Atypical antipsychotic clozapine has a special therapeutic impact on tardive dyskinesia and treatment-resistant schizophrenia. Clozapine also has important adverse effects such as epileptic seizures. For this reason, most clinicians avoid using clozapine in patients with schizophrenia and epilepsy. Therefore, treating patients with schizophrenia, tardive dyskinesia, and epilepsy is challenging. Here, we describe the case of a 32-year-old woman who was already suffering from epilepsy, schizophrenia, and tardive dyskinesia. She experienced clozapine-related seizures. But at the same time, clozapine dose adjustments successfully improved her psychosis and tardive dyskinesia and also stabilized her epilepsy. This case study indicates that epilepsy does not preclude the use of this important agent whenever it is clinically appropriate.
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http://dx.doi.org/10.5152/pcp.2023.23651 | DOI Listing |
Front Pharmacol
December 2024
Department of Clinical Psychology, The Third Affiliated Hospital of Soochow University, Changzhou, China.
Background: Deutetrabenazine is a widely used drug for the treatment of tardive dyskinesia (TD), and post-marketing testing is important. There is a lack of real-world, large-sample safety studies of deutetrabenazine. In this study, a pharmacovigilance analysis of deutetrabenazine was performed based on the FDA Adverse Event Reporting System (FAERS) database to evaluate its relevant safety signals for clinical reference.
View Article and Find Full Text PDFNeuropsychopharmacology
January 2025
Neurocrine Biosciences, Inc., San Diego, CA, USA.
Positron emission tomography (PET) is frequently used to obtain target occupancy (%TO) of central nervous system (CNS) drug candidates during clinical development. Obtaining %TO with PET can be particularly powerful when the %TO associated with efficacy is known for a protein target. Using the radiotracer [F]AV-133, the relationship between plasma concentration (PK) and %TO of NBI-750142, an experimental inhibitor of the vesicular monoamine transporter type 2 (VMAT2) was obtained in both nonhuman primate (NHP) and human.
View Article and Find Full Text PDFNat Commun
January 2025
Shanghai Fifth People's Hospital, Fudan University, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism (Ministry of Science and Technology), Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Vesicular monoamine transporter 2 (VMAT2) is crucial for packaging monoamine neurotransmitters into synaptic vesicles, with their dysregulation linked to schizophrenia, mood disorders, and Parkinson's disease. Tetrabenazine (TBZ) and valbenazine (VBZ), both FDA-approved VMAT2 inhibitors, are employed to treat chorea and tardive dyskinesia (TD). Our study presents the structures of VMAT2 bound to substrates serotonin (5-HT) and dopamine (DA), as well as the inhibitors TBZ and VBZ.
View Article and Find Full Text PDFExpert Opin Pharmacother
December 2024
Department of Neurology, UTHealth Houston McGovern Medical School, Houston, TX, USA.
Introduction: Chorea is a motor manifestation of Huntington's disease (HD), which can lead to decreased functional independence and falls. Even though multiple classes of medications have been used to treat this symptom, only the vesicular monoamine transporter 2 (VMAT2) inhibitors tetrabenazine, deutetrabenazine, and valbenazine have been approved by the FDA for this indication.
Areas Covered: This article reviews the pharmacological properties, clinical efficacy, safety, and tolerability of valbenazine in the treatment of chorea in HD.
Ment Health Clin
December 2024
(Corresponding author) Clinical Pharmacist Specialist, Vanderbilt Specialty Pharmacy Services, Nashville, Tennessee,
Vesicular monoamine transporter 2 inhibitors (VMAT2i) are currently Food and Drug Administration-approved for the treatment of Huntington disease chorea and tardive dyskinesia. Additionally, they are often used for other hyperkinetic movement disorders in clinical practice. Due to a lack of head-to-head clinical trials, management of VMAT2i in the clinical setting may be unclear and rely on the clinical experience of the practitioner.
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