- 5-Amino-1MQ (5-amino-1-methylquinolinium) is a small-molecule NNMT (nicotinamide N-methyltransferase) inhibitor with a molecular weight of 174.2 Da.
- Supplied in oral 50mg capsule format — distinct from the injectable lyophilized peptides in the metabolic research category.
- Research investigates NAD+ metabolism, SAM/SAH methylation balance, adipocyte differentiation, and energy expenditure pathway interactions.
What is 5-Amino-1MQ?
5-Amino-1MQ (5-amino-1-methylquinolinium) is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT) with a molecular weight of 174.2 Da. Unlike the other compounds in the metabolic research category — which are peptides supplied as lyophilized powders for injection — 5-Amino-1MQ is supplied in oral capsule format (50mg per capsule) reflecting its small-molecule chemistry and oral bioavailability. Researchers can access 5-Amino-1MQ research capsules from Advanced Peptide Science.
Research Background and the NNMT Pathway
NNMT (nicotinamide N-methyltransferase) catalyses the methylation of nicotinamide using S-adenosylmethionine (SAM) as the methyl donor. The reaction has two metabolic consequences: depletion of nicotinamide (a key NAD+ precursor via the salvage pathway) and consumption of the methyl-donor SAM pool. Both effects make NNMT a significant node in cellular metabolism with broad downstream implications for NAD+-dependent signalling (sirtuins, PARPs) and methylation-dependent regulation. Pharmacological NNMT inhibition is investigated as a research tool to elevate cellular NAD+ availability via the salvage pathway and to shift the SAM/SAH methylation balance.
Mechanism of Action
Mechanism research investigates 5-Amino-1MQ competitive inhibition at the NNMT active site. Downstream effects include preservation of cellular nicotinamide for NAD+ resynthesis via the salvage pathway, elevation of cellular NAD+ pools, altered SAM/SAH ratio with consequent effects on DNA and histone methylation, and downstream signalling through NAD+-dependent enzymes including sirtuin family deacetylases (SIRT1-7) and PARP enzymes.
Active research areas include AMPK pathway activation downstream of altered cellular NAD+, mitochondrial biogenesis signalling through PGC-1α coactivator pathway engagement, and adipocyte-specific differentiation effects driven by the combined NAD+-elevation and methylation-balance effects of NNMT inhibition.
Key Research Findings
NAD+ Pathway Modulation
Research investigates 5-Amino-1MQ effects on cellular NAD+ pools via preservation of the nicotinamide salvage pathway. The pathway is one of two NAD+ biosynthesis routes — preservation of substrate availability via NNMT inhibition is investigated alongside direct NAD+ precursor supplementation strategies as complementary research approaches.
Methylation Balance Effects
Inhibition of the SAM-dependent NNMT methylation reaction shifts the cellular SAM/SAH ratio. Research investigates downstream effects on DNA methylation, histone methylation, and methylation-dependent regulatory signalling — a research area at the intersection of NAD+ biology and epigenetic regulation.
Adipocyte Differentiation and Energy Expenditure
NNMT is highly expressed in adipose tissue, where its inhibition is investigated for effects on adipocyte differentiation pathways and energy expenditure. Research focuses on white-adipocyte vs brown/beige-adipocyte programming and the role of NNMT in determining adipose tissue metabolic phenotype.
Comparison with Other Metabolic Research Compounds
5-Amino-1MQ occupies a distinctive mechanistic niche in the Metabolic & Weight Management category. The GLP-1-class compounds (Semaglutide, Tirzepatide, Retatrutide) act through incretin receptor signalling. AOD-9604 acts on adipocyte lipolytic signalling. 5-Amino-1MQ acts through enzyme inhibition affecting NAD+ availability and methylation balance — a fundamentally different mechanism, enabling complementary research designs across the category. Related longevity research compounds including MOTS-c (AMPK activation) and SS-31 (mitochondrial-targeted) intersect with the NAD+ pathway research framework.
Research Specifications
| Molecular Weight | 174.2 Da |
| Chemistry | Small molecule (5-amino-1-methylquinolinium) — not a peptide |
| Target | Nicotinamide N-methyltransferase (NNMT) |
| Format | Oral capsule, 50mg per capsule |
| Storage | Room temperature, dry conditions |
| Available in | 30 / 60 / 90 count bottles |
Frequently Asked Questions
What is the research significance of NNMT inhibition?
NNMT catalyses methylation of nicotinamide (a NAD+ precursor) using SAM as methyl donor. Inhibition preserves cellular NAD+ pools via the salvage pathway and shifts the SAM/SAH methylation balance — two effects with broad downstream implications for NAD+-dependent and methylation-dependent signalling.
Why is 5-Amino-1MQ supplied as a capsule rather than an injectable?
5-Amino-1MQ is a small molecule (174.2 Da), not a peptide. Small molecules typically have suitable oral bioavailability, distinct from peptides which are typically degraded by gastrointestinal proteases. The 50mg capsule format is appropriate for the molecule’s chemistry.
Where can researchers source 5-Amino-1MQ?
5-Amino-1MQ research capsules are available at Advanced Peptide Science in 30, 60, and 90 count bottles.
Is 5-Amino-1MQ approved for human use?
Advanced Peptide Science supplies 5-Amino-1MQ exclusively for in vitro and in vivo scientific research. Not for human consumption. Research use only.
For Research Use Only. Not for human consumption. Not intended to diagnose, treat, cure, or prevent any disease.
