Cardio Lab · DeCure for X

DeCure for Restrictive cardiomyopathy

DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for restrictive cardiomyopathy — screening already-approved drugs against its 12-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.

Disease module12 genesLead labCardio
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CardioDOID:397$DeCureCardio

The disease map

Disease moduleRestrictive cardiomyopathy maps to a 12-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 restrictive cardiomyopathy 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

estrogen receptor 2 (ESR2)ESR2 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 3-fluoro-4-hydroxyphenyldrag to rotate · scroll to zoom

RCSB Protein Data Bank · entry 1YYE · 2.03 Å · ligand 3-(3-FLUORO-4-HYDROXYPHENYL)-7-HYDROXY-1-NAPHTHONITRILE (196). Experimental structure, not a prediction.

What the evidence adds up to

Restrictive cardiomyopathy is defined as heart-muscle disease that impairs ventricular filling, with normal or decreased diastolic volume of either or both ventricles. Systolic function usually remains normal, at least early in the disease, and wall thickness may be normal or increased, depending on the underlying cause. The condition usually results from increased stiffness of the myocardium, causing pressure within the ventricle to rise precipitously with only small increases in volume. It may cause symptoms and signs of right or left ventricular failure, and right-sided findings often predominate.

Restrictive cardiomyopathy is a rare cardiac disease causing severe diastolic dysfunction, ventricular stiffness and dilated atria. It induces heart failure often with preserved ejection fraction and is associated with a high mortality. Because of a poor clinical prognosis, patients frequently require heart transplantation. The disease is quite rare in childhood, and a 15-year-old patient with heart failure signs was diagnosed with restrictive cardiomyopathy in one case report. Right heart failure signs, thromboembolism and cardiac arrhythmia can be seen in clinical presentation.

Genetic as well as non-genetic factors contribute to restrictive cardiomyopathy, and a significant portion of cases remains of unknown etiology. The genetic forms and the involved molecular pathomechanisms are only partially understood. No drug treatment is discussed in any of these abstracts, and no survival or response rates are reported.

What is still missing is any clinical trial data for pharmacological intervention, adequate patient stratification by genetic cause, and funding for studies that could move beyond case reports and reviews toward prospective treatment testing.

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 · 1997 · 410 citations

Restrictive Cardiomyopathy

AbstractRestrictive cardiomyopathy is defined as heart-muscle disease that results in impaired ventricular filling, with normal or decreased diastolic volume of either or both ventricles. Systolic function usually remains normal, at least early in the disease, and wall thickness may be normal or increased, depending on the underlying cause.1 The condition usually results from increased stiffness of the myocardium that causes pressure within the ventricle (or ventricles) to rise precipitously with only small increases in volume. Since the condition affects either or both ventricles, it may cause symptoms and signs of right or left ventricular failure. Often, right-sided findings predominate, with . . .

https://doi.org/10.1056/nejm199701233360407
Preprints.org · 2022 · 18 citations · open access

Genetic Insights Into Primary Restrictive Cardiomyopathy

AbstractRestrictive cardiomyopathy is a rare cardiac disease causing severe diastolic dysfunction, ventricular stiffness and dilated atria. In consequence, it induces heart failure often with preserved ejection fraction and is associated with a high mortality. Since a poor clinical prognosis, patients with restrictive cardiomyopathy require frequently heart transplantation. Genetic as well as non-genetic factors contribute to restrictive cardiomyopathy and a significant portion of cases remains of unknown etiology. However, the genetic forms of restrictive cardiomyopathy and the involved molecular pathomechanisms are only partially understood. In this review, we summarize the current knowledge about primary genetic restrictive cardiomyopathy and describe its genetic landscape, which might be of interest for geneticists as well as for cardiologists.

https://doi.org/10.20944/preprints202203.0265.v1
Postgraduate Medical Journal · 1986 · 7 citations · open access

Restrictive cardiomyopathy

AbstractJournal Article Restrictive cardiomyopathy Get access E G J Olsen E G J Olsen National Heart Hospital, London W1M 8BA, UK Correspondence: E.G.J. Olsen, M.D., F.R.C.Path., F.A.C.C. Search for other works by this author on: Oxford Academic Google Scholar Postgraduate Medical Journal, Volume 62, Issue 728, June 1986, Pages 607–608, https://doi.org/10.1136/pgmj.62.728.607 Published: 01 June 1986

https://doi.org/10.1136/pgmj.62.728.607
The Annals of Clinical and Analytical Medicine · 2013 · 0 citations · open access

Restrictive Cardiomyopathy in Childhood: Case Report

AbstractRestrictive cardiomyopathy is quite rare in childhood. The disease is characterized by diastolic dysfunction without systolic dysfunction or ventricular dilatation.Right heart failure signs, tromboembolism and cardiac arrhytmia can be seen in clinic presentation. In this case report, a 15 year-old patient who had heart failure signs was diagnosed with restrictive cardiomyopathy .

https://doi.org/10.4328/jcam.2140

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.