects in mice
What were the efficacy arms?	10 or 32 mg/kg/day subcutaneously versus vehicle for 28 days
Was food intake the explanation?	Changes were not explained simply by reduced food intake
Were metabolic measures assessed?	Yes: fed insulin, OGTT, insulin sensitivity, liver triglycerides, histology, ALT, AST, and ketone bodies
What happened to liver pathology?	Less steatosis and macrophage infiltration, smaller/lighter livers, lower liver triglycerides
Does it establish human weight loss?	No
Does it establish long-term human liver safety?	No

Muscle function in aged mice

Group	Preclinical finding
Sedentary control	Reference condition
5-Amino-1MQ without training	Improved grip strength and altered muscle molecular profiles
Exercise alone	Improved strength and running performance
Exercise + 5-Amino-1MQ	Produced additive improvements in several functional measures

The study used 22-month-old female mice given 10 mg/kg/day subcutaneously for eight weeks. Findings are hypothesis-generating and do not prove improved strength, recovery, sarcopenia treatment, or muscle preservation in humans.

Muscle regeneration after injury in aged mice

A separate 2019 study administered 5 or 10 mg/kg/day subcutaneously around an experimental muscle injury. NNMT inhibition increased aged muscle-stem-cell proliferation and subsequent fusion into regenerating fibers. This is a controlled mouse injury model—not evidence that the compound accelerates gym recovery, heals human tendon injuries, or treats sarcopenia.

Does 5-Amino-1MQ preserve muscle during weight loss?

No human study has tested whether 5-Amino-1MQ preserves lean mass during dieting or GLP-1 treatment. Connecting mouse fat-loss and aged-muscle studies into a claim that it “prevents GLP-1 muscle loss” is an unsupported extrapolation.

No controlled study was identified for a 5-Amino-1MQ plus semaglutide or tirzepatide combination.

5-Amino-1MQ Side Effects

Human side effects are unknown. There is no reliable human adverse-event table. Headache, nausea, fatigue, insomnia, anxiety, heart-rate changes, or appetite changes sometimes listed online are anecdotal claims, not rates from a controlled 5-Amino-1MQ trial.

Safety question	Current evidence
Common human adverse events	Unknown
Serious human adverse events	Unknown
Maximum tolerated human dose	Unknown
Human liver safety	Unknown
Human kidney safety	Unknown
Cardiovascular safety	Unknown
Drug interactions	Not systematically studied
Pregnancy and reproductive safety	Unknown
Carcinogenicity and genotoxicity program	No complete public human-development package identified
Neurologic/psychiatric safety	Unknown; stimulation/focus/insomnia claims are anecdotal
Long-term safety	Unknown

What animal tolerability can—and cannot—tell us

Published mouse studies did not report an obvious pattern of acute toxicity at the regimens used, and body-weight effects were not driven by reduced food intake. That is weaker than a formal safety conclusion. Small efficacy experiments may miss uncommon events, organ toxicity, reproductive effects, immune effects, or harms that emerge only after long exposure.

Mechanism-based uncertainties

NNMT sits at the intersection of nicotinamide handling, NAD+ salvage, and one-carbon metabolism. Inhibiting it can change nicotinamide and 1-methylnicotinamide concentrations, NAD+ availability in a tissue-dependent manner, SAM and S-adenosylhomocysteine balance, methyl-donor availability, and adipose, liver, muscle, stromal, and tumor-cell metabolism.

These changes are why NNMT is scientifically interesting—and why long-term systemic inhibition should not automatically be assumed safe.

Product-quality risk

Products sold online may use different salts, concentrations, excipients, or purity specifications. A certificate of analysis does not establish clinical sterility, human safety, accurate pharmacokinetics, or regulatory approval. Research-grade labeling generally means the material was not approved for human use.

How 5-Amino-1MQ Works

NNMT normally attaches a methyl group to nicotinamide. That reaction consumes nicotinamide that could otherwise participate in the NAD+ salvage pathway and uses SAM, a major cellular methyl donor. 5-Amino-1MQ blocks NNMT in laboratory models, reducing this metabolic diversion.

NNMT mechanism

Nicotinamide + SAM → NNMT → 1-MNA + SAH

1
Nicotinamide
Substrate
2
SAM
Methyl donor
3
NNMT
Inhibition target
4
1-MNA + SAH
Downstream products
5
NAD+ salvage
Preclinical possibility
6
Methyl-donor balance
Preclinical possibility

Downstream NAD+ salvage and methyl-donor changes are preclinical possibilities, not guaranteed human effects. IC50 ≈ 1.2 µM describes enzyme inhibition in an assay — not a human dose.

