5-Amino-1MQ
Research OnlyAlso known as: 5-Amino-1-Methylquinolinium, NNMT Inhibitor
A small molecule NNMT inhibitor studied for metabolic effects in animal models. No human clinical trials have been conducted. Increases NAD+ levels in adipose tissue in preclinical studies.
Research Statistics
Preclinical NAD+ metabolic data is promising but only 1 human study available.
Research Dossier
Overview
What is 5-Amino-1MQ and what does the research say?
Mechanism of Action
The proposed mechanisms of 5-Amino-1MQ are based entirely on animal and in vitro studies. No human mechanistic data exists.
How It Works (Simplified)
5-Amino-1MQ acts by blocking NNMT, an enzyme that depletes important cellular resources:
Blocks NNMT enzyme activity, preventing it from consuming NAD+ precursors and SAM (the universal methyl donor).
Preserves nicotinamide for NAD+ synthesis, increasing cellular NAD+ levels especially in adipose tissue.
Higher NAD+ activates sirtuins (SIRT1-7), master regulators of metabolism, mitochondrial function, and energy expenditure.
In mice, leads to increased energy expenditure, adipose browning, and weight loss without reduced food intake.
Scientific Pathways
NNMT Inhibition Pathway (Target Engagement)
5-Amino-1MQ → Binds NNMT active site → Blocks nicotinamide methylation
↓
Nicotinamide preserved for NAD+ synthesisNAD+ / Sirtuin Pathway (Metabolic Effects)
NNMT blocked → NAD+ levels increase → Sirtuin activation → Enhanced metabolism
↓
SAM preserved → Improved methylation capacityThermogenic Pathway (Energy Expenditure)
Sirtuin activation → PGC-1a upregulation → UCP1 expression → Adipose browning
↓
Increased energy expenditureKey Research: Neelakantan H et al. (UTMB, 2018) demonstrated 7% weight reduction in diet-induced obese mice with 11 days of treatment. PMID:29155253
Important Limitations
- Zero human trials - All efficacy data is from mice only
- Translation to human adipose tissue metabolism is unconfirmed
- Human pharmacokinetics (absorption, half-life, dosing) completely unknown
- NNMT expressed in multiple tissues (liver, brain, muscle) - systemic effects uncharacterized
- Potential cardiovascular concerns from vascular NNMT inhibition (NNMT may protect endothelium)
- No long-term safety data in any species
Evidence-Chained Benefits
Evidence-Chained Benefits
Research findings linked to mechanisms and clinical outcomes
What to Expect
Timeline based on observations from published studies. Individual responses may vary.
Based on preclinical data: NNMT inhibition should begin immediately upon administration. Mouse studies used 11-day treatment periods. No human pharmacokinetic data available to predict onset.
In mouse studies, measurable weight reduction (~7%) observed by end of 11-day treatment. NAD+ elevation in adipose tissue documented. Human timeline completely unknown.
No long-term preclinical studies available. Sustained effects, tolerance development, and long-term metabolic adaptations are uncharacterized.
Completely unknown. Long-term safety and efficacy data do not exist in any species. Chronic NNMT inhibition effects unstudied.
Research-Based Observations
This timeline reflects observations from published clinical and preclinical studies. Individual responses may vary significantly. This is not a guarantee of effects or a dosing schedule. Consult qualified healthcare providers for personalized guidance.
Quality Checklist
Visual indicators to help evaluate 5-Amino-1MQ product quality
Good Signs (6 indicators)
Warning Signs (5 indicators)
Bad Signs (6 indicators)
For Research Evaluation Only
These quality indicators are general guidelines based on typical peptide characteristics. Professional laboratory testing (HPLC, mass spectrometry) provides definitive quality verification. This checklist is for initial visual evaluation only.
Peptide Interactions
Known and theoretical interactions when combining 5-Amino-1MQ with other peptides. Based on published research and mechanistic considerations.
