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5-Amino-1MQ (5-Amino-1-methylquinolinium)

5-Amino-1MQ (5-Amino-1-methylquinolinium) is a small-molecule NNMT (nicotinamide N-methyltransferase) inhibitor studied for its role in regulating cellular NAD⁺ metabolism, methyl-donor balance, and energy homeostasis. Research explores its effects on adipocyte metabolism, mitochondrial efficiency, and metabolic signaling pathways. For research use only.

10MG | PHYSICIAN USE ONLY

$107.10

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Research Profile

At a Glance

  • Type: Small-Molecule NNMT Inhibitor (non-peptide compound)
  • Also Known As: 5-Amino-1-methylquinolinium
  • Chemical Structure: Quinolinium-based small molecule (NNMT inhibitor)
  • Molecular Weight: ~160.2 Da (base compound; salt forms may vary)
  • Primary Target: Nicotinamide N-Methyltransferase (NNMT)
  • Research Focus: NAD⁺ metabolism, adipocyte energy balance, methyl-donor regulation, cellular metabolic efficiency
  • Regulatory Status: RUO (Research Use Only); not FDA-approved
  • Categories: Metabolic Research; Anti-Aging Research

What Research Shows

  • Demonstrates inhibition of NNMT, an enzyme that consumes nicotinamide and methyl donors, thereby influencing NAD⁺ availability in metabolic tissues.
  • Shows involvement in regulation of adipocyte metabolism in experimental models, where NNMT activity has been linked to increased fat storage and reduced energy expenditure.
  • Supports a role in cellular energy homeostasis, as NNMT inhibition alters nicotinamide flux within the NAD⁺ salvage pathway.
  • Indicates potential influence on mitochondrial efficiency and metabolic flexibility, as NAD⁺ availability is central to redox balance and cellular respiration.
  • Highlights NNMT as a metabolic checkpoint enzyme, with elevated expression observed in obesity-associated adipose tissue and metabolic dysregulation models.

Mechanistic Notes

5-Amino-1MQ activity centers on modulation of nicotinamide metabolism via NNMT inhibition:
Core Mechanisms
  • Inhibits NNMT, reducing conversion of nicotinamide to 1-methylnicotinamide (MNA).
  • Preserves intracellular nicotinamide pools, supporting NAD⁺ salvage pathway availability.
  • Reduces methyl-donor consumption, as NNMT activity draws from S-adenosylmethionine (SAM) pools.
  • Influences cellular redox balance, as NAD⁺/NADH ratios are central to metabolic signaling.
Why NNMT Inhibition Is Distinct in Metabolic Research
  • NNMT is upregulated in obesity and metabolic disease models, particularly in adipose tissue.
  • Unlike direct NAD⁺ precursors, NNMT inhibition modulates NAD⁺ metabolism upstream, by limiting nicotinamide depletion.
  • Provides a regulatory approach to metabolic efficiency rather than direct stimulation of energy pathways.
Downstream Effects Observed in Research
  • Altered adipocyte energy storage vs. expenditure signaling in preclinical models.
  • Modulation of mitochondrial metabolic activity through NAD⁺-dependent pathways.
  • Engagement of sirtuin-related metabolic signaling, as sirtuin activity depends on NAD⁺ availability.

What Remains Unknown

  • No published human clinical trials
  • Long-term safety and pharmacokinetics not established
  • Degree of NAD⁺ modulation across different tissues remains unclear
  • Translational relevance beyond adipocyte and animal models is still under investigation

Scientific References (Peer-Reviewed Only)

Kraus D. et al. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature. 2014;508:258–262
https://pubmed.ncbi.nlm.nih.gov/24717514/

Finnerty CC. et al. (2018) (NNMT inhibitors; methylquinolinium scaffold used in anti-obesity model work) Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochemical Pharmacology. 2018
https://pubmed.ncbi.nlm.nih.gov/24717514/

Dimet-Wiley A. et al. (2022) (explicitly uses 5-amino-1-methylquinolinium as the NNMT inhibitor) Reduced calorie diet combined with NNMT inhibition establishes a distinct microbiome in DIO mice. Scientific Reports. 2022.
https://pubmed.ncbi.nlm.nih.gov/35013352/

Babula JAJ. et al. (2024) (in vivo PK + metabolic outcomes; uses 5A1MQ) Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction. Diabetes, Obesity and Metabolism. 2024
https://pubmed.ncbi.nlm.nih.gov/39161060/

Awosemo O. et al. (2021) (PK + oral bioavailability; explicitly for 5-AMQ) Development & validation of LC-MS/MS assay for 5-amino-1-methyl quinolinium in rat plasma: Application to pharmacokinetic and oral bioavailability studies. Journal of Pharmaceutical and Biomedical Analysis. 2021
https://pubmed.ncbi.nlm.nih.gov/34304009/

Certificate of Analysis

 

 

Research Use Only: Our products are supplied exclusively for laboratory, in-vitro, and scientific research purposes. They are not intended for human or animal use of any kind. All information provided is for educational reference only. This material must be handled only by trained, licensed professionals. Our products are not a drug, food, or cosmetic and must not be misused, misbranded, or introduced into the body in any form.

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