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Pharmacotherapeutic Group: Antiepileptic agent.
Pharmacology: Depakene is chemically unrelated to other drugs used to treat seizure disorders. Valproic acid has no nitrogen or aromatic moiety characteristic of other antiepileptic drugs. The mechanism by which Depakene exerts its antiepileptic effects has not been established. It has been suggested that its activity is related to increased brain levels of γ-aminobutyric acid (GABA). The effect on the neuronal membrane is unknown.
Pharmacokinetics: Valproic acid/valproate is rapidly distributed and at therapeutic drug concentrations, drug is highly bound (90%) to human plasma proteins. Increases in dose may result in decreases in the extent of protein-binding and variable changes in valproate clearance and elimination.
Elimination of Depakene and its metabolites occurs principally in the urine, with minor amounts in the feces and expired air. Very little unmetabolized parent drug is excreted in the urine. Depakene is primarily metabolized in the liver and is excreted as the glucuronide conjugate. Other metabolites in the urine are products of β, Ω-1 and Ω-oxidation (C-3, C-4 and C-5 positions).
The major oxidative metabolite in the urine is 2-propyl-3-ketopentanoic acid; minor metabolites are 2-propylglutaric acid, 2-propyl-5-hydroxypentanoic acid, 2-propyl-3-hydroxypentanoic acid and 2-propyl-4-hydroxypentanoic acid.
Depakene is rapidly absorbed after oral administration. Peak serum levels of valproic acid occur approximately 1-4 hrs after a single oral dose of Depakene. The serum half-life of the parent compound is typically in the range of 6-16 hrs. Half-lives in the lower part of the previously mentioned range are usually found in patients taking other antiepileptic drugs. A slight delay in absorption occurs when the drug is administered with meals but this does not affect the total absorption.
