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Pharmacology: Pharmacodynamics: Sodium valproate has anticonvulsant properties. The exact mode of action is unknown. However, the most likely mode of action for valproate is related to increased brain concentrations of gamma amino butyric acid (GABA) through an action on the synthesis or metabolism of GABA.
Pharmacokinetics: Valproic acid is rapidly absorbed from gastrointestinal tract, slight delay when taken with food. For delayed-release tablets the time to peak serum concentration could be 3 or 4 hours.
Valproic acid concentration in cerebrospinal fluid is close to free plasma concentration.
Valproate is highly bound to plasma proteins (90-95%). Protein binding decreased in the elderly and with hepatic or renal dysfunction.
Valproic acid is extensively metabolized in the liver. Most of the medicine is converted to the conjugate ester of glucuronic acid, while mitochondrial metabolism, principally by means of beta-oxidation. Some of the metabolites have anticonvulsant activity.
Sodium valproate is mainly excreted in urine following metabolism via glucuro-conjugation and beta-oxidation.
The elimination half-life of sodium valproate varies from approximately 6 to 16 hours. It is usually shorter in children.
