Metabolic Research

5-Amino 1MQ50mg

$89

A potent small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT) — a metabolic enzyme implicated in obesity and adipose dysfunction — with strong preclinical evidence for fat mass reduction and NAD⁺ elevation without caloric restriction.

5-Amino 1MQMetabolic Research

Overview

5-Amino-1-methylquinolinium (5-Amino 1MQ) is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), a metabolic enzyme that consumes S-adenosylmethionine (SAM) to methylate nicotinamide — simultaneously depleting two critical cellular resources: the universal methyl donor (SAM) and the NAD⁺ salvage precursor (nicotinamide). NNMT is normally expressed at low levels in most tissues, but elevated NNMT activity in adipose tissue, muscle, and liver has emerged over the past decade as a consistent molecular signature of obesity, insulin resistance, and age-related metabolic decline.

By inhibiting NNMT, 5-Amino 1MQ restores intracellular NAD⁺ and SAM pools, which drives several downstream metabolic consequences: increased histone methylation (gene expression remodeling), improved mitochondrial biogenesis and fatty acid oxidation, and shifted adipocyte phenotype toward thermogenic metabolism. In rodent models of diet-induced obesity, oral 5-Amino 1MQ produced significant reductions in body weight and adipose mass, reduced lipid accumulation in liver, and improved insulin sensitivity — all without caloric restriction or exercise intervention. These outcomes have positioned the compound as a candidate exercise- and restriction-independent metabolic modulator.

Unlike GLP-1 class agents that act centrally to reduce caloric intake, 5-Amino 1MQ works through peripheral metabolic rewiring — making it mechanistically complementary rather than redundant to appetite-suppressing agents. This distinct mechanism has generated interest in its potential as a research companion compound to GLP-1 investigations, in age-related sarcopenic obesity models, and in fatty liver disease research where hepatic NAD⁺ restoration is mechanistically relevant. The compound is technically a small molecule rather than a peptide but is frequently grouped with metabolic research peptides due to its shared research context and delivery format.

Mechanism of Action

Inhibits NNMT to prevent SAM-dependent methylation of nicotinamide; restores intracellular NAD⁺ and SAM pools; drives mitochondrial biogenesis and fatty acid oxidation; shifts adipocyte phenotype toward thermogenic metabolism.

Research Applications

Areas of peer-reviewed scientific inquiry where this compound has appeared.

  • Obesity and diet-induced weight gain models
  • Adipose tissue phenotype and thermogenesis
  • NAD⁺ restoration and longevity research
  • Non-alcoholic fatty liver disease (NAFLD)
  • Insulin resistance and metabolic syndrome
  • Sarcopenic obesity and age-related metabolic decline

Key Findings from the Literature

  1. 01Reduced body weight and adipose mass in diet-induced obesity without caloric restriction
  2. 02Restores intracellular NAD⁺ and SAM pools via NNMT inhibition
  3. 03Peripheral metabolic mechanism complementary to centrally-acting GLP-1 agents
  4. 04Improved insulin sensitivity and reduced hepatic steatosis in rodent models
  5. 05Elevated NNMT is a consistent molecular signature of obesity and metabolic disease

Certificates of Analysis1

Independent third-party lab reports for this peptide. Each CoA can be verified against its accession number at the testing lab.

1 independent test by Freedom Diagnostics Testing

TestResult
Purity (HPLC)99.712%
Identity (MS)Pass
Endotoxins (LAL)Pass

Lab: Freedom Diagnostics Testing

Accession: 2603200310 / 2603200311

Reports are verifiable against the issuing lab using the accession or batch identifier above.

Other compounds in the metabolic research category.