PCL NAD+ 20mL 100mg/mL

Nicotinamide adenine dinucleotide (NAD⁺) is a pivotal pyridine dinucleotide involved in redox biochemistry and non-redox enzymatic functions across eukaryotic and prokaryotic systems. As a hydride acceptor, NAD⁺ is central to catabolic pathways including glycolysis, the tricarboxylic acid (TCA) cycle, and fatty acid oxidation, where it governs cellular energy metabolism through electron transfer reactions and ATP generation (Covarrubias et al. 2021).

Beyond redox metabolism, NAD⁺ functions as an obligate co-substrate for several classes of NAD⁺-consuming enzymes, such as sirtuins, PARPs, and CD38, with critical roles in DNA repair, epigenetic regulation, circadian rhythms, and intracellular calcium signaling (Li et al. 2017; Covarrubias et al. 2021). These enzymes compartmentalize NAD⁺ usage, and their activation or inhibition contributes to distinct physiological outcomes during stress, aging, and genomic maintenance (Ying 2006; Li et al. 2017).

Cellular NAD⁺ pools are maintained via the de novo pathway from tryptophan, the Preiss– Handler pathway from nicotinic acid, and predominantly the salvage pathway from nicotinamide (Covarrubias et al. 2021). Disruptions in these pathways or increases in NAD⁺-consuming enzyme activity contribute to age-related NAD⁺ decline, which has been associated with mitochondrial dysfunction and impaired genome stability in mammalian models (Zhang et al. 2016; Li et al. 2017).