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disopyramide (Disopyramide Dumles / Dirythmin SA / Dirytmin)

✓ Approved

AstraZeneca UK Limited · SCN5A · Small Molecule

What is disopyramide?

disopyramide is a small molecule developed by AstraZeneca UK Limited. It is approved for therapeutic indications via unknown.

Drug Profile

Brand NamesDisopyramide Dumles, Dirythmin SA, Dirytmin
CompanyAstraZeneca UK Limited
Drug ClassSmall Molecule
Molecular TargetSCN5A
RouteUnknown
StatusApproved

Mechanism of Action

Molecular Targets

disopyramide acts on 1 molecular target:

SCN5Asodium voltage-gated channel alpha subunit 5 (CMD1E, SSS1)
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Therapeutic Indications

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

Therapeutic AreaConditionPhase
Cardiac disordersArrhythmia✓ Approved

Related Research Articles

PubMedAmerican heart journal plus : cardiology research and practice2026-07-12

Ice-cold beer-triggered swallow syncope with reproducible supra-Hisian AV block documented by intracardiac recordings.

Sato Daisuke D, Uchimura Kumi K, Katashima Takashi T, Matsui Yumie Y et al.

Swallow syncope is a rare situational syncope caused by an exaggerated vagal reflex and may result in bradyarrhythmia or atrioventricular block. A 63-year-old man with recurrent syncope triggered by beer ingestion underwent cardiovascular, gastrointestinal, ambulatory electrocardiographic, and electrophysiological evaluation, including provocation testing. Only ice-cold beer reproducibly induced transient AH block. Other foods and beverages, including cold soda, cold sake, and room-temperature beer, were negative. Ambulatory monitoring documented a symptomatic 7.9-second pause. Disopyramide was ineffective. Permanent pacemaker implantation prevented recurrent symptoms despite repeat provocation. This case highlights a highly specific trigger for swallow syncope and the diagnostic value of targeted provocation testing.

PubMedIndian heart journal2026-06-19

Medical management of hypertrophic cardiomyopathy.

Gupta Mohit D MD, Goel Vrinda V, Girish M P MP

Hypertrophic cardiomyopathy (HCM) is a genetically determined myocardial disease in which symptoms are driven not simply by ventricular hypertrophy, but by a combination of dynamic left ventricular outflow tract obstruction (LVOTO), impaired diastolic filling and other factors.The therapy for HCM differs fundamentally from routine heart failure management and must be mechanism based. In obstructive HCM, the pharmacologic objective is to blunt hypercontractility, lengthen diastole, preserve loading conditions, and reduce the LVOT gradient. In non-obstructive HCM, management is focused on symptom control, heart-rate moderation, careful volume management, and treatment of arrhythmias and congestion. Non-vasodilating beta-blockers, non-dihydropyridine calcium-channel blockers, and disopyramide have constituted the foundation of medical therapy. The contemporary era has added sarcomere-directed treatment with cardiac myosin inhibitors, particularly mavacamten and aficamten, The present review provides a pragmatic algorithm for publication-level clinical use in contemporary practice.

PubMedJournal of clinical medicine2026-06-12

Use of Disopyramide in Obstructive Hypertrophic Cardiomyopathy: A European Insight.

Charron Philippe P, Osman Faizel F, Trochu Jean-Noel JN, Zema Carla C et al.

Background/Objectives: Guidelines for obstructive hypertrophic cardiomyopathy (HCM) recommend treatment with disopyramide as an add-on to beta-blockers or calcium-channel blockers when symptoms persist. Data pertaining to effective disopyramide use in practice beyond single-center experience are very limited. This study aimed to quantify disopyramide use in patients with obstructive HCM in England, France and Germany, before the availability of cardiac myosin inhibitors. Methods: This retrospective study used nationally representative databases from England (Clinical Practice Research Datalink and Hospital Episode Statistics, 2010-2019), France (National Healthcare Data System, 2012-2019) and Germany (German statutory health insurance, 2011-2019). Adults (18+) with obstructive HCM were included, based on diagnostic codes for obstructive HCM or any HCM with septal reduction therapy. Disopyramide usage was defined as ≥1 prescription for a patient in a calendar year. Results: Overall, 3730, 6823 and 1141 patients diagnosed with obstructive HCM were identified in the English, French and German databases, respectively. In England, disopyramide use ranged from 4.7% to 5.6% per year with use generally stable over time. The equivalent usage for France was 1.7% to 2.6% per year. As expected, no recorded reimbursed use was reported in Germany during the study period. Conclusions: Disopyramide use is very low in patients with obstructive HCM, possibly due to treatment-related issues, availability or lack of reimbursement. These barriers may drive the uptake of alternative guideline recommended therapies for obstructive HCM treatment.