Technical mechanism

Target or pathway	Proposed preclinical effect
NNMT enzyme	Competitive inhibition at the nicotinamide-binding region
Nicotinamide → 1-MNA reaction	Reduced formation of 1-methylnicotinamide
NAD+ salvage	More nicotinamide may remain available for recycling toward NAD+
SAM/SAH metabolism	Less SAM consumed by NNMT, altering methyl-donor balance
Adipocyte metabolism	Reduced lipogenic activity and changes in adipose metabolites in experimental systems
Muscle metabolism	Proteomic and metabolomic changes associated with better function in aged mice

The early biochemical paper reported an NNMT inhibitory concentration in the low-micromolar range, commonly summarized as an IC50 around 1.2 µM. IC50 is not a human dose.

A necessary correction about NAD+

It is too strong to say that 5-Amino-1MQ universally “boosts NAD+.” NNMT inhibition altered NAD+-related metabolites in adipocyte and animal models, but the direction and importance of effects can depend on tissue, baseline NNMT expression, substrate availability, and disease state. No human trial has shown that taking the compound raises whole-body NAD+ or improves a clinical outcome through that pathway.

5-Amino-1MQ vs Related Compounds

Compound	Type	Mechanism	Human evidence	Regulatory status
5-Amino-1MQ	Small-molecule NNMT inhibitor	Reduces nicotinamide methylation	No published controlled efficacy trial identified	Not FDA approved
Nicotinamide riboside (NR)	Vitamin B3 derivative	NAD+ precursor	Multiple human pharmacokinetic and clinical studies	Sold as a dietary supplement in the U.S.
Nicotinamide mononucleotide (NMN)	NAD+ intermediate	NAD+ precursor	Early human studies; clinical benefit remains uncertain	Not an approved anti-aging drug
Semaglutide	Peptide GLP-1 agonist	Appetite, gastric emptying, insulin/glucagon signaling	Extensive phase 3 and outcomes evidence	FDA approved for specific indications
Tirzepatide	Peptide GIP/GLP-1 agonist	Dual incretin signaling	Extensive phase 3 and outcomes evidence	FDA approved for specific indications

5-Amino-1MQ attempts to reduce a metabolic “drain,” while NR and NMN supply NAD+ precursors. Calling these approaches complementary is mechanistically plausible but clinically untested. No controlled human evidence supports stacking 5-Amino-1MQ with NAD+, NMN, NR, semaglutide, tirzepatide, or another metabolic compound.

Clinical Evidence

No published human clinical efficacy study identified. As of August 2026, searches of the peer-reviewed literature and ClinicalTrials.gov did not identify a completed, results-reported human trial establishing the safety or efficacy of 5-Amino-1MQ. The evidence summaries below are therefore preclinical.

Evidence-level navigator

From assay to animal to (absent) human trials

Human evidence

No completed, results-reported controlled human trial establishing safety or efficacy was identified as of August 2026.

•No established human dosage
•No published human adverse-event rates
•Commercial 50–150 mg/day protocols are anecdotal

No completed results-reported controlled human trial was identified as of August 2026.

