Nicotinamide Adenine Dinucleotide
100mg / vial
NAD+ (Nicotinamide Adenine Dinucleotide) is an essential coenzyme present in every living cell. It plays a central role in cellular energy production, DNA repair, and the regulation of hundreds of metabolic processes. NAD+ levels decline significantly with age — a finding that has driven substantial research interest in supplementation and restoration strategies.
NAD+ is a dinucleotide coenzyme consisting of adenine and nicotinamide connected via two phosphate groups. It exists in two interconvertible forms: the oxidised form (NAD+) and the reduced form (NADH), and this redox cycling is fundamental to cellular energy production. NAD+ functions as a critical electron carrier in mitochondrial oxidative phosphorylation (the electron transport chain), and as a substrate for three major enzyme families: sirtuins (SIRT1-7, involved in gene regulation, stress response, and longevity), PARP enzymes (poly-ADP-ribose polymerases, involved in DNA repair), and CD38/CD157 (enzymes that consume NAD+ to generate calcium-signalling molecules, and whose activity increases with age). At 663.4 g/mol, NAD+ is a small molecule compared to the peptides in the catalogue.
As a sirtuin substrate, NAD+ enables SIRT1 and SIRT3 to deacetylate target proteins, regulating mitochondrial biogenesis, inflammatory responses, and cellular stress adaptation. SIRT1 activation in particular has been linked to caloric restriction mimicry and lifespan extension in multiple model organisms. As a PARP substrate, NAD+ supports DNA strand break repair — a process that becomes increasingly important as oxidative damage accumulates with age. Research has shown that restoring NAD+ levels in aged cell and animal models reverses markers of cellular ageing, improves mitochondrial function, enhances DNA repair capacity, and reduces chronic inflammation (inflammageing). The age-related decline in NAD+ is now understood to involve primarily CD38 upregulation, which consumes NAD+ faster than it can be synthesised.
NAD+ research spans mitochondrial biology, ageing and longevity science, neurodegeneration, cardiovascular health, and metabolic disease. Studies have been conducted at institutions including Harvard (David Sinclair's laboratory), the Salk Institute, Washington University St. Louis, and the National Institutes of Health. Key publications include work by Yoshino et al. demonstrating NAD+ decline with age and restoration with precursors, and work by Imai et al. establishing the role of NAD+ in sirtuin-mediated longevity. Research in neurodegeneration has shown NAD+ repletion to be protective in models of Alzheimer's, Parkinson's, and ALS.
Commonly researched with