5-Amino-1MQ
A selective small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT) studied for metabolic enhancement, adipose remodelling, and NAD+ preservation in obesity and ageing research models.
⏱ Half-Life
Short duration profile
5-Amino-1MQ demonstrates a short half-life characteristic in research literature, shaping how observation windows and study timelines are typically structured.
⚡ Onset Characteristics
Gradual measurable response
Onset is observed as gradual — a property that influences how researchers structure comparative studies versus other compounds in the metabolic research category.
🧠 Key Notes
What makes it distinct
- 01Selectively inhibits NNMT, reducing nicotinamide methylation
- 02Preserves NAD+ precursor pools by blocking the NNMT consumption pathway
- 03Studied for fat-mass reduction independent of appetite suppression
🧬 Mechanism of Action
How it works
5-Amino-1MQ (5-amino-1-methylquinolinium) is a selective, membrane-permeable small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), a cytosolic enzyme that methylates nicotinamide using S-adenosylmethionine (SAM) to produce N-methylnicotinamide. In obesity and ageing, NNMT is upregulated in adipose tissue, accelerating nicotinamide turnover and depleting the NAD+ salvage pathway. By inhibiting NNMT, 5-Amino-1MQ preserves intracellular nicotinamide and NAD+ levels, reduces SAM depletion, and shifts adipocyte metabolism toward lipolysis and oxidative phosphorylation. This produces fat-mass reduction and improved insulin sensitivity in research models without direct appetite suppression or hormonal manipulation.
✨ Documented Benefits
What the research shows it supports
🔍 Research Insights
What the literature shows
Inhibits NNMT selectively without affecting other methyltransferases, preserving SAM pools for other cellular methylation reactions.
Fat-loss effects are mechanistically distinct from GLP-1/GIP agonists — it remodels adipose metabolism rather than reducing energy intake.
Combined with low-fat diet, normalised adiposity and weight to age-matched lean controls faster than diet switch alone.
🧪 Typical Research Use Cases
Where it appears in study design
NNMT-pathway and NAD+ metabolism research.
Adipose-tissue remodelling and lipolysis studies.
Comparative metabolic work vs GLP-1 agonists and GH fragments.
📚 References
Peer-reviewed literature
Primary research sources cited on this profile. All links resolve to PubMed or the publishing journal.
- [01]
Neelakantan, H. et al. (2017). Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochemical Pharmacology, 147, 67–76.
Biochemical Pharmacology ↗ - [02]
Pirani, A. et al. (2022). Reduced calorie diet combined with NNMT inhibition establishes a distinct microbiome in DIO mice. Scientific Reports, 12, 267.
Scientific Reports ↗ - [03]
Babula, J. et al. (2024). Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction. Diabetes, Obesity and Metabolism, 26(3), 1189–1201.
Diabetes, Obesity and Metabolism ↗ - [04]
Kraus, D. et al. (2014). Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature, 508(7495), 258–262.
Nature ↗
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