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26-Week Repeated-Dose Toxicity Study of a Novel Antiarrhythmic Drug Sulcardine Sulfate in Sprague-Dawley Rats.
J Appl Toxicol
January 2025
School of Pharmaceutical Sciences, Nanjing Tech University, Nanjing, China.
Sulcardine sulfate (Sul) is a novel antiarrhythmic agent blocking multiple channels and exhibits unique pharmacological properties such as lower APD-dependent prolongation and reduced arrhythmia risk. Sul is currently in Phase III clinical trials, yet studies on its long-term toxicological profile and potential target organs remain unexplored. This study investigated the related toxicity of Sul in Sprague Dawley (SD) rats through repeated oral administration for 26 weeks, followed by a 4-week recovery period.
View Article and Find Full Text PDFImpact of Preventive Intravenous Amiodarone on Reperfusion Ventricular Fibrillation in Patients With Left Ventricular Hypertrophy Undergoing Open-Heart Surgery: Randomized Controlled Clinical Trial.
JMIR Form Res
January 2025
Department of Anesthesiology and Perioperative Medicine, The First Affiliated Hospital of Nanjing Medical University, No. 300 Guangzhou Road, Nanjing, 210029, China, 86 2568303569.
Background: Ventricular fibrillation (VF) is a vicious arrhythmia usually generated after removal of the aortic cross-clamp (ACC) in patients undergoing open-heart surgery, which could damage cardiomyocytes, especially in patients with left ventricular hypertrophy (LVH). Amiodarone has the prominent properties of converting VF and restoring sinus rhythm. However, few studies concentrated on the effect of amiodarone before ACC release on reducing VF in patients with LVH.
View Article and Find Full Text PDFArtemisinin protected human bronchial epithelial cells from amiodarone-induced oxidative damage via 5'-AMP-activated protein kinase (AMPK) activation.
Redox Rep
December 2025
Pharmaceutical Science, Faculty of Health Sciences, University of Macau, Taipa, People's Republic of China.
Background: Amiodarone, a common antiarrhythmic drug, is known for its severe side effects, including pulmonary toxicity, which involves oxidative stress and apoptosis. Artemisinin, an antimalarial drug, has shown cytoprotective properties by inhibiting oxidative stress and apoptosis. This study investigated the protective effects of artemisinin against amiodarone-induced toxicity in human bronchial epithelial cells (BEAS-2B) and mouse models.
View Article and Find Full Text PDFA python approach for prediction of physicochemical properties of anti-arrhythmia drugs using topological descriptors.
Sci Rep
January 2025
Department of Mathematical Sciences, Faculty of Science, Somali National University, Mogadishu Campus, Mogadishu, Somalia.
In recent years, machine learning has gained substantial attention for its ability to predict complex chemical and biological properties, including those of pharmaceutical compounds. This study proposes a machine learning-based quantitative structure-property relationship (QSPR) model for predicting the physicochemical properties of anti-arrhythmia drugs using topological descriptors. Anti-arrhythmic drug development is challenging due to the complex relationship between chemical structure and drug efficacy.
View Article and Find Full Text PDFFlecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca/Ba Current Is Present.
Int J Mol Sci
December 2024
Institute of Molecular Physiology and Genetics, Centre of Biosciences, Slovak Academy of Sciences, Dubravska cesta 9, 840 05 Bratislava, Slovakia.
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a highly arrhythmogenic syndrome triggered by stress, primarily linked to gain-of-function point mutations in the cardiac ryanodine receptor (RyR2). Flecainide, as an effective therapy for CPVT, is a known blocker of the surface-membrane Na channel, also affecting the intracellular RyR2 channel. The therapeutic relevance of the flecainide-RyR2 interaction remains controversial, as flecainide blocks only the RyR2 current flowing in the opposite direction to the physiological Ca release from the sarcoplasmic reticulum (SR).
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