Comparative Pharmacology
Head-to-head clinical analysis: LATUDA versus ZIPRASIDONE HYDROCHLORIDE.
Peer-Reviewed Evidence
Head-to-head clinical analysis: LATUDA versus ZIPRASIDONE HYDROCHLORIDE.
LATUDA vs ZIPRASIDONE HYDROCHLORIDE
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Lurasidone is an atypical antipsychotic with high affinity for dopamine D2, serotonin 5-HT2A, and serotonin 5-HT7 receptors, and moderate affinity for serotonin 5-HT1A receptors. It acts as an antagonist at D2 and 5-HT2A receptors, and as a partial agonist at 5-HT1A receptors. The exact mechanism of action in schizophrenia and bipolar depression is unknown but is thought to involve modulation of these receptors.
Ziprasidone is an atypical antipsychotic with high affinity for serotonin 5-HT2A and dopamine D2 receptors. It also antagonizes 5-HT2C, 5-HT1D, and alpha1-adrenergic receptors, and has moderate affinity for histamine H1 and alpha2-adrenergic receptors. It exhibits partial agonism at 5-HT1A receptors.
40 mg orally once daily initially, titrated to 80-160 mg once daily; maximum 160 mg/day. Administer with food (at least 350 calories).
20 mg PO BID with food, titrated up to max 80 mg PO BID; IM: 10-20 mg q2h or q4h, max 40 mg/day
None Documented
None Documented
Terminal elimination half-life is approximately 20–40 hours (mean about 29 hours) in adults, supporting once-daily dosing. Steady-state is reached within 7 days.
Terminal elimination half-life is approximately 7 hours (range 6–10 hours) for oral administration; clinically, steady state is achieved within 1–3 days.
Approximately 80% of the dose is eliminated in feces (mostly as unchanged drug and metabolites) and about 10% in urine. Less than 2% is excreted as unchanged lurasidone in urine.
Primarily hepatic metabolism via aldehyde oxidase and CYP3A4; <1% excreted unchanged in urine, approximately 20% in feces as metabolites.
Category C
Category A/B
Atypical Antipsychotic
Atypical Antipsychotic