Catalog No.S5714 Synonyms: SM-13496
Molecular Weight(MW): 492.68
Lurasidone is a second-generation antipsychotic agent that exhibits full antagonism at dopamine D2 and serotonin 5-HT2A receptors with binding affinities Ki = 1 nM and Ki = 0.5 nM, respectively. It also has high affinity for serotonin 5-HT7 receptors (Ki = 0.5 nM), partial agonist activity at 5-HT1A receptors (Ki = 6.4 nM) and lacks affinity for histamine H1 and muscarinic M1 receptors.
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|Description||Lurasidone is a second-generation antipsychotic agent that exhibits full antagonism at dopamine D2 and serotonin 5-HT2A receptors with binding affinities Ki = 1 nM and Ki = 0.5 nM, respectively. It also has high affinity for serotonin 5-HT7 receptors (Ki = 0.5 nM), partial agonist activity at 5-HT1A receptors (Ki = 6.4 nM) and lacks affinity for histamine H1 and muscarinic M1 receptors.|
Lurasidone is a new atypical antipsychotic in the benzoisothiazoles class of chemicals. Like most second-generation antipsychotics it is a full antagonist at dopamine D2 and serotonin 5-HT2A receptors, and is a partial agonist at 5-HT1A receptors. It has much greater affinity for 5-HT7 subtype receptors than other atypical antipsychotics. Lurasidone also has high affinity for the 5-HT1A subtype, α2c-adrenergic receptors and low affinity for α1-adrenergic receptors. It has minimal affinity for 5-HT2C receptors and negligible affinity for histamine H1 and muscarinic receptors.
|In vivo||Lurasidone is rapidly absorbed, reaching peak concentrations within 1.5–3 hours (tmax) after single and multiple oral doses. Once absorbed, it extensively distributes in tissues and rapidly enters the CNS. Lurasidone has high binding to human plasma albumin and alpha-1-glycoprotein (≥99%). Long-term treatment of schizophrenia with lurasidone has been shown to reduce the risk of relapse. The elimination half-life of lurasidone is about 20-40 h. Mean Cmax and area under the curve (AUC) for lurasidone were approximately threefold and twofold greater, respectively, in a comparison of administration with food v. fasting. Lurasidone absorption is independent of food fat content. Lurasidone is metabolised primarily via CYP3A4. In animal studies, lurasidone penetrated the placental barrier and distributed into the fetus, and was excreted in milk during lactation.|
|In vitro||DMSO||7 mg/mL (14.2 mM)|
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Clinical Trial Information
|NCT Number||Recruitment||interventions||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03627195||Completed||Drug: DSP-1349M|Drug: placebo||Schizophrenia||Sunovion||June 7 2018||Phase 1|
|NCT02731612||Recruiting||Drug: lurasidone|Other: Placebo||Bipolar Disorder||Nazlin Walji|University of British Columbia||May 8 2017||Phase 3|
|NCT02147379||Completed||Drug: Lurasidone||Bipolar I Disorder||University of British Columbia||May 2014||Phase 3|
|NCT02174523||Completed||Drug: 40mg lurasidone|Drug: placebo||Schizophrenia||Sumitomo Pharmaceutical (Suzhou) Co. Ltd.|Xuhui Central Hospital Shanghai||April 2014||Phase 1|
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