DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for hypertrophic cardiomyopathy 15 — 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 moduleHypertrophic cardiomyopathy 15 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 hypertrophic cardiomyopathy 15 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.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
European Heart Journal · 1997 · 104 citations
Induction of subaortic septal ischaemia to reduce obstruction in hypertrophic obstructive cardiomyopathy: Studies to develop a new catheter-based concept of treatment
AbstractAIM: To develop a new catheter-based method of treatment in patients with hypertrophic obstructive cardiomyopathy. METHOD: Does abolition of the blood supply to the subaortic part of the septum lead to regional myocardial ischaemia and a decrease in the left ventricular outflow tract gradient? To find this out, in 10 consecutive patients the first larger septal branch of the left anterior descending coronary artery was temporarily occluded with conventional percutaneous transluminal coronary angioplasty. The intracoronary electrocardiogram was registered for objective verification of the intended ischaemia. The intraventricular pressure was measured at rest and at the post extrasystolic beat under programmed electrostimulation of the right ventricle. RESULTS: During occlusion, regional ischaemia was observed in all patients. Simultaneously, there was a significant reduction of the intraventricular gradient from 56.2 mmHg to 32.2 mmHg (P < 0.05) followed by an increase from 32.2 mmHg to 61.1 mmHg (P < 0.01) after release of occlusion of the septal branch. During ischaemia there was no increase in left ventricular end-diastolic pressure. CONCLUSION: We conclude that the results form the basis for a new catheter interventional therapy in hypertrophic obstructive cardiomyopathy.
Genetic Mutations and Mitochondrial Dysfunction as Modulating Factors in Hypertrophic Cardiomyopathy: An Updated Scoping Review
AbstractHypertrophic cardiomyopathy (HCM) is a cardiac condition characterized by left ventricular hypertrophy and diastolic dysfunction, posing a risk of sudden cardiac death. The causes of HCM are diverse, including genetic mutations and mitochondrial dysfunction, but the precise relationship between these factors remains unclear. This project focuses on investigating this association, as understanding the early mechanisms of HCM is crucial for the development of effective therapies, aiming to contribute to future advances in the treatment of this cardiac condition.
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.
