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NADH (sodium salt hydrate) is an orally effective reduced coenzyme. NADH disodium hydrate plays a role in regenerating electron donors during cellular energy metabolism, including glycolysis, β-oxidation, and the tricarboxylic acid (TCA) cycle. NADH disodium hydrate regulates calcium homeostasis by promoting the opening of IP3-gated Ca2+ channels and inhibiting Ryanodine receptor, and affects mitochondrial function through direct interaction with VDAC. NADH disodium hydrate is used in cytoprotective studies related to cerebral ischemic injury, neurodegenerative diseases, aging, and signal transduction。

NADH (sodium salt hydrate) (5 mM; 1-20 min) hydrate reduces Na+binding ability in purified V-ATPase, with Kd values of 20 µM and 15 µM in the presence and absence of ATP, respectively。
NADH (sodium salt hydrate) inhibits PARP-1-mediated cell death and increases intracellular NAD+levels in mouse astrocytes, and can be transported into cells through P2X7 receptor mediation。

NADH (10-20 mg/kg; nasal administration; Single dose administration; Disodium hydrate, administered 2 hours after ischemic attack, has the effect of reducing infarct formation and neurological dysfunction in a 2-hour transient focal cerebral ischemia rat model.