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Animal / Lab

5-Amino-1MQ

A small-molecule NNMT inhibitor studied in obese mice for reducing fat mass and raising cellular NAD+ and SAM levels.

In plain English

5-Amino-1MQ (5-amino-1-methylquinolinium) is a small research molecule — not a true peptide — that blocks an enzyme called NNMT (nicotinamide N-methyltransferase). NNMT is highly active in fat tissue, where it burns through the cell's supply of NAD+ precursors and methyl groups. The idea is that by inhibiting NNMT, fat cells keep more NAD+ and energy-related cofactors, shift toward burning fuel rather than storing it, and shrink. In mice on a high-fat diet, NNMT inhibitors and NNMT knockdown reduced fat gain without changing how much the animals ate. That has made 5-Amino-1MQ popular in online fat-loss and longevity communities — but there are no published human trials, and it is not approved by the FDA for any use. Everything known about it comes from cell and rodent studies.

What it is

5-Amino-1MQ is a membrane-permeable small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT). Despite being grouped with research peptides by suppliers, it is a quinolinium-based compound, not an amino-acid chain. It is a research chemical, not a registered drug.

Mechanism (summary)

NNMT methylates nicotinamide using the methyl donor S-adenosylmethionine (SAM), consuming both nicotinamide (an NAD+ precursor) and SAM. In adipose tissue, high NNMT activity is associated with reduced NAD+ and a more fat-storing metabolic state. By inhibiting NNMT, 5-Amino-1MQ is hypothesized to preserve cellular NAD+ and SAM, increase energy expenditure in fat cells, and reduce adiposity. The human pharmacology is uncharacterized.

Why people research it

  • Reducing fat mass and diet-induced obesity in animal models
  • Raising intracellular NAD+ via NNMT inhibition
  • Metabolic health and insulin-related signaling
  • Preserving muscle and lean mass during fat loss

Human evidence

There are no published randomized controlled trials of 5-Amino-1MQ in humans. Interest is driven entirely by preclinical NNMT research and anecdotal supplement use; human pharmacokinetics, efficacy, and safety are unknown.

Animal / lab evidence

Genetic knockdown of NNMT and small-molecule NNMT inhibitors reduced fat-pad weight and protected against high-fat-diet-induced obesity in mice, with associated increases in cellular energy cofactors and no reduction in food intake.

Key studies

Each summary explains the design, what was found, and what it doesn't prove.

Animal2014·Mice on a high-fat diet
Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity

When researchers lowered NNMT activity in mouse fat and liver, the mice gained much less fat on a high-fat diet even though they ate the same amount.

Finding: Knocking down NNMT in white adipose tissue and liver protected mice from diet-induced obesity and improved metabolic parameters, without reducing food intake.
Limitations: Genetic knockdown in mice, not a drug given to humans. Establishes NNMT as a target but not the efficacy or safety of 5-Amino-1MQ specifically.
Animal2018·Diet-induced obese mice
Small-molecule NNMT inhibitors reduce adiposity in diet-induced obese mice

Drug-like NNMT blockers (the class 5-Amino-1MQ belongs to) reduced body fat in obese mice, but the work stops at rodents.

Finding: Membrane-permeable small-molecule NNMT inhibitors lowered fat-pad weight and body fat in obese mice, supporting NNMT inhibition as a pharmacological approach to obesity.
Limitations: Rodent-only, short duration. No human pharmacokinetics, dosing, or long-term safety data.

History

Interest in NNMT as a metabolic target grew after a 2014 Nature study showed that knocking down NNMT in fat and liver tissue protected mice from diet-induced obesity. Small-molecule NNMT inhibitors such as 5-Amino-1MQ were subsequently developed and tested in rodent obesity models.

Important:

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