DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for dilated cardiomyopathy 1W — 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 1W 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 1w 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
vinculin (VCL) — VCL 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 adpdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 6UPW · 2.9 Å · ligand ADENOSINE-5'-DIPHOSPHATE (ADP). Experimental structure, not a prediction.
What the evidence adds up to
In a 1994 follow-up of 235 patients aged 16–70 enrolled from 1978 to 1992, two-year and four-year survival for dilated cardiomyopathy improved across three consecutive five-year periods. Group 1 (1978–1982, 26 patients) had 73.8% and 53.8% survival; group 2 (1983–1987, 65 patients) had 87.7% and 72.3%; group 3 (1988–1992, 144 patients) had 90.3% and 82.9% (P = 0.02). Patients in later groups were younger and less severely affected, but the survival improvement remained significant after stratification for disease severity, suggesting treatment effects. A progressively higher proportion received ACE inhibitors and later beta blockers. In group 2, patients treated with ACE inhibitors showed better survival than those not treated, after stratification for heart failure severity. In group 3, beta blockers had a significant additive effect with conventional therapy: four-year survival in mild and moderate-to-severe heart failure patients treated with beta blockers, usually with digitalis and ACE inhibitors, was 90% and 87.5% respectively.
A 1989 review states that the natural history of dilated cardiomyopathy varies from death within two years in 50% of patients to survival beyond ten years in 25%. The incidence was reported as at least 11,000 new cases per year in the United States. Traditional therapy at that time included cardiac glycosides and diuretics. The same review notes that immunosuppression was being considered, but no efficacy data from that paper are provided here.
By 2016, causative genetic mutations had been identified in more than 40 genes encoding proteins of different cellular structures and pathways. A 2025 review lists genes encoding contractile proteins and regulatory elements in sarcomeres, Z-disks, cytoskeletons, desmosomes, and ion channels. It describes specific forms such as desmosomal-dependent cardiomyopathy, desmoplakin cardiomyopathy, and RBM20 cardiomyopathy, and argues for introducing genetic testing into clinical practice for personalised management and pre-nosological risk identification in family members.
What is still missing is a prospective trial that stratifies patients by the specific genetic mutations now known to underlie the disease, rather than by clinical severity alone. The 1994 survival data are observational and from a single centre; the genetic reviews do not provide outcome data linking genotype to treatment response. Money is needed for genotype-stratified randomised trials, and for the development of therapies targeting the specific pathways identified in the genetic studies.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Heart · 1994 · 76 citations · open access
Changing mortality in dilated cardiomyopathy
AbstractOBJECTIVE: To analyse the changes in mortality in dilated cardiomyopathy over the past 15 years and to identify the factors that might have influenced survival. DESIGN: Follow up study of 235 patients (aged 16-70) systematically enrolled on a register from 1 January 1978 to 31 December 1992. SETTING: Hospital department of cardiology. PATIENTS: Three groups corresponding to three periods of 5 years: group 1 (diagnosis between 1 January 1978 and 31 December 1982) 26 patients; group 2 (diagnosis between 1 January 1983 and 31 December 1987) 65 patients; and group 3 (diagnosis between 1 January 1988 and 31 December 1992) 144 patients. MAIN OUTCOME MEASURES: Death or heart transplantation. RESULTS: Two and four year survival was 73.8% and 53.8% in group 1, 87.7% and 72.3% in group 2, and 90.3% and 82.9% in group 3 (P = 0.02). During the 15 years of the study period the number of cases increased progressively and the baseline clinical characteristics changed (that is, patients were younger and less severely affected), partly explaining the improvement in survival. None the less, the three mortality curves tended to diverge progressively and the improvement in survival in the different groups was still significant after stratification for the severity of the disease, suggesting that treatment had a sustained effect. A progressively higher proportion of patients were treated with angiotensin converting enzyme (ACE) inhibitors and more recently with beta blockers. In group 2, after stratification for the severity of heart failure, patients who were treated with ACE inhibitors showed a better survival than patients who were not. Furthermore, analysis of group 3 showed that beta blockers had a significant additive effect with conventional therapy both by intention to treat and actual treatment. Four year survival in patients with mild and moderate to severe heart failure treated with beta blockers, and usually digitalis and ACE inhibitors, was respectively 90% and 87.5%. CONCLUSIONS: The improvement in the survival of patients with dilated cardiomyopathy over the past 15 years may be explained by earlier diagnosis, new treatments, and a change in the clinical characteristics of the patients at enrolment.
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.
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 . . .
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.
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