DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for dilated cardiomyopathy 1E — 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 1E 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 1e 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
sodium voltage-gated channel alpha subunit 5 (SCN5A) — SCN5A 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 qdndrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 6LQA · 3.3 Å · ligand Quinidine (QDN). Experimental structure, not a prediction.
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. Causative genetic mutations have been identified in more than 40 genes, and a great diversity of pathways has been implied in the pathogenesis depending on the affected genes. Once dilated cardiomyopathy is discovered, a careful history and laboratory tests may reveal a potential toxic cause. The heterogeneity in etiology and clinical presentation makes timely diagnosis and treatment challenging.
The natural history of the disease varies from a course progressing to death within 2 years in 50 percent of afflicted patients to survival for more than 10 years in 25 percent. The incidence is increasing, with at least 11,000 new cases diagnosed each year in the United States. In India, a new case of heart failure is diagnosed every 23 seconds. Even after diagnosis, only 25 to 40 percent of patients receive guideline-directed medical therapy.
The traditional approach to therapy includes cardiac glycosides and diuretics. No abstract in this set reports any drug repurposing trial, any survival benefit from a specific drug, or any response rate for a repurposed agent in dilated cardiomyopathy. The 1989 abstract mentions immunosuppression only in its title and does not provide any efficacy data.
What is still missing is any randomised trial testing a repurposed drug specifically for dilated cardiomyopathy, adequate funding for such trials, and a method to stratify patients by the specific genetic or toxic cause of their disease. Without that, the evidence base remains limited to general heart failure management.
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.
AbstractDilated cardiomyopathy is defined by the presence of left ventricular dilatation and contractile dysfunction in the absence of abnormal loading conditions and severe coronary artery disease. Once dilated cardiomyopathy is discovered, a careful and detailed history with laboratory tests may reveal a potential toxic cause. In this article, we present the case of a patient with suspected toxic dilated cardiomyopathy, and then discuss the common causes and treatment of toxic dilated cardiomyopathy.
Family Medicine · 2019 · 0 citations · open access
Clinical Case of Dysmetabolic Cardiomyopathy in the Practice of a Family Doctor
AbstractThe article highlights the classification of dilated cardiomyopathy, the etiological factors responsible for the occurrence of this pathology, modern principles of diagnosis and treatment of dysmetabolic cardiomyopathy as one of the types of dilated cardiomyopathy. Clinical and main instrumental diagnostic methods are presented, a clinical case of dysmetabolic cardiomyopathy is considered.
AbstractPreviewThe recognition that distinctive pathophysiologies are involved in the three types of cardiomyopathy and that the clinical and laboratory findings of each type are unique has provided new directions in treatment. Part 1 of this two-part article presents an overview of cardiomyopathy and describes the features, diagnosis, and treatment of dilated (congestive) cardiomyopathy. Part 2, beginning on page 95, continues with a discussion of hypertrophic and restrictive/obliterative cardiomyopathies.
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.
