NAD+

Research Overview

NAD+ occupies a central position in cellular biochemistry as both a redox carrier in metabolic reactions and a consumable substrate for NAD+-dependent regulatory enzymes. Its role as the obligate substrate for sirtuins (SIRT1–7) — class III histone deacetylases that regulate gene expression, mitochondrial biogenesis, and DNA damage response — and for PARP enzymes in DNA break repair has established it as a multifunctional research tool in metabolic and longevity biology. The documented age-dependent decline of intracellular NAD+ pools and the associated attenuation of sirtuin activity provides a framework for studying the molecular basis of metabolic ageing in cell models. Supplied exclusively for laboratory and research use.

NAD+ metabolism sits at the convergence of energy substrate catabolism, epigenetic regulation, and genome maintenance — three processes whose coordinated decline has been proposed as a unifying mechanism in biological ageing research. Sirtuin-catalysed NAD+ hydrolysis produces O-acetyl-ADP-ribose and nicotinamide, linking metabolic flux to histone modification state and downstream transcriptional regulation. PARP1/2-mediated NAD+ consumption during DNA strand break repair represents a competing demand on the cellular NAD+ pool, placing NAD+ availability at the intersection of genomic integrity and metabolic signalling. These relationships have driven substantial preclinical research using exogenous NAD+ as a substrate supplement in in vitro ageing and metabolic dysfunction models. All outcomes referenced pertain to preclinical models and do not constitute evidence of clinical efficacy or safety in humans.