Lurasidone 74mg tablets

Cognitive deficits are associated with schizophrenia and show a progressive worsening, often being unresponsive to treatment. New antipsychotic molecules acting as antagonist at the serotoninergic 5-hydroxytryptamine receptor 7 (e.g. lurasidone) or partial agonists at dopamine D3 receptor (e.g. cariprazine) could have an impact on cognition in this patient group. The aim of the systematic review is to explore the efficacy of lurasidone and cariprazine in improving cognition in both animal models and human studies. The following terms: (lurasidone AND cognit*) OR (cariprazine AND cognit*) were searched in Web of Science from inception to December 2021. We included all studies that assessed changes in cognitive function after treatment with cariprazine or lurasidone. Of 201 selected articles, 36 were included. Twenty-four articles used animal models (rats, mice and marmosets), five evaluating the effects of cariprazine and 19 the effects of lurasidone. Twelve articles were clinical studies (cariprazine n = 2; lurasidone n = 10). In both animal and human studies lurasidone showed a greater efficacy on cognitive performance compared to placebo, quetiapine, ziprasidone or treatment-as-usual. Cariprazine was superior to other antipsychotics in improving cognitive functions in both animal and human studies. The cognitive effect of lurasidone could be explained by its potent antagonism at the 5-HT7 receptors combined with partial agonism at 5-HT1A receptors. The pro-cognitive effect of cariprazine is probably explained by its very high affinity for D3 receptors. Head-to-head studies comparing lurasidone and cariprazine are needed to establish the “first-choice” treatment for cognitive dysfunction associated with schizophrenia.

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BackgroundLurasidone is a second-generation antipsychotic with antidepressant properties, but its effect on depressive symptoms across diagnostic domains is not known.AimsThis systematic review aims to synthesise the evidence for the transdiagnostic efficacy of lurasidone in reducing depressive symptoms.MethodElectronic databases were searched up to October 2024 to identify randomised controlled trials comparing the effects of lurasidone and placebo on depressive symptoms, as measured by any standardised scale, in populations with different psychiatric diagnoses. Acceptability, tolerability and safety were also measured. The Cochrane risk of bias tool was used to assess study quality, and the GRADE tool to evaluate certainty of evidence. A random-effects meta-analysis was performed to estimate standardised mean differences (SMDs, for continuous outcomes) or relative risks (for dichotomous outcomes) with 95% CI.ResultsFourteen trials met inclusion criteria. Pooled analysis of 5239 participants found lurasidone to be more efficacious than placebo in improving depression scores (SMD -0.26, 95% CI -0.37, -0.15) across multiple diagnoses (including schizophrenia, bipolar disorder and major depressive disorder). Secondary analyses showed better acceptability (relative risk 0.55, 95% CI 0.43, 0.71) and safety (relative risk 0.73, 95% CI 0.58, 0.91) and comparable tolerability (relative risk 0.74, 95% CI 0.54, 1.02) between lurasidone and placebo. The main limitations were the high risk of bias of several included studies and the high heterogeneity observed in our findings.ConclusionLurasidone is a potentially efficacious and safe strategy for reducing depressive symptomatology across a range of psychiatric diagnoses. Further long-term, robust trials employing precision psychiatry methods are needed to support its broader use to target depressive symptoms transdiagnostically.

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BackgroundThere is a need to provide up-to-date, clinically translatable data as it relates to the treatment of a major depressive episode (MDE) with mixed features.MethodsPubMed and OVID were searched from inception to July 22, 2024. Randomized controlled trials (RCTs) investigating the efficacy of pharmacological agents for adults with bipolar disorder (BD) or major depressive disorder (MDD) in an MDE with mixed features were included. Risk of bias was assessed using the Cochrane Risk of Bias Tool for Randomized Studies (RoB2).ResultsA total of seven studies were included in this systematic review. The studies identified were all short-term acute studies ranging from 6 to 8 weeks. Treatment with lurasidone, olanzapine, cariprazine, lumateperone, quetiapine, and ziprasidone was associated with statistically significant reduction of depressive symptoms in MDEs with mixed features. Only lumateperone is studied in both BD subtypes [bipolar I disorder (BD-I), bipolar II disorder (BD-II)] and MDD, wherein efficacy in mixed features was the prespecified primary outcome. Lurasidone has a single study in MDD, while ziprasidone has data in a mixed sample of BD-II and MDD. Data for the other agents in mixed features is post hoc. Co-occurring hypomanic symptoms generally improved, and there was no significant difference between the above treatments and placebo with respect to hypomanic symptom severity intensification or treatment-emergent affective switching.ConclusionSelect atypical antipsychotics are effective in alleviating depressive symptoms in persons with mixed features; albeit, much of the data is obtained from post hoc analysis. Minimal evidence exists for the efficacy of lithium or valproate in the treatment of depressive episodes with mixed features. Antidepressant monotherapy has not been adequately evaluated in depressive episodes with mixed features. In addition, there is a pressing need for a consistent definition of mixed presentations to guide future interventional studies.