PubMedArchives of gerontology and geriatrics2026-06-07

Microglial PICALM: A novel genetic driver and therapeutic target in vascular dementia.

Chai Zhaohui Z, Xu Qiuhan Q, Cheng Dan D, Zhang Yuning Y et al.

Vascular dementia (VaD) lacks well-defined genetic mechanisms. Cell-type-specific effects of GWAS loci remain unexplored. We integrated single‑cell eQTL data (183 donors, eight cell types) with VaD GWAS (3624 cases, 475,484 controls) using Mendelian randomization and Bayesian colocalization, replicated in an independent cohort (2074 cases, 456,366 controls). Subtype, snRNA‑seq, cell‑cell communication, PheWAS, expression profiling, and drug prediction with BBB permeability assessment were performed. Microglial PICALM was the only robustly replicated signal (OR = 0.8334, p = 5.3 × 10⁻⁴; colocalization PP.H4 > 0.75). The effect was strongest in multiple infarctions dementia (OR = 0.7746). Exploratory snRNA-seq analysis (4 VaD vs. 4 controls; GSE282111) provided supporting evidence for microglial PICALM enrichment and downregulation (p < 0.001). PICALM‑high microglia showed enhanced neurovascular‑ and phagocytosis‑related communication (e.g., SPP1, GAS6, GRN). PheWAS revealed no pleiotropy. In silico drug repurposing prioritised three FDA-approved BBB-penetrant compounds (disopyramide, benzocaine, amantadine) as candidates warranting further mechanistic validation. Microglial PICALM is identified as a likely genetic determinant of VaD, especially in the multiple infarctions subtype. Upregulating PICALM may be associated with a neuroprotective microglial phenotype, highlighting PICALM as a candidate therapeutic target warranting further experimental validation.

PubMedJRSM cardiovascular disease2026-05-29

Pharmacologic therapies for hypertrophic cardiomyopathy: The past, the present, and the future.

Halațiu Vasile-Bogdan VB, Cozac Dan Alexandru DA, Scridon Alina A

Hypertrophic cardiomyopathy (HCM) stands as the most common monogenic cardiac disease, with an estimated prevalence historically reported as 1:500, but likely closer to 1:200 based on contemporary population studies in the general population. The past decade has marked a fundamental shift in therapeutic strategy: from symptomatic relief toward interventions directly targeting pathological sarcomeric hypercontractility. Conventional therapy relies on beta-blockers and non-dihydropyridine calcium channel antagonists, which provide symptomatic benefits through negative inotropic effects. For refractory left ventricular outflow tract obstruction, disopyramide constitutes an effective third-line option, although its anticholinergic profile requires cautious administration. Cardiac myosin inhibitors, mavacamten and aficamten, have introduced a novel therapeutic paradigm through direct modulation of actin-myosin cross-bridge formation. Pivotal clinical trials have demonstrated significant improvements in exercise capacity, reduction in obstruction severity, and enhancement of functional status, validating for the first time a therapeutic strategy that directly targets the underlying sarcomeric mechanism of hypercontractility. The therapeutic horizon includes next-generation myosin modulators, metabolic pathway interventions, and gene-based strategies. Current challenges involve accessibility to these therapies, substantial costs, and the requirement for mandatory regular echocardiographic monitoring. Future perspectives are oriented toward precision personalized medicine, integrating molecular therapeutics with genetic profiling to enable increasingly individualized risk stratification and therapeutic decision making.

PubMedClinical toxicology (Philadelphia, Pa.)2026-03-30

Recommendations from the Clinical Toxicology Recommendations Collaborative on the administration of activated charcoal in acute oral overdose.

Hoegberg Lotte C G LCG, Gosselin Sophie S, Buckley Nicholas A NA, Wood David M DM et al.

