NADPH tetrasodium salt is the reduced form of the electron acceptor nicotinamide adenine dinucleotide phosphate, which acts as an electron donor in a variety of biological reactions. NADPH tetrasodium salt is also an endogenous inhibitor of iron death.

METHODS: Neurons were pretreated with NADPH tetrasodium salt (2.5-10 μM) for 1-8 h, then treated with Kainic acid (KA, 100 μM) for 8 h. Cell viability was measured by CCK-8 assay.
RESULTS: KA treatment significantly reduced the cell viability of primary cortical neurons in a time-dependent and dose-dependent manner, and NADPH pretreatment significantly promoted neuronal survival, which was more effective at 10 μM for 4 or 8 h. The RESULTS showed that Kainic acid (KA, 100 μM) treatment significantly reduced the cell viability of primary cortical neurons. [1]
METHODS: Neurons were pretreated with NADPH tetrasodium salt (10 μM) for 4 h, and then treated with Kainic acid (KA, 100 μM) for 8 h. The expression levels of target proteins were detected by Western Blot.
RESULTS: The expression of TIGAR was decreased after KA treatment, and it was significantly reversed by NADPH. [1]

METHODS: To examine the effects on Kainic acid (KA)-induced excitotoxicity and its mechanism, NADPH tetrasodium salt (1-2 mg/kg in saline) was administered intravenously to KA-induced rats once a day for seven days.
RESULTS: NADPH reduced KA-induced increase in striatal lesion size, improved KA-induced dyskinesia, and reversed KA-induced glial cell activation. [1]
METHODS: NADPH tetrasodium salt (2.5 mg/kg) was intravenously injected into ICR mice to determine whether exogenous NADPH could enter the brain tissues and neurons of mice.
RESULTS: Injection of NADPH significantly increased the levels of NADPH in the blood and brain tissue of mice.The half-life of NADPH in the blood of mice is about 6 h and in the brain tissue is 7 h. [2]

DMSO: 1.25 mg/mL (1.5 mM)

H2O: 35 mg/mL (42.00 mM)