Comparative Pharmacology
Head-to-head clinical analysis: DEPAKOTE versus DIVALPROEX SODIUM.
Peer-Reviewed Evidence
Head-to-head clinical analysis: DEPAKOTE versus DIVALPROEX SODIUM.
DEPAKOTE vs DIVALPROEX SODIUM
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Increases GABA levels by inhibiting GABA transaminase and succinic semialdehyde dehydrogenase; also blocks voltage-gated sodium channels and T-type calcium channels.
Increases brain concentrations of gamma-aminobutyric acid (GABA), blocks voltage-gated sodium channels, and modulates T-type calcium channels.
Initial dose 750 mg/day PO in divided doses; increase by 250-500 mg/day every 3-7 days; maintenance dose 1000-2000 mg/day PO divided BID or TID; maximum 60 mg/kg/day.
10-15 mg/kg/day orally in divided doses; increase by 5-10 mg/kg/week; maximum 60 mg/kg/day. Extended-release: 25 mg/kg/day orally; increase by 15 mg/kg/day at weekly intervals; maximum 60 mg/kg/day.
None Documented
None Documented
Terminal: 9-16 hours (mean 12 h); extended with hepatic dysfunction, co-administered enzyme inhibitors, or in elderly.
9-16 hours (terminal); shorter in children (6-9 hours) and longer in hepatic disease or elderly; clinical context: twice-daily dosing provides stable trough concentrations.
Renal: <3% as unchanged drug; >95% as metabolites (glucuronide conjugates, oxidation products). Biliary/fecal: minor, <5%.
Renal: <3% unchanged; primarily hepatic metabolism (glucuronidation, beta-oxidation, cytochrome P450), metabolites eliminated renally; fecal: negligible.
Category C
Category D/X
Anticonvulsant
Anticonvulsant