DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for dilated cardiomyopathy 2A — screening already-approved drugs against its 1-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleDilated cardiomyopathy 2A maps to a 1-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 dilated cardiomyopathy 2a 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.
What the evidence adds up to
Idiopathic dilated cardiomyopathy remains a condition whose origins are not fully understood, and clinicians continue to face challenges in identifying and treating its causes to improve symptoms and survival. A 2002 review describes the then-current diagnostic and therapeutic options and treatment goals, but offers no specific drug or trial data. By 2016, causative genetic mutations had been identified in more than 40 genes encoding proteins from different cellular structures and pathways, with ventricular dilation and progressive systolic dysfunction as the hallmark features. The 2025 review lists genes encoding contractile proteins, regulatory elements in sarcomeres, Z-disks, cytoskeletons, desmosomes, and ion channels, and notes that pathogenic variants are linked to disease onset, structural myocardial disorders, arrhythmogenic complications, and progression of heart failure. New terms such as desmosomal-dependent cardiomyopathy, desmoplakin cardiomyopathy, and RBM20 cardiomyopathy have been proposed.
No abstract reports a clinical trial, a repurposed drug, or any quantitative outcome such as survival or response rates. The 2025 review argues for further introduction of genetic testing into clinical practice for personalised management and pre-nosological risk identification in family members, but it does not describe any therapeutic intervention. The 2002 and 2016 papers are reviews that summarise existing knowledge without presenting new experimental data.
What is still missing is any randomised trial testing a specific drug in dilated cardiomyopathy 2A, any patient stratification by the genetic subtypes now recognised, and the funding to conduct such studies. The genetic heterogeneity described in the abstracts suggests that a single treatment is unlikely to work for all patients, but no abstract provides evidence for any drug at all.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Cleveland Clinic Journal of Medicine · 2002 · 44 citations
Idiopathic dilated cardiomyopathy: a common but mystifying cause of heart failure.
AbstractWhile researchers try to elucidate the origins of idiopathic dilated cardiomyopathy, clinicians continue to face the challenges of identifying and treating the causes of this condition to improve symptoms and survival. We review classification schemes for dilated cardiomyopathy and the current range of diagnostic and therapeutic options and treatment goals.
Journal of Cardiovascular Medicine · 2016 · 15 citations
Genetic bases of dilated cardiomyopathy
AbstractCardiomyopathies represent a wide and heterogeneous group of diseases wherein a genetic cause has been consistently identified.Dilated cardiomyopathy (DCM) is characterized by ventricular dilation and progressive systolic dysfunction, and it is the most common form of cardiomyopathy.Causative genetic mutations have been identified in more than 40 genes encoding proteins belonging to different cellular structures and pathways.A great diversity of pathways has been implied in the pathogenesis of DCM, depending on the affected genes and on the dislodged intracellular structures or mechanisms.This review describes the major genes and focus on the pathophysiologic mechanisms of DCM, with a special consideration of the most recent discoveries in the field.
Current Opinion in Cardiology · 1991 · 1 citations
Dilated cardiomyopathy
AbstractDilated cardiomyopathy is the most common form of cardiomyopathy and is anatomically defined by large atrial and ventricular chambers, thin or normal myocardial walls, and poor systolic function. In the United States, up to 10,000 deaths every year have been determined to be secondary to cardiomyopathy, and of these 80% were due to the dilated form of the disease. This review describes recent advances of DCM, which can be grouped into the following headings: 1)etiologies and mechanisms of disease; 2) pathophysiology of the dilated heart; 3) diagnostic approaches; 4) clinical findings and prognosis; and 5) therapy.
Clinical and genetic heterogeneity of dilated cardiomyophathy. Review
AbstractThis article contains an overview of published scientific sources from the MEDLINE database on the PubMed, Web of Science, Scopus platforms regarding the dilated cardiomyopathy with an emphasis on clinical and genetic aspects. Taking into account the etiological origins, various classification categories of myocardial damages are presented — non‑syndromic, acquired (secondary), syndromic cardiomyopathies. The modern definition of dilated cardiomyophaty is presented in accordance with the recommendations of international experts. The review focuses on cardiomyocyte components that are important for energy generation and transmission, mechanical and signaling functions, and maintenance of electrolyte homeostasis. A list of genes encoding contractile proteins and their regulatory elements in components of sarcomeres, Z‑disks, cytoskeletons, desmosomes, and ion channels of cardiomyocytes is provided. The role of pathogenic gene variants associated with mechanisms contributing to the initiation, clinical manifestation, and prognosis of dilated cardiomyopathy is summarized. The causal relationships of mutations in the relevant genes with various clinical scenarios of dilated cardiomyopathy are shown: onset of the diseases, structural myocardial disorders, arrhythmogenic complications, and progression of heart failure. Genetic analysis has become a stimulus for enriching the classification spectrum of cardiomyopathies through the creation of new terms. Specific forms of cardiomyophaties include desmosomal‑dependent cardiomyophathy, desmoplakin cardiomyophathy, RBM20 cardiomyophathy, and others. The argumentation for the further introduction of genetic testing into clinical practice is underlined for the purpose of personalized management of patients with cardiomyopathies and timely identification of risk factors for the disease in their family members at the pre‑nosological stage.
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.
DeCure is a research and publication project, not medical advice and not a treatment. "DeCure for X" describes a research goal, not a claim that a cure exists. Backing a cure is a contribution to fund the research — it is not an investment, and confers no yield, royalty, equity or IP ownership. Papers are published open-access by the DeCure.ai DAO.
