NADH disodium salt hydrate, also known as Disodium NADH hydrate, functions as an orally active reduced coenzyme. It serves as a donor of ADP-ribose units in ADP-ribosylation reactions and acts as a precursor to cyclic ADP-ribose. Additionally, it contributes to cellular energy metabolism by acting as a renewable electron donor in processes such as glycolysis, β-oxidation, and the tricarboxylic acid (TCA) cycle [1].

NADH is stable under alkaline conditions but unstable under acidic conditions [2]. At concentrations of 0-1 mM over 0-12 hours, NADH increases NAD+ levels in various mammalian cell lines [3]. Additionally, NADH at 1 mM for 24 hours exhibits low toxicity and protects cells from genotoxicity [3].

NADH, administered intraperitoneally at 5 μmol/mouse, enhances urinary excretion of nicotinamide and its metabolites in male ICR mice [2]. At a dosage of 500 mg/kg, orally administered NADH promotes alcohol metabolism and protects against early liver injury from acute alcohol exposure in male C57BL/6J mice by modulating blood acetaldehyde levels and maintaining the NAD+/NADH redox balance [3]. Additionally, a 1000 mg/kg intraperitoneal dose of NADH increases tissue NAD+ levels in these mice [3].