Comparative Pharmacology
Head-to-head clinical analysis: DEPAKENE versus DILANTIN.
Peer-Reviewed Evidence
Head-to-head clinical analysis: DEPAKENE versus DILANTIN.
DEPAKENE vs DILANTIN
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Increases GABA concentration in the brain by inhibiting GABA transaminase and blocking voltage-gated sodium channels; also modulates histone deacetylase activity.
Phenytoin stabilizes neuronal membranes and decreases seizure activity by increasing efflux or decreasing influx of sodium ions across cell membranes in the motor cortex during generation of nerve impulses. It acts by blocking voltage-dependent sodium channels, thereby inhibiting the spread of seizure activity.
Oral: Initial 15 mg/kg/day divided into 1-3 doses, increase by 5-10 mg/kg/day weekly; typical maintenance 30-60 mg/kg/day. Intravenous: Same total daily dose as oral, administered as continuous infusion or divided q6h.
300–400 mg/day orally in 2–3 divided doses; IV loading dose 15–20 mg/kg at max 50 mg/min, then 300 mg/day IV divided 2–3 times daily.
None Documented
None Documented
10-16 hours (monotherapy); 5-9 hours in patients on enzyme-inducing co-medications; prolonged in hepatic impairment (up to 30 hours) or neonates.
Average 22 hours (range 7-42 hours) in adults. Dose-dependent; increases with higher concentrations due to saturable metabolism. In neonates: 10-15 hours. In chronic use, half-life may increase.
Renal: <3% unchanged; primarily hepatic metabolism via glucuronidation (50%) and beta-oxidation (40%), with metabolites excreted renally. Fecal: negligible.
Primarily hepatic metabolism to inactive metabolites (p-hydroxyphenyltoin and glucuronide conjugate). Less than 5% excreted unchanged in urine. Fecal excretion minimal (<2%).
Category C
Category C
Anticonvulsant
Anticonvulsant