The Clinical Toxicology Recommendations Collaborative was established by three international clinical toxicology societies and tasked to produce recommendations on the management of poisonings. The Activated Charcoal in Clinical Toxicology Workgroup (the Workgroup) was formed to provide recommendations on the administration of activated charcoal for gastrointestinal decontamination and enhanced elimination in poisoning. Based on a systematic review of the literature, 43 poisons or poison categories were selected for appraisal. Voting statements were drafted using a predetermined format. Strength of consensus was measured using the Disagreement Index as defined by the RAND/University of California at Los Angeles Appropriateness Method. A two-round modified Delphi method was used to reach expert consensus. The Workgroup concluded that there is no role for activated charcoal in poisoning from arsenic, caesium, copper, ethanol, methanol, ethylene glycol, iron, lead, lithium, and metformin. Activated charcoal is appropriate after ingestion of antidysrhythmics (types I and III not discussed specifically), beta-adrenergic antagonists, bupropion, calcium-channel blockers, carbamazepine, cardiac glycosides, chloroquine, cocaine, colchicine, cyanide, dapsone, diphenhydramine, disopyramide, factor Xa inhibitors, ibuprofen, isoniazid, lamotrigine, methotrexate, moclobemide, opioids, organophosphorus insecticides, paracetamol (acetaminophen), paraquat, phenobarbital, phenytoin, quinidine and quinine, salicylates, selective serotonin reuptake inhibitors, sulfonylureas, thallium, theophylline, tricyclic antidepressants, valproic acid, venlafaxine, and warfarin. An additional dose of activated charcoal to complete gastrointestinal decontamination is appropriate after ingestion of carbamazepine, paracetamol, paraquat, phenobarbital, salicylates, thallium, theophylline, valproic acid and verapamil. The maximum time post-ingestion for which activated charcoal administration is recommended differs for each poison and different formulations. According to an individualized risk assessment, activated charcoal is appropriate up to 6 h post-ingestion for many poisons. If ongoing absorption is suspected, which may occur, for example, with pharmacobezoar formation, certain modified-release preparations, or when drug burden exceeds the limits of solubility, then activated charcoal can be administered beyond 6 h post-ingestion for gastrointestinal decontamination. Multiple-dose activated charcoal for enhanced elimination is appropriate in poisoning with carbamazepine, cardiac glycosides, colchicine, dapsone, phenobarbital, phenytoin, thallium and theophylline. Before deciding to perform endotracheal intubation to assist with the administration of activated charcoal, every clinician needs to weigh the potential complications and adverse effects of this procedure against the toxicity expected to be prevented by the administration of activated charcoal. This is a challenging decision, and a local poison centre and/or a bedside toxicology consultation can assist with this decision. Endotracheal intubation is not a benign procedure and is associated with a high rate of various adverse events, such as new haemodynamic instability, severe hypoxaemia, and cardiac arrest, which seem more common in children. In three studies that evaluated the risks of endotracheal intubation in over 2,200 poisoned patients, the rates of hypotension were between 1.5% and 11.8%, desaturation between 3.4% and 7.1%, and cardiac arrest in 0.4%. The risk of aspiration following administration of activated charcoal after endotracheal intubation is reported to be low (1-4%). Therefore, the decision to endotracheally intubate a patient to administer activated charcoal needs to carefully assess the patient's other comorbidities and the expected toxicity of the ingestion, which needs to be clinically significant to outweigh the risk of endotracheal intubation. Endotracheal intubation may also be considered if another treatment, such as haemodialysis or extracorporeal circulation, might be required or for transportation to another institution for ongoing clinical care. In these situations, for which endotracheal intubation has been performed for another indication, the risk-benefit will change in favour of activated charcoal administration. The following good practice statements were adopted to address the use of endotracheal intubation to facilitate the administration of activated charcoal. Endotracheal intubation should not be performed solely for the purpose of administration of activated charcoal in patients not anticipated to develop clinically significant complications of poisoning.In patients in whom endotracheal intubation is clinically indicated (e.g., compromised or unprotected airway, respiratory failure, significantly diminished level of consciousness, refractory seizures, hemodynamic instability), insertion of a nasogastric or orogastric tube is reasonable to facilitate gastrointestinal decontamination with activated charcoal.In patients with a clinically significant risk of developing life-threatening toxicity, endotracheal intubation is reasonable to safely facilitate gastrointestinal decontamination, especially if other treatment options are nonexistent or unavailable.Use of nasogastric or orogastric tube insertion without endotracheal intubation to facilitate the administration of activated charcoal: The following good practice statement was adopted: Nasogastric or orogastric tube insertion without endotracheal intubation should not be performed solely for the purpose of administration of AC. The decision to use activated charcoal is complex and depends primarily on the nature of the poison(s), the time since ingestion, the severity of the symptoms present at the time of decision or expected based on the dose ingested or patient comorbidities, and the availability of antidotes or other treatments. Although the existing level of evidence is primarily of low or very low quality, clinical decisions are still necessary. The Workgroup recommends the administration of a single-dose of activated charcoal beyond the traditional 1 h post-ingestion time point in selected poisons and introduces the concept of an additional dose of activated charcoal to prevent further absorption of poisons that may remain in the gastrointestinal tract for prolonged periods of time. Multiple-dose activated charcoal is also recommended to enhance elimination in selected clinical scenarios.

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