Longevity & Cellular Aging

Aging is increasingly understood as a cellular process driven by mitochondrial dysfunction, NAD+ depletion, oxidative stress, and impaired autophagy. Peptide research in this domain targets these mechanisms directly:

**MOTS-c** is a mitochondrial-derived peptide encoded in the 12S rRNA gene. It activates AMPK and translocates to the nucleus under metabolic stress, regulating adaptive gene expression. In C2C12 myotubes, it activates AMPK at 0.5–10 µM.

**NAD+** is the central coenzyme for sirtuins (SIRT1–SIRT7), PARPs, and CD38. Without NAD+, sirtuin activity collapses. NAD+ depletion is a hallmark of cellular aging. Buffered NAD+ maintains physiological pH in cell-culture media.

**Glutathione** is the cell's primary low-molecular-weight thiol antioxidant. It scavenges free radicals, serves as cofactor for glutathione peroxidase, and conjugates xenobiotics in Phase II detoxification.

**Vitamin B12 (methylcobalamin)** supplies methyl groups to the one-carbon cycle, supporting SAM-dependent methylation of DNA, proteins, and neurotransmitters.

Aurex longevity compounds are tested for endotoxin (<0.5–1.0 EU/mg), heavy metals (ICP-MS), and purity (≥98–99% HPLC-UV) before release.