Research Profile
NAD+ (nicotinamide adenine dinucleotide) is an essential coenzyme in every living cell, participating in 500+ enzymatic reactions. It serves as substrate for sirtuins (SIRT1–7: gene expression, metabolism, stress resistance), PARPs (DNA repair), and CD38/CD157 (calcium signalling). NAD+ levels decline with age in liver, brain, skeletal muscle, and skin.
Direct injectable NAD+ bypasses rate-limiting biosynthesis steps, providing immediate substrate availability — unlike oral precursors (NMN, NR) which require enzymatic conversion.
Ageing and longevity — restoring NAD+ improves mitochondrial bioenergetics, reduces oxidative stress, and activates sirtuin longevity pathways: SIRT1 (metabolic regulation), SIRT3 (mitochondrial function), SIRT6 (DNA repair, telomere maintenance).
Mitochondrial function — primary electron carrier in the ETC. Restores mitochondrial biogenesis (PGC-1α), ATP production efficiency, and attenuates age-related sarcopenia preclinically.
DNA repair — PARP hyperactivation depletes NAD+ under oxidative stress, impairing further repair. NAD+ supplementation restores capacity. Active investigation in cancer biology and radiation injury.
Neurodegeneration — SIRT1/SIRT3 activation reduces amyloid burden and tau pathology preclinically. NAD+/PARP axis mediates neuronal death after ischaemic injury.
Metabolic syndrome — SIRT1 activation improves insulin sensitivity and regulates hepatic gluconeogenesis.
IV NAD+ commonly causes transient flushing, chest tightness, nausea at rates above 100 mg/hour — dose and rate dependent, resolves promptly. Subcutaneous generally better tolerated. Reconstitute in sterile saline; use within 24 hours.