DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for hypertrophic cardiomyopathy 9 — screening already-approved drugs against its 3-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 9 maps to a 3-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 9 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
myomesin 1 (MYOM1) — MYOM1 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 2-methoxyethoxydrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 2Y23 · 2.5 Å · ligand 2-(2-METHOXYETHOXY)ETHANOL (PG0). Experimental structure, not a prediction.
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. No drug treatment was described in that review.
In 1997, a catheter-based method was tested in 10 consecutive patients with hypertrophic obstructive cardiomyopathy. Temporary occlusion of the first large septal branch of the left anterior descending coronary artery produced regional ischaemia in all patients. During occlusion the mean intraventricular gradient fell from 56.2 mmHg to 32.2 mmHg (P < 0.05), and 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 the results formed the basis for a new catheter interventional therapy, not a drug therapy.
A 2023 scoping review states that hypertrophic cardiomyopathy is characterised by left ventricular hypertrophy and diastolic dysfunction, with risk of sudden cardiac death. The causes include genetic mutations and mitochondrial dysfunction, but the precise relationship between these factors remains unclear. No drug treatment is evaluated in that review.
No drug has been tested in these abstracts for hypertrophic cardiomyopathy. What is still missing is any randomised controlled trial of a pharmacological agent, a defined patient stratification by genotype or mitochondrial phenotype, and funding for such a trial.
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 . . .
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.
Journal of Contemporary Medical Practice · 2022 · 0 citations · open access
Progress in Clinical Treatment of Hypertrophic Cardiomyopathy with Traditional Chinese and Western Medicine
AbstractHypertrophic cardiomyopathy refers to cardiac hypertrophy caused by hypertension, aortic stenosis and other factors, with dyspnea, precardiac pain, fatigue, palpitations and other clinical manifestations, and ultimately can progress to heart failure; The clinical incidence of this disease is increasing year by year, and the complications are numerous, which seriously affect the prognosis. For the treatment of this disease, Chinese and western medicine have their own opinions, through combing the latest domestic and foreign relevant literature, systematically elaborated in recent years about the progress of Chinese and western medicine treatment of this disease, for the majority of doctors reference.
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.
