NAD+ and Epithalon target two of the most documented mechanisms of biological aging: metabolic dysfunction driven by NAD+ depletion, and telomere attrition driven by declining telomerase activity. The pairing is rational because the mechanisms are independent — addressing one does not substitute for addressing the other.
Why these two compounds
NAD+ (Nicotinamide Adenine Dinucleotide) is a coenzyme central to cellular energy metabolism, DNA repair, and sirtuin signaling. NAD+ levels decline 40–50% between age 20 and 60. This decline impairs mitochondrial function, reduces SIRT1/SIRT3 activity (longevity-associated deacetylases), and accumulates DNA damage. Restoring NAD+ levels is one of the most evidence-backed interventions in the longevity research space, with preclinical data from multiple species and emerging human trial data.
Epithalon (Epitalon) is a synthetic tetrapeptide (Ala-Glu-Asp-Gly) derived from Epithalamin, a pineal gland extract studied extensively by Professor Vladimir Khavinson’s team at the St. Petersburg Institute of Bioregulation. Its primary documented mechanism is upregulation of telomerase — the enzyme that maintains telomere length. Animal model data across multiple species shows telomere extension with Epithalon treatment, alongside documented effects on melatonin secretion and antioxidant status. It has over 40 years of Russian research behind it and is one of the few peptides with direct telomere data.
NAD+ addresses the metabolic and mitochondrial layer of aging. Epithalon addresses the genetic/telomere layer. They are not substitutes — they are additive across different aging hallmarks.
Protocol reference
Research protocol: NAD+ 500mg–1g IV or subcutaneous as per research design; Epithalon 5–10mg subcutaneous daily for 10-day cycles, typically 2–4 cycles per year. Epithalon is cycled, not run continuously.
What’s included
For research use only. Not for human consumption. Not medical advice. COA available on every batch. HPLC-verified ≥99% purity on all compounds.
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