Summary
5-Amino-1MQ is a small molecule that blocks nicotinamide N-methyltransferase (NNMT), an enzyme that is overexpressed in the fat tissue of obese animals. In diet-induced obese mice, it reduced fat mass and body weight without changing food intake.
How it works
NNMT consumes the methyl donor SAM and nicotinamide. Inhibiting it is thought to raise cellular NAD+ and SAM levels in fat cells and shift metabolism toward energy use.
Research use cases
Areas where 5-Amino-1MQ has been studied. Inclusion here does not mean it works for that purpose.
- Adipocyte metabolism
- Diet-induced obesity models
- Muscle stem cell function in aged mice
What the research found
Diet-induced obesity
Obese mice treated for 11 days lost weight and white fat mass, and adipocytes shrank, with no change in food intake.1
Aged muscle
In aged mice, NNMT inhibition improved muscle stem cell activity and regeneration after injury.2
Safety and open questions
No human safety data have been published.
Regulatory status
Not approved. No published human trials. Sold for research use.
Status was accurate when this page was last reviewed on October 26, 2026. Regulations change; check with the relevant authority before relying on it.
5-Amino-1MQ: common questions
Is 5-Amino-1MQ a peptide?
No. It is a small quinolinium molecule. It is included because it is commonly discussed alongside metabolic peptides.
Is 5-Amino-1MQ approved for human use?
Not approved. No published human trials. Sold for research use.
References
- Neelakantan H, Vance V, Wetzel MD, et al. (2018). Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochemical Pharmacology.
- Neelakantan H, Brightwell CR, Graber TG, et al. (2019). Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. Biochemical Pharmacology.
Links open a PubMed search for the exact title, or the original source where one is given.