Cardio Lab · DeCure for X

DeCure for Hypertrophic cardiomyopathy 6

DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for hypertrophic cardiomyopathy 6 — 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:0110312$DeCureCardio

The disease map

Disease moduleHypertrophic cardiomyopathy 6 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 6 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

In ten patients with hypertrophic obstructive cardiomyopathy, temporary balloon occlusion of the first septal branch of the left anterior descending artery produced regional ischaemia and reduced the left ventricular outflow tract gradient from 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 findings form the basis for a new catheter-based interventional therapy.

A 1996 review of medical therapy for symptomatic hypertrophic cardiomyopathy states that no therapies have been proven to improve prognosis and that there are few randomised trials of symptomatic treatment. The drugs available for symptom relief are beta-blockers, calcium antagonists and disopyramide. A 2015 review notes that despite advances in understanding the disease as the most common monogenic disorder in cardiology, it remains unclear how flaws in individual sarcomere components produce the observed phenotype.

The catheter-based concept from 1997 has not been tested in a randomised controlled trial against medical therapy or surgical myectomy. The long-term effects of deliberately inducing septal ischaemia on ventricular function, arrhythmia risk and survival are not established. What is still missing is a randomised trial with adequate power to compare this approach with standard care, along with clear criteria for patient stratification by outflow tract gradient, symptom burden and genetic subtype.

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.

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
Cardiology in Review · 1996 · 0 citations

Medical Therapy for Symptomatic Patients with Hypertrophic Cardiomyopathy

AbstractHypertrophic cardiomyopathy is a relatively uncommon myocardial disease with a heterogeneous presentation and complex pathophysiology. The condition is often asymptomatic; when symptoms are present, however, they are usually multiple, and each has several potential mechanisms. No therapies have been proven to improve prognosis, and there are few randomized trials of symptomatic treatment. Within these limitations, an approach to assessing the symptomatic patient is presented. The major drugs available for symptomatic therapy, namely beta-blockers, calcium antagonists and disopyramide, are reviewed. An overall management plan and a step-by-step strategy for the treatment of the symptomatic patient are presented.

https://doi.org/10.1097/00045415-199609000-00007

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.