Delving into the Latest Updates on Cibenzoline Succinate with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Cibenzoline, Cifenline, コハク酸シベンゾリン

+ [10]

Target

SCNA

Action

blockers

Mechanism

SCNA blockers(Sodium voltage-gated channel alpha subunits blockers)

Therapeutic Areas

Cardiovascular Diseases

Active Indication

Tachycardia

Inactive Indication-

Originator Organization

UPSA SAS

Active Organization

TOA Eiyo Ltd.

Inactive Organization-

License Organization-

Drug Highest PhaseApproved

First Approval Date

Japan (28 Sep 1990),

Tachycardia

Regulation-

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Structure/Sequence

Molecular FormulaC22H24N2O4

InChIKeyXFUIOIWYMHEPIE-UHFFFAOYSA-N

CAS Registry100678-32-8

View All Structures (2)

BACKGROUNDChanges in left ventricular (LV) remodeling, especially in relation to the duration of therapy, are poorly understood in patients with hypertrophic non-obstructive cardiomyopathy (HNCM).METHODS AND RESULTSThis study included 254 consecutive patients with HNCM. Patients were divided into 3 groups according to the length of chronic cibenzoline therapy (CCT): Group I (n=104), CCT ≥10 years; Group II (n=85), 5 years≤CCT<10 years; and Group III (n=65), 1 year ≤CCT<5 years. SV1+RV5 and the maximum depth of precordial negative T waves were measured on electrocardiograms (ECG). In addition to routine echocardiographic indices, we measured the distance between the mitral valve and the apex (i.e., the "LV long distance" [LVLD]). After CCT, ECG indices and LV wall thicknesses were decreased in all 3 groups. LV dimensions and LV fractional shortening were preserved, and did not differ significantly among the groups. Left atrial dimension and the E/A ratio also did not differ among the groups, whereas the E/early diastolic annular velocity (Ea) ratio was decreased in Groups I and II. After CCT, LVLD was increased in all groups (all P<0.0001). These improvements were greater in Group I than in Groups II and III.CONCLUSIONSCCT preserved LV systolic function and reduced LV hypertrophy in patients with HNCM. The E/Ea ratio was improved in Groups I and II. Thus, CCT aids in treating patients with HNCM.

21 Feb 2025·Biological and Pharmaceutical Bulletin

<i>α</i><sub>1</sub>-Adrenoceptor Blockade by Class I Antiarrhythmic Drugs in Guinea Pig Thoracic Aorta as Revealed by Mechanical and Fluorescence Displacement Analysis

Article

Author: Tanaka, Hikaru ; Igarashi, Hiro ; Namekata, Iyuki ; Shirai, Kuniaki ; Kawazoe, Ayaka ; Tsukada, Kohei ; Seki, Maika ; Hamaguchi, Shogo ; Miyahara, Marina

The effects of thirteen Vaughn Williams class I antiarrhythmic drugs on the α₁-adrenergic receptor-mediated contraction were examined in thoracic aorta tissue preparations isolated from the guinea pig. Cibenzoline, quinidine, aprindine, and ranolazine, as well as prazosin, inhibited the phenylephrine-induced contraction with pA₂ values of 5.64, 5.59, 5.61, 5.08, and 8.50, respectively, but not prostaglandin F_2α-induced. These drugs reduced the staining of the smooth muscle layer by fluorescent prazosin. Propafenone inhibited the phenylephrine-induced contraction with an apparent pA₂ value of 5.31 and reduced the staining by fluorescent prazosin, but also inhibited the prostaglandin F_2α-induced contraction. Other class I antiarrhythmic drugs, disopyramide, pirmenol, procainamide, lidocaine, mexiletine, flecainide, pilsicainide, and GS-458967, affected neither the contraction by phenylephrine nor the fluorescent staining by prazosin. These results indicate that among the class I antiarrhythmic drugs, cibenzoline, aprindine, and propafenone, as well as quinidine and ranolazine, have α₁-adrenoceptor-blocking activity at therapeutically relevant concentrations.

27 Jun 2024·Cureus

A Case of New-Onset Atrial Tachyarrhythmias With Apical Hypertrophic Cardiomyopathy and Bronchiectasis in a Very Elderly Patient: A Therapeutic Dilemma

Article

Author: Fujiwara, Hitoshi ; Kurisu, Satoshi

Hypertrophic cardiomyopathy (HCM) is a primary myocardial disease that is genetically transmitted as an autosomal dominant trait. Even apical HCM (ApHCM) induces atrial fibrillation (AF) based on underlying left ventricle (LV) diastolic dysfunction, where anticoagulation therapy is recommended. However, anticoagulation for AF in patients at high risk of bleeding is a double-edged sword. A 98-year-old woman living in a nursing home presented to our hospital with sudden-onset dyspnea and palpitation persisting for two hours. The patient had a history of apical HCM and bronchiectasis. An electrocardiogram showed a regular tachycardia with a heart rate of 130 bpm, suggesting atrial flutter with 2:1 atrioventricular conduction. Intravenous verapamil (5 mg) resulted in the conversion into AF, and subsequent cibenzoline (70 mg) failed to restore sinus rhythm. Given the impossibility of continuous anticoagulation, electrical cardioversion was planned. Electrical cardioversion was successful in converting AF into sinus rhythm. Given the very high risk of hemoptysis, anticoagulation was avoided. This case gives an insight into how to manage a practical therapeutic problem, which is the coexistence of AF and bronchiectasis. A variety of individual factors should be considered for clinical decision-making and management of patients with concomitant HCM and AF.

100 Deals associated with Cibenzoline Succinate

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