New Exclusive BlendNAD+ / MOTS-c / 5-Amino-1MQ
Nicotinamide Adenine Dinucleotide / MOTS-c / 5-Amino-1-Methylquinolinium Blend
The NAD+ / MOTS-c / 5-Amino-1MQ (100mg/10mg/10mg) blend is a multi-component formulation designed for laboratory investigation of mitochondrial function, energy homeostasis, and cellular metabolism. By combining an essential metabolic coenzyme (NAD+), a mitochondrial-derived signaling peptide (MOTS-c), and a targeted small molecule inhibitor of nicotinamide N-methyltransferase (5-Amino-1MQ), this blend offers researchers a unified system to examine converging metabolic pathways. NAD+ serves as a fundamental substrate for sirtuins and PARPs, playing a pivotal role in redox reactions and cellular survival. MOTS-c acts downstream to promote metabolic flexibility, regulate glucose utilization, and stimulate AMPK signaling. Concurrently, 5-Amino-1MQ prevents the degradation of nicotinamide and preserves methyl pools by selectively inhibiting NNMT, thereby sustaining cellular NAD+ concentrations and modulating epigenetic markers. This tri-phasic complex is extensively utilized in pre-clinical research models focusing on age-related metabolic decline, mitochondrial biogenesis, adipogenesis, and cellular resilience against metabolic stress.
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- Purity
- ≥99%
- Form
- Lyophilized powder
- Available sizes
- 120mg
Mechanism of Action
The mechanisms of this blend converge on the regulation of intracellular energy sensing and nucleotide balance. 5-Amino-1MQ functions as a cell-permeable, selective inhibitor of NNMT, an enzyme that consumes nicotinamide and S-adenosylmethionine (SAM). In vitro NNMT inhibition rescues intracellular NAD+ levels and upregulates SAM/SAH ratios, promoting enhanced metabolic efficiency and suppressing lipogenic pathways. Simultaneously, direct supplementation of NAD+ fuels crucial enzyme families including sirtuins (SIRT1-7), driving mitochondrial renewal and DNA repair mechanisms. MOTS-c complements this action by translocating to the nucleus under metabolic stress and regulating nuclear gene expression, directly stimulating the AMPK pathway and modulating the folate-methionine cycle to optimize cellular respiration.
Research Areas
- ●Mitochondrial biogenesis and respiration
- ●AMPK and Sirtuin signaling pathways
- ●Nicotinamide N-methyltransferase (NNMT) inhibition
- ●Cellular energy homeostasis and longevity
- ●Metabolic and lipid flux dynamics
Selected References
- Lee C, et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces diet-induced obesity. Cell Metab. 2015.
- Neelakantan H, et al. Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochem Pharmacol. 2018.
- Cantó C, et al. The regulation of mitochondrial fitness, healthspan, and longevity by NAD+ and its precursors. Cell Metab. 2015.
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