Also known as: 5-amino-1-methylquinolinium · 5A1MQ · 5-amino-1MQ chloride
5-amino-1MQ is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT) — an enzyme highly overexpressed in adipose tissue that drives fat accumulation and suppresses energy expenditure. By blocking NNMT, it elevates NAD+ precursor availability, activates SIRT1 pathways, and promotes lipolysis without stimulant effects. Strong preclinical results for obesity and metabolic syndrome.
5-amino-1MQ (5-amino-1-methylquinolinium) is a small quinolinium salt, not a peptide — included in the metabolic category due to its NNMT inhibition mechanism and common use alongside peptide-based weight loss protocols.
NNMT is dramatically overexpressed in white adipose tissue in obesity, acting as a metabolic brake by consuming SAM while depleting NAD+ precursors. 5-amino-1MQ blocks NNMT, restoring SAM availability and NAD+ levels, which activates SIRT1/SIRT3 and promotes fatty acid oxidation in adipocytes.
5-amino-1MQ binds the nicotinamide pocket of NNMT with ~50 nM potency, preventing nicotinamide methylation and depletion. Elevated NAD+ activates SIRT1 in adipose tissue, driving PGC-1α deacetylation, mitochondrial biogenesis, and fatty acid oxidation.
NNMT inhibition reduces lipid droplet size, upregulates fatty acid oxidation genes (CPT1A, HADHA), and suppresses lipogenic transcription factors. Effects resemble a shift toward beige/brown adipocyte phenotype with increased UCP1 expression.
Restoring SAM availability enables proper function of DNA and histone methyltransferases, potentially reversing obesity-associated epigenetic marks in adipose tissue for durable metabolic reprogramming.
5-amino-1MQ is NOT a peptide — it is a small-molecule NNMT inhibitor included in the metabolic category due to its fat-loss mechanism and common use alongside GLP-1/peptide protocols. Human safety and dosing data are essentially non-existent beyond preclinical studies. All human protocols are extrapolated from rodent data. Use with significant caution and awareness of the complete lack of clinical trial data. No significant adverse effects were noted in rodent studies at research doses.
Cycling protocols for 5-amino-1MQ are entirely derived from community research practice — no clinical cycling data exists. Short cycles are used to assess effects and monitor for any adverse responses. The epigenetic changes in adipose tissue SAM methylation may persist beyond the treatment period — potentially creating residual metabolic improvements during the off-cycle. This is speculative based on mechanism.
Key preclinical study: Obese mice treated with 5-amino-1MQ showed 7% body weight reduction, 30% fat mass reduction, improved glucose tolerance, and reduced liver fat without changes in food intake — within 14 days. No completed human clinical trials as of 2024. All human dosing extrapolated from rodent data.
Ask anything about 5-amino-1MQ — mechanisms, dosing protocols, interactions, or research comparisons.
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