The NAD+/MOTS-c/5-amino-1MQ blend is an investigational synergistic formulation that combines direct NAD+ replenishment, the mitochondria-derived peptide MOTS-c (AMPK/glucose homeostasis activator), and the NNMT inhibitor 5-amino-1MQ (NAD+- and SAM-preserving fat-loss agent) to collectively restore mitochondrial function, improve insulin sensitivity, reduce adiposity, enhance energy metabolism, and exert geroprotective and neuroprotective effects in preclinical models of obesity, diabetes, and aging.
Store in a cool, dark place or freeze at -20°C for long term storage. Refrigerate after reconstitution
NAD+: 100MG
MOTS-c: 10MG
5amino 1MQ: 10MG
The NAD+/MOTS-c/5-amino-1MQ peptide blend represents a synergistic investigational formulation designed to target mitochondrial dysfunction, metabolic dysregulation, and age-related cellular decline, combining direct NAD+ replenishment (100 mg) as a critical redox cofactor for sirtuin activation, DNA repair, and energy metabolism; MOTS-c (10 mg), a 16-amino-acid mitochondria-derived peptide (MRWQEMGYIFYPRKLR) encoded by mtDNA that translocates to the nucleus under metabolic stress to activate AMPK, upregulate antioxidant and glucose homeostasis genes, enhance insulin sensitivity, and mitigate diet-induced obesity and insulin resistance; and 5-amino-1MQ (10 mg), a small-molecule NNMT inhibitor that preserves endogenous NAD+ by blocking nicotinamide methylation, thereby elevating intracellular NAD+ and SAM levels, suppressing lipogenesis in adipocytes (reducing fat cell size by up to 30–40% in preclinical models), stimulating brown adipose thermogenesis, and promoting muscle regeneration in aged or dystrophic tissues. Preclinical studies in diet-induced obesity mice demonstrate that this triad collectively improves glucose tolerance, reduces white adipose mass and plasma lipids (e.g., 30% lower cholesterol), enhances mitochondrial efficiency and redox balance, and extends healthspan by countering immunosenescence and neuroinflammation, with emerging evidence suggesting neuroprotective benefits against cognitive impairment in Alzheimer’s models and geroprotective effects via SIRT1 activation.
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