Cardio Lab · DeCure for X

DeCure for Hypertrophic cardiomyopathy 12

DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for hypertrophic cardiomyopathy 12 — 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 module1 genesLead labCardio
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CardioDOID:0110318$DeCureCardio

The disease map

Disease moduleHypertrophic cardiomyopathy 12 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 12 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

Hypertrophic cardiomyopathy was first recognised in the late 1950s, and by 1987 investigators had assembled observations on its clinical identification, morphology, pathophysiology, and natural history, though the intrinsic complexities of the disease continued to create uncertainty and debate. In 1997, a study of 10 consecutive patients with hypertrophic obstructive cardiomyopathy tested whether temporarily occluding the first larger septal branch of the left anterior descending coronary artery could reduce the left ventricular outflow tract gradient. During occlusion, regional ischaemia was observed in all patients, and the intraventricular gradient fell from a mean of 56.2 mmHg to 32.2 mmHg (P < 0.05). After release of the occlusion, the gradient rose to 61.1 mmHg (P < 0.01). Left ventricular end-diastolic pressure did not increase during ischaemia. The authors concluded that these results formed the basis for a new catheter interventional therapy, but the study was small and did not report long-term outcomes or survival.

By 2015, hypertrophic cardiomyopathy was described as the most common monogenic disorder in cardiology, but it remained unclear how flaws in individual sarcomere components were responsible for the observed phenotype. The 2015 review focused on alterations in cardiac mechanical properties as a pathophysiological mechanism, but offered no new clinical trial data or therapeutic intervention. No drug treatment was tested or discussed in any of these abstracts.

What is still missing is a large, randomised trial of any catheter-based or pharmacological intervention for hypertrophic cardiomyopathy, with long-term follow-up on mortality, symptom relief, and arrhythmia risk. Patient stratification by genotype and obstruction severity has not been systematically applied in a prospective treatment study. Funding for such a trial, and for basic research linking sarcomere mutations to mechanical dysfunction, remains inadequate.

Evidence

Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.

New England Journal of Medicine · 1987 · 900 citations

Hypertrophic Cardiomyopathy

Abstract(First of Two Parts)HYPERTROPHIC cardiomyopathy has fascinated and often confused physicians for the quarter of a century since its recognition in the late 1950s.1 2 3 4 5 During this time, investigators have assembled an impressive array of observations spanning numerous aspects of the clinical identification, morphology, pathophysiology, and natural history of the disease. Much understanding has emerged from these investigative efforts; however, the intrinsic complexities of hypertrophic cardiomyopathy continue to create uncertainty and debate.Numerous studies have explored specific facets of hypertrophic cardiomyopathy, and several have comprehensively reviewed the broader aspects of its clinical profile and course, including the findings on physical . . .

https://doi.org/10.1056/nejm198703263161305
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.

https://doi.org/10.1093/oxfordjournals.eurheartj.a015350
Frontiers in Physiology · 2015 · 3 citations · open access

Mechanical aberrations in hypetrophic cardiomyopathy: emerging concepts

AbstractHypertrophic cardiomyopathy is the most common monogenic disorder in cardiology. Despite important advances in understanding disease pathogenesis, it is not clear how flaws in individual sarcomere components are responsible for the observed phenotype. The aim of this article is to provide a brief interpretative analysis of some currently proposed pathophysiological mechanisms of hypertrophic cardiomyopathy, with a special emphasis on alterations in the cardiac mechanical properties.

https://doi.org/10.3389/fphys.2015.00232
Journal of Clinical and Nursing Research · 2025 · 0 citations · open access

Progress in Interventional and Surgical Treatment of Obstructive Hypertrophic Cardiomyopathy

AbstractTo improve the treatment effect of obstructive hypertrophic cardiomyopathy, this article focuses on the treatment of obstructive hypertrophic cardiomyopathy and conducts a comprehensive analysis of the disease. It highlights the limitations of traditional treatment methods and elaborates on interventional and surgical treatments. Additionally, this article compares the indications, risks, treatment effects, and costs of the two different treatment methods, providing a reference for doctors and patients in selecting clinical treatment plans.

https://doi.org/10.26689/jcnr.v9i4.10405

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.