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The Peptide Effect
preclinicalFat Loss & Metabolism

5-Amino-1MQ

Also known as: 5-Amino-1-Methylquinolinium, 5-Amino-1-MethylQuinolinium chloride, NNMT inhibitor

5-Amino-1MQ is a small molecule inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme increasingly linked to obesity, metabolic dysfunction, and cellular aging. Although not technically a peptide, it is widely sold alongside peptides in the research compound marketplace due to overlapping customer interest in metabolic optimization. Its mechanism of action — boosting NAD+ in adipose tissue and promoting white-to-beige fat conversion — represents a novel approach to fat loss that is distinct from stimulant-based or hormonal interventions.

Key Facts

Mechanism
5-Amino-1MQ inhibits NNMT, a cytosolic enzyme that methylates nicotinamide (a form of vitamin B3) using S-adenosylmethionine (SAM) as a methyl donor. NNMT is highly expressed in white adipose tissue and liver, and its overactivity depletes both NAD+ and SAM — two critical metabolic cofactors. By blocking NNMT, 5-Amino-1MQ restores intracellular NAD+ pools in fat cells, reactivates SAM-dependent metabolic pathways, and promotes the thermogenic "browning" of white adipocytes. This browning process converts energy-storing white fat cells into energy-burning beige fat cells that express uncoupling protein 1 (UCP1). In animal models, NNMT inhibition also reduced adipocyte size and inhibited adipogenesis (new fat cell formation) without affecting food intake.
Research Status
preclinical
Half-Life
Not well established in humans
Molecular Formula
C₁₀H₁₁N₂⁺
Primary Use
Fat Loss & Metabolism
Table of Contents

Benefits

  • Promotes fat cell shrinkage (reduced adipocyte size) and inhibits new fat cell formation (adipogenesis) in preclinical modelspreliminary
  • Increases intracellular NAD+ levels in adipose tissue by preventing NNMT-mediated nicotinamide degradationmoderate
  • Drives white-to-beige fat cell conversion (browning), increasing thermogenic energy expenditurepreliminary
  • May improve overall metabolic rate and insulin sensitivity through restored NAD+ and SAM pathwayspreliminary
  • Potential treatment for diet-resistant obesity — works independently of appetite suppression or caloric restrictionpreliminary

Dosage Protocols

RouteDosage RangeFrequencyNotes
Oral capsule50–100 mg1–2× dailyMost common protocol in the research community. Taken with or without food. Some users titrate up from 50 mg once daily.
Oral capsule (higher dose)100–150 mg1× dailyHigher-end dosing used by some; limited data to support doses above 100 mg providing additional benefit. Not clinically validated.
Subcutaneous injection (research)Variable (mg/kg dosing from animal studies)DailyInjectable form used in preclinical research settings. Oral bioavailability appears reasonable for this small molecule, making injection unnecessary for most users.

Medical disclaimer

Dosage information is provided for educational reference only. Always follow your prescriber's instructions and consult a qualified healthcare provider before starting any peptide protocol.

Side Effects

  • Gastrointestinal discomfort — nausea, bloating, or mild stomach upset reported by some userscommon
  • Headache — occasionally reported, typically during initial dosing periodcommon
  • Fatigue or mild lethargy during first few days of userare
  • Potential disruption of methylation pathways — NNMT inhibition alters SAM/SAH ratios, which could theoretically affect DNA methylation, neurotransmitter synthesis, and other methylation-dependent processesserious
  • Unknown long-term safety profile — no published human clinical trials exist as of 2026serious

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Frequently Asked Questions

Why is 5-Amino-1MQ sold alongside peptides if it is not a peptide?
5-Amino-1MQ is a small molecule (quinolinium salt), not a peptide. It is sold by peptide vendors because it targets the same customer base — people interested in metabolic optimization, body composition, and cutting-edge research compounds. Many peptide suppliers have expanded their catalogs to include non-peptide research chemicals like 5-Amino-1MQ, NAD+ precursors, and SARMs. The compound is popular in peptide communities specifically because it complements fat-loss peptide stacks.
How does 5-Amino-1MQ cause fat loss without affecting appetite?
Unlike GLP-1 agonists (semaglutide, tirzepatide) that reduce appetite, 5-Amino-1MQ works directly at the fat cell level. By inhibiting NNMT, it restores NAD+ in adipocytes, which reactivates metabolic pathways that promote fat burning and "browning" of white fat. In animal studies, treated mice lost significant fat mass without any reduction in food intake. The fat cells themselves become smaller and shift from energy storage to energy expenditure through increased expression of UCP1 (uncoupling protein 1).
What is NNMT and why does inhibiting it matter?
Nicotinamide N-methyltransferase (NNMT) is an enzyme that methylates nicotinamide using SAM as a methyl donor. This reaction simultaneously depletes two critical metabolic cofactors: NAD+ (essential for cellular energy metabolism) and SAM (the universal methyl donor). NNMT is overexpressed in obese individuals and in white adipose tissue. By inhibiting NNMT, you preserve NAD+ and SAM pools, reactivating metabolic pathways that promote fat oxidation, thermogenesis, and healthy cellular function. Think of NNMT as a metabolic "brake" — inhibiting it releases that brake.
Is there any human clinical trial data for 5-Amino-1MQ?
As of February 2026, there are no published peer-reviewed human clinical trials for 5-Amino-1MQ. All efficacy data comes from in vitro studies and animal models (primarily mice). The compound has shown promising results in preclinical work, but the lack of human safety and efficacy data is a significant limitation. Anyone considering this compound should understand they are essentially self-experimenting with a research chemical that has not been through the standard drug development process.
Can 5-Amino-1MQ be stacked with other fat loss peptides?
Many users in the research community combine 5-Amino-1MQ with other fat-loss compounds such as AOD-9604, MOTS-c, or even GLP-1 agonists. The rationale is that 5-Amino-1MQ works through a unique mechanism (NNMT inhibition at the adipocyte level) that is complementary to appetite suppression (GLP-1s) or GH-fragment-based fat metabolism (AOD-9604). However, there is zero clinical data on these combinations, and stacking multiple research compounds compounds the unknown risk profile. This is not medical advice.

References

  1. 1
    NNMT inhibition effectively activates NAD+ salvage pathway in adipocytes and prevents diet-induced obesity(2020)PubMed ↗
  2. 2
    Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity(2014)PubMed ↗
  3. 3
    Small molecule NNMT inhibitors for the treatment of obesity and metabolic syndrome(2021)PubMed ↗
  4. 4
    Nicotinamide N-methyltransferase: an emerging protagonist in cancer and metabolic disease(2017)PubMed ↗

Last updated: 2026-02-14