5-Amino-1MQ
An orally active small-molecule NNMT inhibitor with reproducible fat-loss and muscle data in mice but zero published human trials.
5-Amino-1MQ is a small-molecule selective inhibitor of nicotinamide N-methyltransferase (NNMT), the enzyme that methylates and inactivates nicotinamide using S-adenosylmethionine (SAM) as the methyl donor. By blocking NNMT, it is proposed to preserve cellular NAD+ precursor and SAM pools and shift adipocyte metabolism toward a thermogenic, fat-reducing phenotype. Despite being sold alongside peptides, it is not a peptide but a methylated quinolinium derivative, and all supporting evidence comes from preclinical rodent obesity and muscle studies — no human pharmacokinetic, safety, or efficacy data has been published.
Class
Small-molecule quinolinium NNMT inhibitor (not a peptide)
Half-life
Not characterized in humans; approximately 6–12 hours (oral) is cited by some vendor sources but is not from peer-reviewed human data
Routes
Oral, Subcutaneous/injectable (research protocols)
Category
Weight Loss & Metabolic
Researched benefits
What it's studied for
Fat mass reduction
In diet-induced obese mice, 5-Amino-1MQ and related NNMT inhibitors reduced body weight and fat mass and decreased adipocyte size. The foundational Neelakantan 2018 study reported roughly 7% body weight reduction over 11 days on a high-fat diet, apparently by increasing adipocyte energy expenditure rather than suppressing appetite.
Increased metabolic rate / thermogenesis
NNMT inhibition is reported to shift white adipocyte metabolism toward a thermogenic phenotype and raise energy expenditure in rodent models, the proposed basis for its anti-obesity effect.
NAD+ pool preservation
By reducing NNMT-mediated methylation of nicotinamide, the compound preserves nicotinamide for the NAD+ salvage pathway, increasing NAD+ availability in target tissues in animal-model research.
Improved insulin sensitivity
Preclinical studies in obese mice using 5-Amino-1MQ and related inhibitors reported improved glucose tolerance, better insulin sensitivity, and lower hepatic triglyceride content.
Muscle function in aging (preclinical)
A widely circulated 2021 aged-mouse study reported that 5-Amino-1MQ increased muscle stem cell activity, accelerated muscle regeneration after injury, and improved grip strength and muscle mass, generating interest in it as a dual metabolism-and-sarcopenia compound. Human translation is untested.
Mechanism
How it works
5-Amino-1MQ is a selective small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme that transfers a methyl group from S-adenosyl-L-methionine (SAM) to nicotinamide (vitamin B3 amide), producing 1-methylnicotinamide (1-MNA) and S-adenosyl-L-homocysteine (SAH). NNMT is overexpressed in adipose tissue, liver, and certain cancers, where its activity diverts nicotinamide away from NAD+ synthesis and consumes SAM, altering the cellular methyl-donor balance that governs epigenetic marks and lipid metabolism.
By inhibiting NNMT, 5-Amino-1MQ is proposed to preserve intracellular nicotinamide and NAD+ precursor pools and to raise SAM availability, shifting the methylation balance in adipocytes toward suppression of adipogenesis and promotion of thermogenic gene expression. Structural work characterized it as a bisubstrate-competitive inhibitor that occupies both the nicotinamide-binding pocket and part of the SAM-binding site, which is thought to confer selectivity over other methyltransferases.
The rationale traces to 2014 genetic work (Kraus et al., Nature) showing that adipocyte-specific NNMT knockdown in mice produced lean body composition on a high-fat diet, improved glucose tolerance, and increased energy expenditure — establishing NNMT as a metabolic target. 5-Amino-1MQ provides a pharmacologic tool to test whether inhibiting NNMT reproduces the benefits of that genetic knockdown, and preclinical studies in diet-induced obese mice reported reduced adiposity and improved metabolic parameters.
Important caveats attach to this model. The published evidence is entirely preclinical, and counter-evidence exists: Brachs et al. (Diabetes 2019) reported that global NNMT-knockout mice show only a mild metabolic phenotype, partially contradicting the strong-effect interpretation. Because NNMT sits within broader methyl-donor and NAD+ metabolism, chronic inhibition raises unresolved questions about methylation homeostasis (homocysteine, SAM:SAH ratio, DNA methylation) that have not been measured under chronic dosing in any published in vivo study.