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Background/Objectives: Lurasidone ((3aR,4S,7R,7aS)-2-{(1R,2R)-2-[4-(1,2-benzisothiazol-3-yl)piperazin-1-ylmethyl]cyclohexylmethyl}hexahydro-4,7-methano-2H-isoindole-1,3-dione) is a second-generation antipsychotic approved for schizophrenia and mood disorders. Adolescents and children with bipolar disorder receive treatments that expose them to weight gain and metabolic syndrome. Lurasidone is relatively free from such side effects, so it may constitute a useful alternative for the treatment of these patients. We focused on the use of lurasidone in children and adolescents with bipolar disorder. Methods: On 11 June 2025, we used the following strategy on PubMed: lurasidone AND (“bipolar disorder” OR “bipolar depression” OR mania OR manic). We filtered for humans and ages 0–18 years and included case reports and clinical studies. Similar strategies adapted to each database were used to carry out our systematic review on CINAHL, PsycINFO/PsycARTICLES, Scopus, and the ClinicalTrials.gov register on the same date. We excluded reports without children/adolescent participants, those grouping adult participants with children/adolescents without providing data separately, reviews, and opinions/editorials with no data. Eligibility was determined through Delphi rounds; it was required that consensus was reached among all authors. We followed the PRISMA-2020 Statement. Results: Our search produced 38 results on PubMed on 11 June 2025. We included four case reports/series and five studies. One additional eligible study emerged from our Scopus inquiry, raising the number of eligible studies to six. One case series was moderately positive; one case report was neutral, another was positive, and one reported the induction of mania. The six longitudinal studies involved 16,735 participants and showed generally good efficacy. Conclusions: The use of lurasidone in adolescents/children with bipolar disorder obtains favorable results regarding the excitatory and depressive symptoms of bipolar disorder with no significant side effects.

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BackgroundAtypical antipsychotics (AAs) are commonly used in the treatment of schizophrenia and are often preferred as first-line therapy over typical antipsychotics (TAs) due to their lower risk of extrapyramidal side effects. Both groups are efficacious in treating symptoms of schizophrenia, but increasing research has highlighted AAs as being associated with a risk of developing dyslipidaemia. Existing research has pointed to the need for more data focusing on the effects of individual AAs on dyslipidaemia in this population.MethodsThe scoping review was conducted using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping reviews (PRISMA-ScR) checklist. The thematic analysis was used to synthesize data from 12 studies selected through structured searches across six databases. Inclusion criteria focused on primary studies between 2015 and 2025 involving adult patients with schizophrenia (18-65 years) treated with AAs and reporting on lipid abnormalities. The themes were identified via Braun and Clarke's six-step framework.ResultsClozapine and olanzapine were most strongly associated with increased LDL, total cholesterol, and triglycerides, and reduced HDL. Aripiprazole and lurasidone showed minimal impact. Identified biomarkers included asprosin, IGFBP-2, MIF, and white blood cell counts. Pharmacogenetic markers such as APOA1 gene polymorphisms and specific SNPs were also linked to lipid profile variability. Anthropometric indicators like waist-to-hip ratio were correlated with dyslipidaemic risk.ConclusionThe review shows significant associations between specific AAs and lipid abnormalities, particularly with clozapine and olanzapine. Biomarkers and genetic polymorphisms offer promising avenues for monitoring and personalized treatment. Evidence for certain AAs, such as amisulpride, paliperidone, and ziprasidone, remains sparse, highlighting the need for further targeted research. These findings support informed prescribing and the development of predictive tools to mitigate metabolic risks in the treatment of schizophrenia.

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This network meta-analysis evaluates the efficacy and safety of pharmacological and physical treatments for depressive episodes in adolescents with bipolar disorder (BD), incorporating evidence from six randomized controlled trials (RCTs), total N = 879. Due to the absence of shared comparators, pharmacological treatments and non-invasive brain stimulation (NIBS) were analyzed in separate evidence networks rather than being directly compared.Pharmacological treatments included lurasidone, olanzapine-fluoxetine combination (OFC), and quetiapine, while NIBS consisted of transcranial direct current stimulation (tDCS) and intermittent theta-burst stimulation (iTBS). P-scores probabilities showed lurasidone as the most effective for reducing depressive symptoms (CDRS-R SMD: -0.41, 95% CI: -0.62 to -0.19) and improving response rates (RR: 1.64, 95% CI: 1.30-2.04). OFC had the highest remission rates (RR: 1.39, 95% CI: 1.03-1.89). Quetiapine demonstrated limited antidepressant efficacy (CDRS-R SMD: -0.12, 95% CI: -0.38-0.15) but significantly reduced treatment-emergent mania risk (RR: 0.22, 95% CI: 0.05-0.97). In NIBS, tDCS outperformed both iTBS and placebo for reducing depressive (HAMD SMD: -2.56, 95% CI: -3.40 to -1.73) and anxiety symptoms (HAMA SMD: -3.21, 95% CI: -4.15 to -2.28). These results suggest that lurasidone and tDCS may be promising options for symptom management in adolescents with BD, while quetiapine may be considered for preventing manic switching. Further studies, including head-to-head trials, are needed to better understand the long-term effects and address gaps in suicide risk management and multimodal treatment strategies.

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