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sotalol

✓ Approved

Hyloris Pharmaceuticals SA · ADRB1 · Small Molecule

What is sotalol?

sotalol is a small molecule developed by Hyloris Pharmaceuticals SA. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

CompanyHyloris Pharmaceuticals SA
Drug ClassSmall Molecule
Molecular TargetADRB1, ADRB2, KCNH2
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Hyloris Pharmaceuticals SA

Mechanism of Action

Molecular Targets

sotalol acts on 3 molecular targets:

ADRB1adrenoceptor beta 1 (B1AR, RHR)
ADRB2adrenoceptor beta 2 (ADRBR, B2AR)
KCNH2potassium voltage-gated channel subfamily H member 2 (ERG1, H-ERG)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

sotalol is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Cardiac disordersAtrial fibrillation✓ Approved

Related Research Articles

PubMedJACC. Case reports2026-10-07

Sustained Monomorphic Ventricular Tachycardia Decades After Ventricular Septal Defect Repair.

Kothia Darpan D, Mouselli Asaad A, Short Lillian L, Thomson Erica E et al.

Ventricular tachycardia can occur decades after ventricular septal defect repair, but surface electrocardiogram (ECG) and noninvasive imaging cannot prove patch-dependent reentry. A 57-year-old man with ventricular septal defect patch repair in infancy and no adult congenital heart disease follow-up presented with chest pain, dyspnea, and near-syncope. ECG showed sustained monomorphic ventricular tachycardia at 209 beats/min. Transthoracic echocardiography showed left ventricular ejection fraction 30%, right ventricular dysfunction, moderate-to-severe tricuspid regurgitation, and possible right ventricular thrombus. Transesophageal echocardiography demonstrated fixed postoperative-appearing tissue rather than thrombus. Coronary angiography showed no obstructive disease. After cardioversion, a secondary-prevention dual-chamber implantable cardioverter-defibrillator was placed, and sotalol was initiated with renal and ECG monitoring. The case provides a framework for suspected but unproven postoperative scar-related ventricular tachycardia by separating substrate plausibility from circuit proof. Repaired ventricular septal defect carries lifelong arrhythmic risk; patch dependency requires electroanatomic mapping, whereas prevention decisions should follow clinical risk.

PMID 42841831
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PubMedCardiovascular toxicology2026-09-29

Substrate-Dependent Pro- and Antiarrhythmic Action of Omecamtiv Mecarbil at the Ventricular and Atrial Level: Insights from a Langendorff-Perfused Rabbit Heart Model.

Wolfes Julian J, Neff Katharina K, Wegner Felix F, Rath Benjamin B et al.

Omecamtiv mecarbil is a cardiac-selective myosin activator and potential heart failure treatment, but its electrophysiological profile remains incompletely characterized. We investigated omecamtiv mecarbil in a Langendorff-perfused rabbit heart model. Forty-eight rabbit hearts were retrogradely perfused; twenty-four in a ventricular and twenty-four in an atrial setup. In the ventricular setup, action potential duration at 90% repolarization (APD90), QT interval, and dispersion of repolarization were assessed during pacing at seven cycle lengths. After baseline recordings, Group 1 (n = 12) received 1, 5 and 10 µM omecamtiv mecarbil sequentially, while Group 2 (n = 12) received 100 µM sotalol followed by 5 µM omecamtiv mecarbil. In the atrial setup, Group 3 (n = 12) received 5 and 10 µM omecamtiv mecarbil, and Group 4 (n = 12) received isoproterenol/acetylcholine (IsoACh) to increase atrial fibrillation (AF) susceptibility, followed by 5 µM omecamtiv mecarbil. Omecamtiv mecarbil alone shortened ventricular APD90 and QT interval, increased dispersion of repolarization, and raised ventricular arrhythmia incidence. Sotalol prolonged APD90, QT interval, and dispersion, with a marked rise in VT episodes; additional omecamtiv mecarbil did not further prolong repolarization but increased arrhythmia susceptibility further. In the atrial setup, omecamtiv mecarbil alone prolonged conduction time and increased AF inducibility. Under IsoACh, which shortened atrial APD and refractoriness and increased AF episodes, additional omecamtiv mecarbil slowed atrial conduction and markedly suppressed AF. In summary, omecamtiv mecarbil was proarrhythmic at the ventricular level, particularly under reduced repolarization reserve, but showed antiarrhythmic effects in an IsoACh-induced AF model and proarrhythmic properties in the healthy atrium, indicating a substrate-dependent electrophysiological profile.

PMID 42806179
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PubMedJournal of electrocardiology2026-09-18

Pregnancy-associated idiopathic ventricular arrhythmia: Serial electrocardiographic evolution during pregnancy and postpartum.

Bueno Sávia S, de Oliveira Patricia P, Avila Walkiria Samuel WS, Scanavacca Maurício M

Pregnancy can trigger or exacerbate ventricular arrhythmias even in structurally normal hearts. A 41-year-old woman at 22 weeks' gestation developed symptomatic monomorphic premature ventricular contractions (PVCs) and frequent nonsustained ventricular tachycardia (NSVT), with 11% PVC burden and 313 NSVT episodes. Metoprolol reduced arrhythmic burden but not symptoms. Sotalol, introduced with serial QT monitoring, was followed by complete symptomatic and Holter suppression. One month postpartum, asymptomatic ventricular arrhythmia recurred off therapy, then resolved spontaneously by three months. Serial monitoring illustrates marked pregnancy-related variability and the potential dissociation between symptoms and arrhythmic burden.

PMID 42759417
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PubMedPharmacology2026-09-15

Comparative analysis of infarct-reducing properties of ß1 -, ß2 -, and ß3 -adrenergicreceptor ligands in ischemia and reperfusion of the heart.