Dosing protocols
Dosing & administration
Dosing reflects protocols reported in research and community literature for educational purposes. It is not medical advice or a recommendation. Most peptides here are not approved for human use.
Reconstitution
Sold as oral capsules (commonly 50 mg and 100 mg) or as lyophilized vials (5–50 mg) for research reconstitution. There is no standardized human reconstitution or dosing protocol; injectable research protocols use bacteriostatic water but no validated concentration exists.
Common self-report range
- Dose
- 100–150 mg daily
- Frequency
- Once daily
- Timing
- Typically morning with food
- Duration
- Cycled; users often run multi-week cycles
- Route
- Oral
Most frequently cited community range. Extrapolated from rodent efficacy via allometric scaling; not validated in any human trial.
Broad self-report range
- Dose
- 50–300 mg daily
- Frequency
- Once daily
- Timing
- With food
- Duration
- Variable
- Route
- Oral
Full span of doses described in self-report communities. Vendor label doses are estimates, not clinically established figures.
Vendor-stated range
- Dose
- 50–150 mg daily
- Frequency
- Once daily
- Timing
- Morning
- Duration
- Variable
- Route
- Oral or injection
Range listed on some vendor pages; no human dose-finding work supports it.
- No human clinical trial has established a dosing protocol for 5-Amino-1MQ; every dose in circulation is extrapolated from rodent studies and carries a false sense of precision.
- Oral administration is the standard route in published animal research; injectable routes appear only in informal research protocols.
- Because chronic NNMT inhibition alters methyl-donor metabolism, some users supplement methyl donors (e.g. trimethylglycine 500–1000 mg, methylfolate 400–800 mcg, methylcobalamin 500–1000 mcg) as a precaution on extended cycles, though no clinical evidence shows this changes outcomes.
- Suggested monitoring before and after each cycle includes comprehensive metabolic panel, CBC, liver function tests, fasting glucose/HbA1c, lipid panel, homocysteine, and B12/folate; any unexplained abnormality warrants stopping and evaluation.
Evidence
Research & clinical studies (7)
NNMT inhibitor in diet-induced obese mice: effects on body weight, body fat, and energy expenditure
NNMT inhibition with a small-molecule inhibitor related to 5-Amino-1MQ significantly reduced body weight and fat mass and increased energy expenditure, identifying NNMT as a potential metabolic target for obesity.
PMID 35013352Small molecule inhibitors of nicotinamide N-methyltransferase (foundational efficacy paper)
Neelakantan et al. reported approximately 7% body weight reduction in high-fat-diet obese mice over 11 days, the foundational efficacy demonstration for 5-Amino-1MQ.
Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity
Kraus et al. showed adipocyte-specific NNMT knockdown produced lean body composition on a high-fat diet, improved glucose tolerance, and increased energy expenditure, validating NNMT as a metabolic target.
Pharmacological inhibition of NNMT with an independent quinolinium scaffold (JBSNF-000088)
Kannt et al. independently confirmed that NNMT inhibition reduced adiposity, improved insulin sensitivity, and lowered hepatic triglyceride content in obese mice using a distinct chemical scaffold.
1-methylnicotinamide, NNMT and SIRT1-mediated metabolic regulation
Hong et al. described the mechanism linking NNMT activity, 1-methylnicotinamide, and SIRT1 signaling in metabolic regulation.
Structural characterization of 5-amino-1MQ as a bisubstrate-competitive NNMT inhibitor
Neelakantan et al. characterized 5-Amino-1MQ as a bisubstrate-competitive inhibitor occupying both the nicotinamide and part of the SAM binding site, conferring selectivity over other methyltransferases.
Global NNMT-knockout metabolic phenotype (counter-evidence)
Brachs et al. reported that global NNMT-knockout mice show only a mild metabolic phenotype, partially contradicting the strong-effect interpretation of earlier target-validation work.
Combinations
Stacking & blends
5-Amino-1MQ + NAD+ precursors
Maximize NAD+ elevation
Mechanistically complementary: 5-Amino-1MQ preserves nicotinamide by reducing NNMT-mediated methylation while NMN or NR supplies additional NAD+ substrate. Theoretical synergy only — no clinical data validate the combination or show it beats either agent alone.
5-Amino-1MQ + L-Carnitine
Support fatty-acid oxidation and energy metabolism
Listed as a synergistic pairing on vendor interaction matrices, combining NNMT inhibition with carnitine's cofactor role in fatty-acid transport; unvalidated in controlled studies.