Study explorer

Published preclinical and PK evidence

Selective NNMT inhibitors in DIO mice
Neelakantan H et al. · Biochemical Pharmacology, 2018
Body compositionMouse2018
Protocol: 20 mg/kg SC three times daily (key experiment) · 11 days · Subcutaneous
Reduced body weight, adipose mass, adipocyte size, and cholesterol without reduced food intake
Small, short mouse study; no human pharmacology or safety
View study →
Rat PK / oral bioavailability
Awosemo O et al. · Journal of Pharmaceutical and Biomedical Analysis, 2021
PharmacokineticsRat2021
Protocol: Study-specific rat oral and IV doses · Short PK sampling period · Oral / IV
Oral bioavailability 38.4%; oral Cmax ≈ 2,252 ng/mL; oral t½ ≈ 6.9 h; IV t½ ≈ 3.8 h
Rat PK cannot establish human bioavailability, dosage, or efficacy
View study →
Diet-switch + microbiome
Dimet-Wiley A et al. · Scientific Reports, 2022
MicrobiomeMouse2022
Protocol: 32 mg/kg API SC once daily · Approximately 7 weeks · Subcutaneous
Drug + lower-fat diet reduced weight/fat beyond diet switch alone; distinct microbiome pattern
Small groups; no treated group kept on Western diet; microbiome associations ≠ causation
View study →
Obesity-related metabolic dysfunction
Babula JJ et al. · Diabetes, Obesity and Metabolism, 2024
MetabolismMouse2024
Protocol: 10 or 32 mg/kg/day SC vs vehicle · 28 days · Subcutaneous
Dose-dependent limitation of weight/fat gain; improved metabolic and liver measures
Animal endpoints; no human translation established
View study →
Aged muscle-stem-cell regeneration
Neelakantan H et al. · Biochemical Pharmacology, 2019
MuscleMouse2019
Protocol: 5 or 10 mg/kg/day SC around injury · 2 weeks · Subcutaneous
Increased muscle-stem-cell activation/proliferation and fusion into regenerating fibers
Short mouse injury model; no human recovery or sarcopenia endpoint
View study →
Aged-mouse muscle function + exercise
Dimet-Wiley AL et al. · Scientific Reports, 2024
MuscleMouse2024
Protocol: 10 mg/kg/day SC · 8 weeks · Subcutaneous
Improved grip strength and molecular muscle measures; additive effects with exercise
Aged-mouse model, not a human sarcopenia or recovery trial
View study →
HeLa cell antiproliferative research
Akar S et al. · 2021
CancerCell2021
Protocol: In-vitro concentrations · Cell assays · In vitro
Antiproliferative or pro-apoptotic signals in tumor-cell systems
Does not establish cancer treatment, prevention, or safety in people
View study →

Evidence Quality

Evidence type	Strength	Interpretation
Biochemical target-engagement studies	Moderate preclinical	NNMT inhibition is well supported in experimental assays
Cell studies	Low for clinical inference	Useful for mechanism, unable to predict whole-human effects
Rodent pharmacokinetics	Low to moderate preclinical	Oral exposure in rats is established; human PK remains unknown
Mouse obesity studies	Low for human efficacy	Repeated preclinical signal, but small and species-specific
Mouse muscle studies	Low for human efficacy	Interesting aging/exercise signal without human validation
Human observational NNMT biology	Indirect	NNMT associations do not prove that this inhibitor is beneficial
Human randomized trials	None identified	No established efficacy or safety
Long-term safety	Unknown	No adequate human dataset
FDA approval	No	No approved indication or dosage

Regulatory and Compounding Status

5-Amino-1MQ is not FDA approved. FDA substance-database entries identify chemical substances; an entry is not approval for human use.

In a January 2026 warning letter, FDA stated that drug products compounded by an outsourcing facility using 5-Amino-1MQ were not eligible for section 503B exemptions because the substance did not appear on the 503B bulks list and was not being used to compound a drug on the shortage list. This is important evidence against marketing 5-Amino-1MQ as an ordinary, FDA-sanctioned compounded medication.

“Not FDA approved” is accurate.
“Appears in an FDA substance database” does not mean approved.
A pharmacy label does not create clinical evidence.
“Compounded” does not mean FDA reviewed for safety, effectiveness, or quality.
“Research use only” does not authorize human administration.

Sports status

5-Amino-1MQ is not necessarily named individually on WADA's list, but WADA's S0 Non-Approved Substances category covers pharmacological substances with no current approval by a governmental health authority for human therapeutic use when not addressed elsewhere. Competitive athletes should therefore treat 5-Amino-1MQ as prohibited and obtain guidance from their anti-doping organization rather than relying on a seller or clinic.

Frequently Asked Questions

What is 5-Amino-1MQ?

5-Amino-1MQ is an experimental small molecule that inhibits nicotinamide N-methyltransferase, or NNMT.

Is 5-Amino-1MQ a peptide?

No. It is a methylquinolinium small molecule and contains no peptide amino-acid chain.

What does 5-Amino-1MQ do?

In laboratory models, it inhibits NNMT and changes nicotinamide, NAD+-salvage, SAM/SAH, adipose, and muscle metabolism.

Does 5-Amino-1MQ work for weight loss?

It reduced body weight and fat mass in obese mice, but human weight-loss efficacy has not been established.

What is the human dosage of 5-Amino-1MQ?

There is no established human dosage because no adequate human dose-ranging or safety trial has been published.

Is 50–150 mg per day a clinically studied dosage?

