5-AMINO-1MQ - 3g

SPECIFICATIONS

Product Code: 5AM003P

Molecular Formula: C10H11N2

Molecular Weight: 286.12 g/mol

CAS: 42464-96-0

Purity: Technical / Research Grade ≥99%

Form: Solid powder

Color: Yellow/Orange

Storage Temperature: -20°C

Source: Synthetic

Safety Classification: Standard handling

DESCRIPTION

5-amino-1MQ is a synthetic small-molecule compound belonging to the class of methylquinolinium derivatives, currently investigated in experimental and preclinical settings for its interaction with cellular metabolic regulation systems. Unlike peptides, this compound is structurally compact and designed to act at the intracellular level, where it interacts with enzymatic pathways involved in energy homeostasis.

At the center of current scientific interest lies its ability to modulate the activity of nicotinamide N-methyltransferase (NNMT), an enzyme that plays a subtle but highly influential role in cellular metabolism. NNMT is located in the cytosol of cells and is expressed across multiple tissues, particularly in metabolically active environments such as adipose tissue, liver, and skeletal muscle. Its biological function consists in catalyzing the methylation of nicotinamide, a precursor of NAD⁺, converting it into 1-methylnicotinamide (1-MNA). While this transformation may appear minor at first glance, it has broader implications for how cells manage energy, maintain redox balance, and regulate metabolic flux.

To understand the significance of 5-amino-1MQ, it is essential to consider the role of NNMT as a metabolic “gatekeeper.” By diverting nicotinamide away from NAD⁺ recycling pathways, NNMT indirectly influences the availability of NAD⁺, a coenzyme that is fundamental to cellular energy production. NAD⁺ participates in oxidative phosphorylation within mitochondria, enabling the conversion of nutrients into usable energy (ATP). It also plays a central role in activating sirtuins, a family of proteins involved in cellular repair, stress resistance, and metabolic regulation.

When NNMT activity is elevated, more nicotinamide is converted into 1-MNA, which can lead to a relative depletion of NAD⁺ pools. This shift may alter cellular efficiency, favoring energy conservation and storage rather than expenditure. In experimental models, increased NNMT expression has been associated with metabolic states characterized by reduced energy utilization and a higher propensity for storing excess calories as fat or glycogen. This has led researchers to explore NNMT as a potential metabolic regulator influencing body composition and energy balance.

5-amino-1MQ is being studied as a functional inhibitor of NNMT, meaning it reduces or modulates the enzyme’s activity. By limiting the conversion of nicotinamide into 1-MNA, more nicotinamide remains available for NAD⁺ biosynthesis through salvage pathways. This shift in biochemical balance is hypothesized to support higher intracellular NAD⁺ levels, which in turn may enhance mitochondrial function and cellular energy output.

One of the most discussed aspects in preclinical research is the potential impact of NNMT inhibition on energy expenditure. In animal models, compounds targeting NNMT have been associated with increased caloric utilization without corresponding increases in food intake. This suggests that cells may become more metabolically active, burning available substrates more efficiently rather than storing them. As a result, reductions in fat mass and changes in adipocyte structure have been observed in controlled experimental settings.

Adipose tissue itself is not merely a passive storage site but an active endocrine organ that communicates with other systems in the body. The size and metabolic behavior of adipocytes (fat cells) can influence systemic metabolic health. In experimental contexts, modulation of NNMT activity has been linked to reductions in adipocyte size, suggesting a shift toward improved lipid turnover and altered fat storage dynamics. However, these findings are based on animal studies and require further investigation before any conclusions can be drawn regarding human physiology.

Another key element in this metabolic network is the glucose transporter GLUT4, which is responsible for insulin-dependent glucose uptake into cells, particularly in muscle and adipose tissue. GLUT4 plays a crucial role in maintaining blood glucose balance and supporting cellular energy supply. Research has indicated that NNMT expression may inversely correlate with GLUT4 levels in certain conditions. When NNMT activity is high, GLUT4 expression may be reduced, potentially impacting glucose uptake efficiency. Conversely, modulation of NNMT may influence GLUT4 dynamics, indirectly affecting how cells handle glucose.

This relationship is particularly relevant when considering metabolic flexibility, which refers to the body’s ability to switch between different energy substrates such as glucose and fatty acids. Efficient metabolic flexibility is associated with better energy utilization and overall metabolic resilience. While the precise mechanisms linking NNMT and GLUT4 are still being studied, their interaction highlights the complexity of metabolic regulation and the interconnected nature of these pathways.

Beyond metabolism, NNMT has also been investigated in the context of muscle physiology and regeneration. Muscle tissue relies on a population of resident stem cells, known as satellite cells, which are responsible for repair and regeneration following injury. Preclinical studies have suggested that NNMT activity may influence the activation and proliferation of these cells. Inhibition of NNMT in animal models has been associated with increased satellite cell activity and enhanced muscle repair processes. This has led to interest in understanding whether metabolic regulation via NAD⁺ pathways could play a role in maintaining muscle integrity over time.

The connection between NNMT and muscle function also extends to mitochondrial performance. Muscle cells have high energy demands, and their function is closely tied to mitochondrial efficiency. By influencing NAD⁺ availability, NNMT modulation may indirectly affect mitochondrial respiration and ATP production. Improved mitochondrial function has been associated, in research contexts, with enhanced cellular performance, reduced oxidative stress, and better adaptation to physiological stressors.

In addition to muscle tissue, NAD⁺ metabolism is critical in the nervous system. Neurons require a constant supply of energy to maintain synaptic transmission and communication. NAD⁺ depletion has been linked, in experimental studies, to impaired neuronal signaling and reduced synaptic efficiency. While 5-amino-1MQ has not been extensively studied in neurological models, its potential to influence NAD⁺ levels has generated interest in its broader implications for brain energy metabolism and cognitive processes.

From a research perspective, 5-amino-1MQ represents a tool for exploring how modulation of a single enzyme—NNMT—can influence multiple interconnected systems, including energy metabolism, mitochondrial function, glucose handling, and cellular repair processes. Its relevance lies not in a single isolated effect, but in its ability to interact with a central metabolic hub that coordinates several aspects of cellular physiology.

REFERENCES

E. Carvalho et al. "Adipose-specific overexpression of GLUT4 reverses insulin resistance and diabetes in mice lacking GLUT4 selectively in muscle" [PubMed]

P. Pssios "Nicotinamide N-Methyltransferase: More Than a Vitamin B3 Clearance Enzyme" [PubMed]

Jie-Ru Liu et al., "Roles of Nicotinamide N-Methyltransferase in Obesity and Type 2 Diabetes" [PMC]

A. Dimet-Wiley et al., "Reduced calorie diet combined with NNMT inhibition establishes a distinct microbiome in DIO mice" [PubMed]

Wei-Dong Sun et al., "Nicotinamide N-methyltransferase (NNMT): a novel therapeutic target for metabolic syndrome" [PMC]

A.H. Apostolatos et al., "Preclinical testing of 5-amino-1-((1R,2S,3S,4R)-2,3-dihydroxy-4-methylcyclopentyl)-1H-imidazole-4-carboxamide: a potent protein kinase C-ι inhibitor as a potential prostate carcinoma therapeutic" [PMC]

Xiao-Yu Li et al., "Nicotinamide N-Methyltransferase: A Promising Biomarker and Target for Human Cancer Therapy" [PMC]

DISCLAIMER

This product is intendend for lab research and development use only. These studies are performed outside of the body. This product is not medicines or drugs and has not been approved by the FDA or EMA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law. This product should only be handled by licensed, qualified professionals.

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