Universal Redox Coenzyme: Central to 500+ enzymatic reactions, glycolysis, citric acid cycle, electron transport chain, 80,000+ PubMed publications since 1906 discovery
Sirtuin/PARP/CD38 Substrate: Essential cofactor for SIRT1-7 longevity proteins, PARPs for DNA repair, CD38 calcium signaling; NAD+ declines 10-65% with aging across tissues
Clinical Development: Multiple Phase 2 RCTs showing 2.6-3.1x NAD+ increases with precursor supplementation, benefits in metabolic disease, cognition, long COVID, well-tolerated safety profile
NAD+ (Nicotinamide Adenine Dinucleotide) is a fundamental redox coenzyme essential for cellular energy metabolism, DNA repair, and sirtuin-mediated aging pathways. Research shows NAD+ levels decline 10-65% with age, and supplementation may restore mitochondrial function and activate longevity pathways.
GHK-Cuis a research peptide composed of the tripeptide sequence Gly-His-Lys bound to copper(II) ions, forming a biologically active peptide–metal complex studied for its role in extracellular matrix modulation and cellular signaling. Preclinical research indicates that GHK-Cu regulates collagen production, gene expression, and enzymatic antioxidant pathways through copper-mediated redox mechanisms. It serves as a model compound for investigating peptide-driven tissue remodeling, metalloprotein r
Synthetic Tuftsin Analogue: Heptapeptide Thr-Lys-Pro-Arg-Pro-Gly-Pro, developed Russian Academy of Sciences, tuftsin core + Pro-Gly-Pro extension for metabolic stability, 20+ years research
Multi-Modal Mechanism: Positive allosteric modulator of GABA-A receptors, upregulates BDNF (hippocampus/cortex), inhibits enkephalinase (IC50 15 μM), modulates monoamines, no tolerance/dependence
Clinical Status: Russian FDA approved 2009 for GAD/neurasthenia (intranasal 0.15%), RCT showed efficacy equal to medazepam with additional nootropic effects, no sedation/amnesia unlike benzodiazepines
