DeCure for Familial isolated arrhythmogenic ventricular dysplasia, biventricular form
DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for familial isolated arrhythmogenic ventricular dysplasia, biventricular form — screening already-approved drugs against its 12-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleFamilial isolated arrhythmogenic ventricular dysplasia, biventricular form maps to a 12-gene Open Targets module — the target space DeCure's AI scientist screens approved drugs against.
DeCure.ai methodSignature reversal (LINCS) plus network proximity (STRING) rank already-approved drugs likely to perturb this module — the same engine that produces DeCure.ai's repurposing hypotheses.
Repurposing thesisScreening approved medicines against this disease module, then publishing the evidence for the strongest candidate. Known pharmacology and human exposure data make the first question sharper — they do not establish safety or efficacy in a new indication.
Research record
01
ResearchComing soon
Candidate research + dossier — target rationale, drug-repurposing thesis and evidence pack.proof: Published dossier + on-chain hash
02
ValidationComing soon
In-vitro biological validation at a contract research org (CRO).proof: CRO contract + in-vitro report
03
Peer review & paperComing soon
Peer-reviewed paper published open-access (preprint + journal).proof: DOI + open-access link + on-chain hash
Current lead
No approved-drug candidate for familial isolated arrhythmogenic ventricular dysplasia, biventricular form is corroborated in the literature DeepSearch retrieved. Some conditions are managed with non-pharmacological care — a device, surgery or physical therapy — rather than a medicine; that may be the case here, or the literature we found may simply be too sparse yet to support a drug-repurposing angle.
Molecular view
LIM domain binding 3 (LDB3) — LDB3 is one of the genes genetically linked to this disease in Open Targets — shown as context, not as a drug target we're pursuing: no approved-drug candidate for this disease is yet corroborated in the literature we found.
Loading structure…
helix sheet gludrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 4YDP · 1.4 Å · ligand GLUTAMIC ACID (GLU). Experimental structure, not a prediction.
What the evidence adds up to
Arrhythmogenic right ventricular dysplasia is described in a 1995 review as a relatively newly recognised clinical entity increasingly identified as a cause of unexpected sudden death in young adults, with or without preceding cardiac symptoms. Familial cases suggest a genetic transmission, and a location on chromosome 14 is implicated. In some patients a superimposed inflammatory process may explain progressive deterioration of left ventricular function. The review states that antiarrhythmic drugs are the first line of therapy and are effective in most cases, with ablative techniques, implantable defibrillators, and heart transplantation used in the most severe examples. A 2003 case report describes a 42-year-old woman resuscitated from ventricular fibrillation whose nephew had died of sudden cardiac death at age 25. Her ECG showed right precordial T wave inversion; echocardiography and angiography revealed inferior wall akinesia of the right ventricle with normal left ventricular function. Endomyocardial biopsy showed focal fibrous infiltration. Ventricular fibrillation could not be reproduced by programmed stimulation. An implantable cardioverter defibrillator (ICD) was placed, and within six months the ICD memory showed no evidence of ventricular fibrillation. The report concludes that concealed arrhythmogenesis as an early manifestation is difficult to detect.
A 2015 lecture summary reviews history, mechanisms, and pathogenesis of arrhythmogenic right ventricular dysplasia, focusing on electrophysiological changes and how this knowledge has modified clinical care, but provides no new efficacy data for any drug or intervention.
No abstract in this set reports a controlled trial of any drug for this condition. The 1995 claim that antiarrhythmic drugs are effective in most cases is not supported by any numerical data on response rates, survival, or sample sizes. The 2003 case report involves a single patient and an ICD, not a drug. What is still missing are prospective, randomised trials of any pharmacological therapy for arrhythmogenic right ventricular dysplasia, particularly for the biventricular familial form, with clearly defined endpoints such as arrhythmia burden, progression to heart failure, or mortality. Patient stratification by genetic subtype and disease stage also remains unaddressed.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Current Opinion in Cardiology · 1995 · 34 citations
Arrhythmogenic right ventricular dysplasia
AbstractArrhythmogenic right ventricular dysplasia is a relatively newly described clinical entity that is more and more frequently recognized. It may explain an increasing number of unexpected, sudden deaths in young adults that are or are not preceded by cardiac symptoms. A genetic transmission of the disease has been suggested by the study of familial cases. A location on chromosome 14 appears to be responsible for this disease. In some patients, a superimposed inflammatory process mixed with the pattern of arrhythmogenic right ventricular dysplasia may explain the progressive deterioration of left ventricular function. The systematic study of electrocardiograms demonstrates prolongation of the QRS complex and repolarization abnormalities in the right precordial leads due to a parietal block. Multiple therapeutic approaches are now available. The first line of therapy remains antiarrhythmic drugs, which are effective in most cases. Ablative techniques, implantable defibrillators, and heart transplantation have been used in the most severe examples of the disease.
Newer Diagnostic and Treatment Options for Patients With ARVC
AbstractThe Intercontinental Lecture, presented by Dr Melvin M. Scheinman, discusses arrhythmogenic right ventricular dysplasia (ARVC). The presenter reviews the history, mechanisms, and pathogenesis of ARVC, with a focus on electrophysiological changes, and then discusses how this new knowledge has modified the clinical approach to the care of this disease.
DMW - Deutsche Medizinische Wochenschrift · 2003 · 0 citations
Arrhythmogene rechtsventrikuläre Dysplasie als Ursache eines überlebten plötzlichen Herztodes
AbstractHISTORY: A 42 year old woman was resuscitated from ventricular fibrillation. 5 months previously she had a syncope. Her nephew had died of sudden cardiac death at the age of 25 years. INVESTIGATIONS: There was no evidence for ST segment elevation, myocardial infarction or pulmonary embolism. The ECG showed right precordial T wave inversion. Coronary artery disease was excluded angiographically. Echocardiography and angiography revealed inferior wall akinesia of the right ventricle with normal left ventricular function and chamber size. Ventricular fibrillation could not be reproduced by programmed stimulation of the right ventricle during an electrophysiologic study. Results of endomyocardial biopsy of the right ventricle showed a focal fibrous infiltration of the myocardium. Magnetic resonance imaging confirmed inferior wall abnormalities of the right ventricle without typical fatty infiltration in the right ventricular myocardium. CLINICAL COURSE: The patient recovered rapidly without neurologic deficits. Arrhythmogenic right ventricular dysplasia was suspected, and a cardioverter defibrillator (ICD) was implanted. Within 6 months after implantation the ICD memory showed no evidence of ventricular fibrillation. CONCLUSION: Arrhythmogenic right ventricular dysplasia is an important cause of ventricular fibrillation with a potential risk of sudden cardiac death in young persons. Concealed arrhythmogenesis as an early manifestation of right ventricular dysplasia is difficult to detect.
Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.
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