Cellular Aging Mechanisms Kit

Epithalon is a synthetic tetrapeptide based on the natural epithalamin produced by the pineal gland. It activates telomerase (hTERT), the enzyme responsible for adding telomeric repeats to chromosome ends, thereby extending telomere length and increasing cellular replicative capacity. It also stimulates melatonin production from the pineal gland, restoring circadian rhythm function that declines with age. Additionally, it modulates antioxidant enzyme expression and has been shown to extend lifespan in animal models.

NAD+ is an essential coenzyme present in all living cells that serves as an electron carrier in metabolic redox reactions (glycolysis, TCA cycle, oxidative phosphorylation) and as a substrate for NAD+-consuming enzymes including sirtuins (SIRT1-7), PARPs, and CD38. Sirtuins are NAD+-dependent deacetylases that regulate DNA repair, mitochondrial biogenesis, inflammation, and stress resistance. NAD+ levels decline with age, and restoring NAD+ activates these protective pathways, enhancing cellular energy production, DNA repair capacity, and stress resilience.

MOTS-c is a mitochondrial-derived peptide encoded by the 12S rRNA gene (MT-RNR1) that acts as a retrograde signaling molecule from mitochondria to the nucleus. It activates AMPK, enhancing glucose uptake and fatty acid oxidation in skeletal muscle. MOTS-c regulates the folate cycle and de novo purine biosynthesis, leading to AICAR accumulation and subsequent AMPK activation. It translocates to the nucleus under metabolic stress to regulate adaptive gene expression, functioning as an exercise mimetic at the molecular level.

SS-31 is a cell-permeable, mitochondria-targeted tetrapeptide that concentrates ~1000-fold in the inner mitochondrial membrane by binding to cardiolipin, a phospholipid unique to this membrane. By stabilizing cardiolipin's interaction with cytochrome c, SS-31 optimizes electron transport chain efficiency, reduces electron leak, and decreases mitochondrial reactive oxygen species (ROS) production. It does not act as a traditional antioxidant scavenger but rather prevents ROS formation at the source by maintaining proper mitochondrial function.