Comparative Pharmacology
Head-to-head clinical analysis: DEPAKOTE versus ZONISADE.
Peer-Reviewed Evidence
Head-to-head clinical analysis: DEPAKOTE versus ZONISADE.
DEPAKOTE vs ZONISADE
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.
Zonisamide is a sulfonamide anticonvulsant. Its precise mechanism of action is unknown, but it is believed to inhibit voltage-sensitive sodium channels and reduce T-type calcium currents, thereby stabilizing neuronal membranes and suppressing neuronal hypersynchronization. It may also modulate GABA and glutamate neurotransmission.
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.
100-200 mg orally every 8 hours; maximum 600 mg/day.
None Documented
None Documented
Terminal: 9-16 hours (mean 12 h); extended with hepatic dysfunction, co-administered enzyme inhibitors, or in elderly.
Terminal elimination half-life: 63-69 hours in adults; allows once-daily dosing; steady-state achieved in 14-21 days
Renal: <3% as unchanged drug; >95% as metabolites (glucuronide conjugates, oxidation products). Biliary/fecal: minor, <5%.
Renal: approximately 62% (35% unchanged, 27% as glucuronide conjugate); fecal: 3%; biliary: negligible
Category C
Category C
Anticonvulsant
Anticonvulsant