5-Amino-1MQ
5-Amino-1-methylquinolinium · NNMT inhibitor
Small-molecule NNMT inhibitor, not a peptide. Mouse/adipocyte papers (PMID 31028097). Not a stimulant fat-burner and not a human obesity drug. Oral; empty vial list - do not run it through reconstitution.
Use-case scores
0–10 against the evidence we have, not a gym ranking. Hidden domains do not apply here.
- Metabolic / weight2.5/10
Neelakantan 2019 (PMID 31028097) is mouse/adipocyte NNMT work. Oral research chemical. Not a fat-loss drug. Mechanism band.
Compound card
- Class
- Small-molecule NNMT inhibitor (not a peptide)
- Formula
- C10H11N2+ (as salt form)
- Status
- Not FDA-approved · research use
How it works
5-Amino-1MQ (5-Amino-1-methylquinolinium) is a cell-permeable small molecule that selectively inhibits nicotinamide N-methyltransferase (NNMT), an enzyme that methylates nicotinamide - diverting SAM (S-adenosylmethionine) and depleting cellular NAD+ precursor pools.
NNMT is overexpressed in obesity, type 2 diabetes, and aged adipose tissue. By inhibiting NNMT, 5-Amino-1MQ raises NAD+ levels, activates SIRT1 (the longevity sirtuin), and promotes a lean metabolic phenotype. In preclinical studies, it prevented diet-induced obesity without reducing food intake, and preserved muscle mass. It represents a distinct mechanism from NMN/NR supplementation - instead of directly adding NAD+ precursors, it stops NAD+ from being wasted.
Source: PMID: 31028097
Background & History
5-Amino-1MQ (5-Amino-1-methylquinolinium) is a small-molecule cell-permeable inhibitor of nicotinamide N-methyltransferase (NNMT) developed by researchers at Vanderbilt University. NNMT is an enzyme expressed primarily in fat tissue that consumes S-adenosylmethionine (SAM) to methylate nicotinamide - effectively diverting NAD+ precursors away from energy metabolism. First published in Nature Communications (2018), 5-Amino-1MQ demonstrated that NNMT inhibition in obese mice prevented weight gain without caloric restriction. It has since exploded in biohacking communities as a novel oral compound for metabolic optimization and fat loss.
Research Use Cases
- ✓Identity: oral NNMT inhibitor, not a peptide
- ✓Mouse papers vs a human obesity NDA (there is not one)
- ✓Empty vial list: skip the reconstitution calculator
Dosing
| Phase | Dose | Frequency | Notes |
|---|---|---|---|
| Research Protocol (Oral) | 50 - 150 mg | 1-2x daily oral | Based on preclinical scaling. No established human clinical dosing. Often cycled for NNMT inhibition. |
Administration
Timeline
Who it is for
NAD+ Optimization
LowNovel NNMT inhibition mechanism raises NAD+ by stopping its depletion. Complementary to NMN/NR supplementation.
Obesity / Metabolic Health
LowPreclinical data shows prevention of diet-induced obesity. No human RCTs yet.
Safety & Considerations
Research compound. Limited human safety data. Preclinical studies show favorable safety profile. Avoid in pregnancy. Monitor liver enzymes with extended use. Not combined with MAOIs.
Regulatory & Legal Status
Not currently on the WADA 2026 Prohibited List. Policies may change - verify before competition.
Research Chemical
US Compounding: Not eligible / not available
⚠️ This information is for educational purposes only and may not reflect the most current regulatory updates. Always verify with official FDA, WADA, and jurisdiction-specific sources before use.
Limits of current evidence
- Empty vial sizes: this is oral. Do not run it through the reconstitution calculator.
- This site will not treat obesity from a 5-Amino-1MQ page.
Verdict
5-Amino-1MQ is a quinolinium small molecule, not a peptide. We list it because the library search box gets it. Mouse NNMT papers are not a BMR-doubling supplement.
Interactions & Contraindications
Very limited human safety data - primarily mouse studies. NNMT inhibition affects SAM methylation metabolism; theoretically could affect methylation of other substrates (neurotransmitters, DNA). Avoid with MAOI medications. Monitor liver enzymes during use. Not approved for human use. Oral compound - no reconstitution required.
Synergies & Common Stacks
5-Amino-1MQ preserves NAD+ precursors by blocking their methylation; NAD+ IV directly replenishes the pool. Together they maximize cellular NAD+ availability from both supply and demand sides.
MOTS-c activates AMPK mitochondrial signaling; 5-Amino-1MQ raises NAD+ which also activates SIRT1/AMPK. Complementary metabolic enhancement from different entry points.
GLP-1 agonist suppresses appetite/caloric intake; 5-Amino-1MQ may enhance lipolysis and metabolic rate via NNMT inhibition. Complementary mechanisms for body composition.
Appears in goal guides
Goal guides are maps, not clinic protocols. A mention here is not a treatment plan.
Frequently Asked Questions
How does 5-Amino-1MQ differ from NMN for NAD+ optimization?▼
References
- Kannt A et al. “"NNMT inhibition rescues age-associated muscle atrophy".” Nature Communications (2018). PMID: 30552329
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