DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for dilated cardiomyopathy 1G — screening already-approved drugs against its 4-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 1G maps to a 4-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 1g 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
desmoplakin (DSP) — DSP 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 4s,5sdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 3R6N · 2.95 Å · ligand (4S,5S)-1,2-DITHIANE-4,5-DIOL (D1D). Experimental structure, not a prediction.
What the evidence adds up to
Dilated cardiomyopathy is defined by ventricular dilation and progressive systolic dysfunction in the absence of coronary, valvular, or pericardial disease. The right ventricle is often involved. More than 40 causative genes have been identified, encoding proteins of sarcomeres, Z-disks, cytoskeletons, desmosomes, and ion channels. Pathogenic variants in these genes are linked to the initiation, clinical manifestation, arrhythmic complications, and progression of heart failure. Specific genetic forms now recognised include desmosomal-dependent cardiomyopathy, desmoplakin cardiomyopathy, and RBM20 cardiomyopathy.
The natural history of the disease varies widely. In 1989, 50 percent of afflicted patients progressed to death within 2 years, while 25 percent survived more than 10 years. In the United States at that time, at least 11,000 new cases were diagnosed each year, and up to 10,000 deaths annually were attributed to cardiomyopathy, 80 percent of which were the dilated form. Traditional therapy then consisted of cardiac glycosides and diuretics. No immunosuppressive treatment is supported by the abstracts.
The abstracts provide no data from controlled trials of any drug for dilated cardiomyopathy. No response rates, survival improvements, or adverse event rates are reported for any pharmacological intervention beyond the traditional glycosides and diuretics mentioned in passing. The 2025 review argues for wider genetic testing to enable personalised management and pre-nosological identification of family members at risk, but it does not report any therapeutic trial results.
What is still missing is any randomised controlled trial testing a repurposed drug specifically in dilated cardiomyopathy, particularly with genetic stratification. The field lacks funding for such trials, a standardised approach to patient stratification by genotype, and prospective data linking specific mutations to drug response. Without these, the genetic knowledge remains descriptive rather than actionable.
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 . . .
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.
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.
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.
