DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for dilated cardiomyopathy 2B — 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 2B 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 2b 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
Dilated cardiomyopathy is defined by left ventricular dilatation and systolic dysfunction with normal wall thickness, in the absence of coronary artery, valvular, or pericardial disease. The right ventricle is often involved. Causative genetic mutations have been identified in more than 40 genes encoding proteins of sarcomeres, Z‑disks, cytoskeletons, desmosomes, and ion channels. The 1989 abstract reports that the natural history varies from progression to death within 2 years in 50 percent of patients to survival for more than 10 years in 25 percent. A 2023 abstract notes that only 25%–40% of diagnosed patients receive guideline-directed medical therapy.
No drug treatment is tested in any of these abstracts. The 1989 paper mentions only the traditional approach of cardiac glycosides and diuretics, and then discusses immunosuppression without presenting trial data. The 2016 and 2025 reviews describe genetic and pathophysiologic mechanisms but do not report any interventional study. The 2023 paper states that heterogeneity in etiology and clinical presentation makes timely diagnosis and treatment challenging, but provides no new treatment results.
The 2025 review argues for further introduction of genetic testing into clinical practice for personalised management and pre-nosological risk identification in family members. It lists specific genetic forms such as desmosomal-dependent cardiomyopathy, desmoplakin cardiomyopathy, and RBM20 cardiomyopathy. No survival benefit, response rate, or any quantitative outcome from a drug trial is reported in any of these abstracts.
What is still missing is any randomised controlled trial testing a specific drug in dilated cardiomyopathy 2B, a clear patient stratification method that accounts for the genetic heterogeneity described, and funding to move from genetic characterisation to interventional studies. The 2023 observation that only a minority of patients receive guideline-directed therapy also points to a gap in implementation, not just discovery.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
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.
New England Journal of Medicine · 1989 · 10 citations
Immunosuppression for Dilated Cardiomyopathy
AbstractThe diagnosis of dilated cardiomyopathy is made when left ventricular dilatation and systolic dysfunction, with normal wall thickness, occur in the absence of coronary artery, valvular, or pericardial disease.1 The right ventricle is also often involved. The natural history of the disease varies from a course progressing to death within 2 years in 50 percent of afflicted patients2 to survival for more than 10 years in 25 percent. The incidence of dilated cardiomyopathy is increasing; at least 11,000 new cases are diagnosed each year in the United States. The traditional approach to therapy includes cardiac glycosides and diuretics. Although increased . . .
Heart failure journal of India · 2023 · 0 citations · open access
Management of non-ischemic dilated cardiomyopathy
AbstractHeart failure (HF) remains a leading cause of morbidity and mortality globally. For every 23 s, a new case of HF is diagnosed in India. Dilated cardiomyopathy is characterized by dilatation of the left ventricle or both ventricles with impaired function, which cannot be fully explained by abnormal loading conditions or coronary artery disease. The heterogeneity in etiology and clinical presentation of dilated cardiomyopathy makes timely diagnosis and treatment challenging. Even after diagnosis, only 25%–40% receive guideline-directed medical 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.