No. The commonly marketed 50–150 mg/day oral schedules are commercial or community protocols, not doses validated in published human trials.

Is 5-Amino-1MQ taken orally?

It is orally bioavailable in rats, poorly orally bioavailable in mice in at least one report, and uncharacterized orally in humans.

Why do clinics sell 5-Amino-1MQ capsules?

Commercial availability reflects marketplace practice, not proof of FDA approval, human bioavailability, safety, or efficacy.

What are the side effects of 5-Amino-1MQ?

Human side effects and their frequencies are unknown because controlled human safety data are absent.

Does 5-Amino-1MQ increase heart rate?

The published preclinical literature does not establish a consistent heart-rate signal, but the effect has not been adequately studied in humans.

Does 5-Amino-1MQ suppress appetite?

Early obese-mouse experiments reported weight and fat loss without lower food intake, so appetite suppression did not appear to explain those results.

Does 5-Amino-1MQ raise NAD+?

It altered NAD+-related metabolism in cells and animals, but no human trial has established a clinically meaningful systemic NAD+ increase.

Does 5-Amino-1MQ preserve muscle?

No human evidence shows muscle preservation during weight loss; aged-mouse studies reported improved muscle function, which is not the same outcome.

Can 5-Amino-1MQ be combined with semaglutide or tirzepatide?

No controlled evidence establishes the safety or benefit of combining 5-Amino-1MQ with a GLP-1-based medication.

How quickly does 5-Amino-1MQ work?

Mouse experiments reported changes over 11 days to several weeks, but there is no established human onset time.

What is the half-life of 5-Amino-1MQ?

A rat study reported an oral elimination half-life around 6.9 hours; a human half-life has not been established.

Is 5-Amino-1MQ FDA approved?

No. It is not FDA approved for weight loss, longevity, muscle function, or any other indication.

Is compounded 5-Amino-1MQ FDA approved?

No. Compounded drugs are not FDA-approved products, and FDA has specifically challenged 503B compounding with 5-Amino-1MQ.

Is 5-Amino-1MQ safe?

Human safety is unknown; small animal efficacy studies cannot establish a safe human dose or long-term risk profile.

Is 5-Amino-1MQ prohibited in sport?

It should be treated as prohibited under WADA's S0 category for non-approved pharmacological substances; athletes should verify status directly with their anti-doping organization.

Is 5-Amino-1MQ an anti-aging drug?

No. Research on NAD+-related metabolism and aged mice does not establish slower aging or longer healthspan in humans.

Does 5-Amino-1MQ treat cancer?

No. Cell and animal oncology findings are preclinical and do not establish cancer treatment in people.

References

Neelakantan H et al.
Selective and membrane-permeable small molecule inhibitors of NNMT reverse high-fat-diet-induced obesity in mice.
Biochemical Pharmacology. 2018.
PMC
Full text of the foundational NNMT-inhibitor study
PMC5826726.
Awosemo O et al.
LC-MS/MS assay and rat pharmacokinetics of 5-amino-1-methylquinolinium.
Journal of Pharmaceutical and Biomedical Analysis. 2021.
Dimet-Wiley A et al.
Reduced calorie diet combined with NNMT inhibition establishes a distinct microbiome in DIO mice.
Scientific Reports. 2022.
Babula JJ et al.
NNMT inhibition mitigates obesity-related metabolic dysfunction.
Diabetes, Obesity and Metabolism. 2024.
Dimet-Wiley AL et al.
NNMT inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice.
Scientific Reports. 2024.
Neelakantan H et al.
NNMT inhibition activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle.
Biochemical Pharmacology. 2019.
Akar S et al.
Small molecule inhibitor of NNMT shows antiproliferative activity in HeLa cells.
2021.
U.S. Food and Drug Administration
Warning letter discussing 5-Amino-1MQ compounding
Genogenix LLC, January 2026.
ClinicalTrials.gov
Search for 5-Amino-1MQ
No completed results-reported efficacy trial identified.
World Anti-Doping Agency
WADA 2026 Prohibited List
S0 Non-Approved Substances category.

Important Safety Information

5-Amino-1MQ is an experimental small-molecule NNMT inhibitor with preclinical metabolic and muscle signals in rodents. It is not a peptide, not FDA approved, and has no established human dosage.

Commercial oral protocols and clinic capsules are marketplace practice, not clinical-trial regimens. Human side effects, bioavailability, and efficacy remain unknown.

This page describes research for educational purposes. It is not individualized medical advice.

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