Nmn
SynergisticTheoretical synergy: NMN provides NAD+ precursor while 5-Amino-1MQ preserves NAD+ by blocking NNMT consumption. Both aim to elevate NAD+ through complementary mechanisms. No combined studies available.
Nicotinamide-Riboside
SynergisticSimilar theoretical synergy as NMN. NR provides substrate for NAD+ synthesis while 5-Amino-1MQ reduces NAD+ depletion. Combined effects unstudied.
AOD-9604
CompatibleDifferent mechanisms of action (5-Amino-1MQ targets NNMT/NAD+ pathway vs AOD-9604's lipolytic effects). No interaction studies available; both target metabolic pathways through distinct routes.
Resveratrol
CompatibleBoth activate sirtuin pathways - resveratrol directly, 5-Amino-1MQ indirectly via NAD+ elevation. Theoretically complementary but unstudied.
Semaglutide
CautionBoth target metabolic and weight management pathways. Semaglutide is a GLP-1 agonist affecting appetite/insulin while 5-Amino-1MQ targets cellular NAD+ metabolism. No interaction data exists.
Research Note: Interaction data is based on published literature, mechanistic understanding, and theoretical considerations. Most peptide combinations lack direct clinical study. This information is for educational purposes only and does not constitute medical advice. Always consult qualified healthcare providers.
References
Key Studies Cited
Full reference list available on request. All citations link to PubMed for verification.
Methodology Note
This dossier synthesizes available evidence from peer-reviewed literature, regulatory documents, and clinical trial registries. Evidence strength ratings follow a modified GRADE approach.
For complete methodology details, see our Methodology page.
Important Disclaimer
This dossier is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before making health decisions.
Get Research Alerts
New dossiers and major study summaries delivered to your inbox. Evidence-graded, citation-backed research you can trust.
No spam. Unsubscribe anytime.
Compare 5-Amino-1MQ
5-Amino-1MQ Calculators
Related Peptides
Amycretin
NNC0487-0111, Oral Amycretin, Subcutaneous Amycretin
A novel single-molecule dual GLP-1/amylin receptor agonist developed by Novo Nordisk. Unlike CagriSema (a fixed-dose combination), amycretin is a unified peptide that activates both pathways. Phase 1 trials showed superior weight loss signals versus semaglutide, with both oral and subcutaneous formulations in development.
Cagrilintide
AM833, NN9838, ZP8396
A long-acting amylin analog developed by Novo Nordisk for weight management. Currently in Phase 3 trials as CagriSema (combination with semaglutide). Phase 2 data shows up to 22-25% weight loss when combined with semaglutide, potentially exceeding tirzepatide efficacy.
CagriSema
Cagrilintide-Semaglutide, NNC0174-0833
A fixed-dose combination of cagrilintide (amylin analog) and semaglutide (GLP-1 agonist) for chronic weight management. Phase 3 REDEFINE trials demonstrate 20-23% weight loss at 68 weeks. NDA submitted to FDA December 2025. First GLP-1/amylin combination therapy.
CT-388
RG-6912
A dual GLP-1/GIP receptor agonist acquired by Roche through the $2.7 billion Carmot Therapeutics acquisition in 2024. Phase 1b results showed 18.8% placebo-adjusted weight loss at 24 weeks, positioning it as a competitive obesity therapeutic with a mechanism similar to tirzepatide.
Liraglutide
Victoza, Saxenda, NN2211
The first long-acting GLP-1 receptor agonist, FDA-approved for type 2 diabetes (Victoza, 2010) and chronic weight management (Saxenda, 2014). Pioneered the therapeutic class with proven cardiovascular benefits in the landmark LEADER trial.
MariTide
AMG 133, maridebart cafraglutide
A bispecific peptide-antibody conjugate combining GLP-1 receptor agonism with GIP receptor antagonism. Unique mechanism opposite to tirzepatide. Phase 2 showed ~20% weight loss at 52 weeks with once-monthly dosing. MARITIME Phase 3 program initiated.