5-amino-1MQ

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5-Amino-1MQ — Small-Molecule NNMT Inhibitor and NAD+ Pathway Modulator

5-Amino-1MQ (5-amino-1-methylquinolinium; also designated 5-A1MQ) is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme that catalyzes the transfer of a methyl group from S-adenosyl methionine (SAM) to nicotinamide (vitamin B3), producing 1-methylnicotinamide and S-adenosyl-homocysteine. The compound was characterized and its mechanism validated in a 2021 Cell Reports paper from the laboratory of Praveen Bhanu at Baylor College of Medicine, which demonstrated that NNMT inhibition with 5-amino-1MQ in diet-induced obese mice reduced adipose tissue mass, increased energy expenditure, and elevated intracellular NAD+ levels — without observed toxicity at research doses. NNMT is overexpressed in the white adipose tissue of obese subjects, where it functions as a methyl sink: by consuming SAM, it simultaneously depletes the cellular methyl pool and reduces NAD+ availability, suppressing SIRT1 and SIRT3 activity. 5-Amino-1MQ is not a peptide — it is a quinolinium salt small molecule — but is included in peptide research contexts due to the convergence of its NAD+ pathway effects with those of related compounds in metabolic biology. It is mechanistically distinct from SLU-PP-332, which is an ERRα/β/γ nuclear receptor agonist; 5-amino-1MQ operates at the level of enzyme inhibition upstream of NAD+ biosynthesis, not receptor activation.

Why NNMT Inhibition as a Metabolic Strategy Differs from Direct NAD+ Supplementation

Direct NAD+ precursor supplementation (e.g., NMN, NR) bypasses NNMT entirely and provides substrate for NAD+ synthesis; 5-amino-1MQ instead blocks the primary enzymatic drain on the methyl pool and NAD+ precursor pool simultaneously. NNMT inhibition also preserves SAM for other methylation reactions — histone, DNA, and protein methylation — meaning the metabolic effect includes both NAD+ elevation and restoration of epigenetic methylation capacity. This dual action on the methyl pool and NAD+ axis makes 5-amino-1MQ a distinct mechanistic probe from NAD+ precursors, useful for dissecting which downstream effects of NAD+ elevation are attributable to NNMT activity specifically.

Aplicaciones de investigación

5-Amino-1MQ is used in studies examining:

• NNMT enzyme inhibition kinetics and selectivity profiling
• NAD+ pathway modulation via SAM/methyl pool preservation
• Adipose tissue biology — adipogenesis, lipid storage, and mitochondrial metabolism
• Epigenetic methylation capacity under NNMT-overexpressing conditions
• SIRT1/SIRT3-dependent metabolic gene expression in adipocyte and hepatocyte models
• Comparative NAD+ pathway studies (NNMT inhibition vs. NMN/NR supplementation as mechanistic probes)
• Diet-induced obesity model metabolic phenotyping

Especificaciones

Reconstitución

5-Amino-1MQ arrives as lyophilized powder. As a small-molecule quinolinium salt, it exhibits limited solubility in aqueous solution alone. For in vitro cell culture applications, dissolve initially in DMSO (typically 10–50mM stock), then dilute into aqueous buffer or media to final working concentration — final DMSO concentration should remain below 0.1% v/v to avoid solvent cytotoxicity. For in vivo rodent studies, dissolve in a vehicle appropriate to the administration route (oral gavage formulations typically use PEG400/water or cyclodextrin solutions). Bacteriostatic water alone is not the preferred reconstitution vehicle for this compound.

Stock solution example: 10mg in 1mL DMSO → approximately 37mM stock (MW ~174 g/mol); dilute to working concentration in aqueous buffer.

Notas sobre el protocolo

In vivo research frameworks for 5-amino-1MQ are derived from the 2021 Baylor College of Medicine Cell Reports study, which remains the primary published pharmacology reference. Human-equivalent dose research is at an early stage with no published clinical data as of the available literature.

• Dose range (rodent literature): 40–80 mg/kg orally in diet-induced obesity mouse models (Baylor, 2021)
• Frequency: Daily oral gavage in published rodent studies
• Study duration: 4–12 weeks in published rodent metabolic phenotyping studies

Pilas de investigación

5-Amino-1MQ is commonly paired in research settings with:

• MOTS-c — Both compounds act on mitochondrial regulatory pathways; MOTS-c operates through AMPK activation while 5-Amino-1MQ inhibits NNMT to shift NAD+ flux, making them complementary targets in metabolic research models.
• NAD+ — 5-Amino-1MQ reduces NNMT-mediated NAD+ consumption, and exogenous NAD+ supplementation is studied alongside to assess combined effects on the NAD+ salvage pathway and cellular energy status.
• SS-31 — SS-31 targets the inner mitochondrial membrane to reduce oxidative stress, providing a complementary intervention point to 5-Amino-1MQ’s upstream metabolic enzyme inhibition in mitochondrial function studies.

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