5-Amino-1MQ + methyl-donor support
Buffer methylation homeostasis on extended cycles
Because chronic NNMT inhibition shifts methyl-donor balance, co-supplementing methyl donors is a mechanism-based precaution; no evidence it changes efficacy or safety outcomes.
5-Amino-1MQ + GLP-1 agonist (discussed, not recommended)
Additive fat loss (promotional claim)
Promoted in some commercial contexts but unsupported by any published combination study in mice or humans; layering an unvalidated research chemical onto a validated GLP-1 therapy adds uncharacterized interaction risk without documented benefit.
Safety
Side effects & considerations
Commonly reported effects
Contraindications & cautions
- Pregnancy and breastfeeding (absolute) — no reproductive/developmental toxicology; methyl-donor balance is critical in embryogenesis
- Trying to conceive — reproductive effects unknown
- Children and adolescents — developmental metabolism, growth, and neurological maturation depend on methylation/NAD+ pathways
- Active malignancy or cancer under surveillance (relative) — NNMT is overexpressed in many cancers; interactions with oncology treatment are uncharacterized
- Inborn errors of methylation (homocystinuria, MTHFR deficiency) (absolute) — pre-existing methyl-donor pathology could be worsened
- Uncorrected folate or B12 deficiency (relative)
- Active cardiovascular disease (relative) — reduced 1-MNA production could theoretically alter vascular signaling
- Hepatic or renal impairment (relative) — liver is a major NNMT tissue; 1-MNA is renally excreted and elimination is uncharacterized
- Concurrent medications with narrow therapeutic windows metabolized via methylation-sensitive pathways (MAOIs, TCAs, clozapine, valproate, warfarin, insulin/sulfonylureas)
Human safety data is entirely absent. The significant unknowns are long-term effects on methylation homeostasis, cancer-surveillance implications of altered methyl-donor metabolism, cardiovascular effects from reduced 1-MNA, and drug interactions through methylation-sensitive pathways. These are theoretical, unresolved concerns rather than documented risks. The most important safeguard is clinical oversight: a physician who knows about the use and can order and interpret follow-up labs.
FAQ
5-Amino-1MQ — common questions
Is 5-Amino-1MQ a peptide?
No. It is a small-molecule quinolinium compound, not a peptide. It is grouped with peptides in research-chemical catalogs because of overlapping buyer interest in metabolic compounds, but it is structurally and pharmacologically distinct.
What does 5-Amino-1MQ do?
It inhibits the enzyme NNMT, preserving NAD+ precursor and SAM pools. In high-fat-diet obese mice this reduced fat mass, decreased adipocyte size, shifted adipocytes toward a thermogenic phenotype, and improved insulin sensitivity — with about 7% body weight reduction over 11 days in the foundational study.
Has 5-Amino-1MQ been tested in humans?
No. As of 2026 there are no published Phase 1 or later trials, no publicly disclosed IND applications, and no registered trials on ClinicalTrials.gov. All human use is self-experimentation with research-chemical supply at unvalidated doses.
How much do people use?
Self-report communities describe 50–300 mg daily, with roughly 100–150 mg as a common range, taken once daily by mouth. These figures are extrapolated from rodent studies via allometric scaling and have not been validated in humans.
Does it produce weight loss in humans?
Unknown. The mouse metabolic data is reproducible and promising, but human translation is unestablished. Anyone seeking evidence-based weight loss should look to FDA-approved GLP-1 options like semaglutide or tirzepatide, which have Phase 3 human data.
How should I stack it with NAD+ precursors like NMN or NR?
The combination is mechanistically complementary — 5-Amino-1MQ preserves nicotinamide while NMN/NR add NAD+ substrate — so there is theoretical synergy for NAD+ elevation. No clinical data validate the combination or show it outperforms either intervention alone.
Is 5-Amino-1MQ FDA approved or legal?
It has no FDA approval for any indication. It is generally legal to purchase as a research chemical for laboratory use in most jurisdictions but is not approved for human consumption.
What are the main safety concerns?
Short-term rodent and self-report tolerability appear reasonable, but the significant unknowns are long-term effects on methylation homeostasis, cancer-surveillance implications, cardiovascular effects from reduced 1-MNA, and methylation-pathway drug interactions. None are documented risks; they remain open because no long-term human data exist.
