5-Amino-1MQWeight Loss / GLP-1

Overview

5-Amino-1MQ (5-amino-1-methylquinolinium) is a small synthetic molecule — not a peptide — designed as a selective, cell-permeable inhibitor of the enzyme nicotinamide N-methyltransferase (NNMT). It is usually supplied for research as the iodide salt (CAS 42464-96-0; the active species is the quinolinium cation). It emerged from academic medicinal-chemistry work on NNMT as an anti-obesity target. All evidence is preclinical — isolated adipocytes and mice; there are no human trials and no human efficacy or safety data. It is research-use-only and not FDA-evaluated.

Mechanism

NNMT transfers a methyl group from S-adenosylmethionine (SAM) to nicotinamide, consuming both a NAD+ precursor (nicotinamide) and the cell's main methyl donor (SAM). In obese animal fat tissue NNMT is over-active. By inhibiting NNMT, 5-Amino-1MQ is reported (in adipocytes and mice) to lower 1-methylnicotinamide and raise intracellular NAD+ and SAM, with downstream increases in adipocyte energy expenditure and suppressed lipogenesis. This mechanism is established in rodent and cell-culture systems only; whether it operates in humans is untested.

Clinical evidence

There is no clinical evidence — no human trials of 5-Amino-1MQ have been conducted. The evidence base is entirely preclinical: in diet-induced obese mice, NNMT inhibitors including 5-Amino-1MQ reduced body weight and white-adipose mass without reducing food intake (Neelakantan 2018), building on a foundational study showing NNMT knockdown protects mice from diet-induced obesity (Kraus 2014). A 2021 review states plainly that clinical trials have not been reported. None of this can be extrapolated to human weight loss.

Safety profile

5-Amino-1MQ has not been studied for safety in humans — no human toxicology, no established dose, no pharmacokinetics, no adverse-event monitoring. Short-term rodent dosing produced no overt adverse findings, but no long-term, carcinogenicity, genotoxicity or reproductive studies exist. Because NNMT and NAD+/SAM metabolism touch methylation, epigenetics and cancer-cell biology, the consequences of chronic NNMT inhibition in humans are genuinely unknown. It is sold research-use-only; not WADA-listed, but that reflects obscurity, not a safety endorsement. Both safety and human-data confidence are scored at the floor.

Compare

• vs MOTS-c

  Another metabolism-focused research compound, but a mitochondrial-derived peptide; both are investigational with limited human data

• vs NAD+

  Targets the same NAD+ biology from the opposite direction — supplying the cofactor rather than inhibiting the enzyme (NNMT) that depletes its precursor