Voronkov NIkita S NS, Maslov Leonid N LN, Naryzhnaya Natalia V NV, Mukhomedzyanov Alexander V AV

In-hospital mortality in patients with acute myocardial infarction and cardiogenic shock can reach 50%. This is because there are currently no drugs approved for clinical use that can radically reduce infarction size and prevent the development of cardiogenic shock. β- Adrenergic receptor (β-AR) ligands could become such drugs. This article presents a comparative study of the cardioprotective properties of β-AR ligands in ischemia and reperfusion (I/R) of the heart. The study was performed in male Wistar rats. Coronary artery occlusion (CAO, 45 min) and reperfusion (120 min) were carried out in anesthetized animals. Fifteen minutes before CAO the following β-AR ligands were injected intravenously: the selective β 1 -AR antagonist atenolol, β 1 - and β 2 -AR antagonist sotalol, β 1 -, β 2 -, and β 3 -AR antagonist bupranolol, selective β 2 -AR antagonist ICI-118,551, selective β 3 -AR antagonist L- 748,337, and selective β 2 -AR agonist formoterol. It was evaluated the infarct size/area at risk (IS/AAR) ratio. Sotalol, bupranolol, atenolol, ICI-118,551, and L-748,337 decreased heart rate. Formoterol increased heart rate. Atenolol only reduced the IS/AAR ratio. β 1 -AR blockade increases cardiac tolerance to I/R in vivo. β 2 -AR blockade and β 2 - AR stimulation do not affect cardiac resistance to I/R in vivo. β 3 -AR blockade does not affect cardiac resistance to I/R in vivo.

PMID 42743088
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PubMedNaunyn-Schmiedeberg's archives of pharmacology2026-09-09

Beyond pooled analysis: sex-specific cardiovascular adverse event reporting signals with antiarrhythmic drugs in FAERS.

Khalifa Mostafa A MA, Dadam Mohammad Najm MN, Aldib Layan S LS, Salem Othman Mariam M

Sex differences in drug metabolism and cardiac electrophysiology may influence the cardiovascular safety profiles of antiarrhythmic drugs (AADs). However, pharmacovigilance studies often pool data, potentially obscuring sex-specific cardiovascular adverse event (CV-AE) reporting patterns. We aim to investigate sex-specific CV-AE reporting profiles associated with commonly used antiarrhythmic drugs using pharmacovigilance data. We analyzed 122,853 medication-role records representing 38,430 unique FAERS reports involving eight AADs. Disproportionality analyses defined index-drug exposure by the primary-suspect role, whereas the report-level XGBoost pipeline separately encoded primary-suspect drugs and secondary-suspect or concomitant medications. Analyses included pooled and sex-stratified disproportionality, drug-adjusted common odds ratios, and a gradient-boosting machine learning model to assess ventricular arrhythmia (VA) reporting patterns. Sex-stratified analysis uncovered "hidden" associations undetected in pooled data, including propafenone-QT prolongation in men and amiodarone-QT prolongation in women. Adverse event profiles were often drug-specific and opposing: cardiogenic shock showed higher reporting odds among males for sotalol, whereas flecainide showed higher reporting odds in females. After adjustment, women had higher odds of torsade de pointes and men of ventricular arrhythmia. However, a machine learning model for VA demonstrated that sex contributed modestly (1.4% SHAP contribution) compared with co-medications and the primary drug, though drug-specific associations differed. Sex-specific CV-AE profiles reporting patterns are often masked in pooled analyses, underscoring the need for sex-stratified pharmacovigilance to guide personalized antiarrhythmic therapy. The identified associations should be considered hypothesis-generating and require validation in datasets with richer clinical information.

PMID 42714472
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PubMedHeart & lung : the journal of critical care2026-09-04

Association of common QT-prolonging medications with arrhythmic risk in patients with bundle branch block: A stratified cohort analysis in left bundle branch block vs. right bundle branch block phenotypes.

Derector Evan E, DO Tirth Patel TP, Watanabe Hiroto H, Solomon Diana D et al.

Bundle branch block (BBB) affects 11-17% of adults over 80 and is associated with mortality and heart failure. Conventional QTc formulae overestimate repolarization in wide QRS complexes, with clinicians holding symptom-management therapies based on inaccurate measurements. This retrospective study utilized the MIMIC-IV database to examine arrhythmogenic risk by drug class and BBB phenotype. Adult ICU admissions with BBB were stratified by drug exposure: amiodarone, high-risk anti-arrhythmics (sotalol, dofetilide, procainamide, ibutilide, quinidine, disopyramide), and common non-cardiac QT-prolonging agents (haloperidol, ondansetron, quetiapine, methadone, levofloxacin, azithromycin). The primary outcome was a composite of ventricular arrhythmia and cardiac arrest; a sensitivity analysis restricted to ventricular arrhythmia was performed. Propensity score matching (1:1) with time-varying Cox regression addressed confounding and immortal time bias. The matched cohort included 1722 admissions (LBBB =1252; RBBB =470). Common non-cardiac agents were not associated with the composite outcome in LBBB (HR 0.96, p = 0.83) or RBBB (HR 0.61, p = 0.24; 28 events, hypothesis-generating). Amiodarone was associated with the composite (LBBB: HR 3.63, p < 0.01; RBBB HR: 3.90, p < 0.01), but not the LBBB sensitivity analysis (HR 1.61, p = 0.19), suggesting confounding by indication. Among patients with QTc >500 ms, common agents remained non-significant. Common non-cardiac QT-prolonging medications were not associated with increased risk in patients with BBB, even with prolonged QTc. The divergence between composite and sensitivity results for amiodarone highlights the influence of confounding by indication. Medication alerts should incorporate stratification by drug class rather than QTc alone.

PMID 42697068
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