DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for heart disease — screening already-approved drugs against its 44-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleHeart disease maps to a 44-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 heart disease 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
lipoprotein(a) (LPA) — LPA 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 2sdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 8TCE · 1.07 Å · ligand (2S)-3-phenyl-2-[(3R)-pyrrolidin-3-yl]propanoic acid (HWF). Experimental structure, not a prediction.
What the evidence adds up to
A 1959 case report describes a 32-year-old woman with complete heart block and aortic stenosis who at autopsy was found to have myocardial sarcoid. The report does not test any drug and offers no treatment data; it is a single pathological description.
A 2010 review of genetic testing in inherited heart disease states that the number of people seeking genetic counselling is growing, that gene-specific studies on long QT syndrome have helped judge the relevance of mutations in specific domains, and that the diagnostic yield of mutation analysis is increasing as more associated genes are identified. The review notes that ongoing research is needed to determine the relevance of all detected mutations and that cascade screening can identify at-risk patients for timely treatment. No drug, no survival or response rates, and no sample sizes are given.
A 2020 prospective observational study examined heart rate changes after sugammadex administration in 99 infants and children (median age 3 years) with comorbid cardiac, cardiovascular, or congenital heart disease. Bradycardia (heart rate below the fifth percentile for age) occurred in 20 of 99 patients (20%), but six of those were already bradycardic before the drug was given. Older patients, male patients, and those with higher body weight were most likely to experience bradycardia. None of the 99 patients required treatment for bradycardia, and the authors conclude that the incidence of bradycardia was low and not associated with clinically significant haemodynamic changes.
What is still missing: no randomised controlled trial of sugammadex in this population exists; the 2020 study is observational and unblinded, with no placebo comparator. Genetic testing studies lack prospective outcome data linking mutation detection to reduced mortality or hospitalisation. The 1959 case report is a single autopsy and cannot inform treatment. No drug has been shown in a controlled trial to improve survival or reduce events in heart disease patients with sarcoid, genetic variants, or perioperative bradycardia risk.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Annals of Internal Medicine · 1959 · 19 citations
MYOCARDIAL SARCOID, COMPLETE HEART BLOCK AND AORTIC STENOSIS
AbstractCase Reports1 October 1959MYOCARDIAL SARCOID, COMPLETE HEART BLOCK AND AORTIC STENOSISROBERT E. BOTTI, M.D., FRANK E. YOUNG, M.D.ROBERT E. BOTTI, M.D., FRANK E. YOUNG, M.D.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-51-4-811 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptComplete heart block in a young adult may pose a difficult diagnostic and therapeutic problem. The subject of this case report illustrates these difficulties and is of unusual interest because of the autopsy finding of myocardial sarcoid in addition to the clinically apparent rheumatic heart disease with aortic stenosis.CASE REPORTA 32 year old white female was admitted to University Hospitals of Cleveland on August 8, 1957, having had fainting spells of six months' duration.This patient had been asymptomatic until six months before admission, when she suddenly became unconscious for a few seconds while playing cards. She awoke...Bibliography1. HudsonChobanianRelman JBAVAS: Hypoaldosteronism, New England J. Med. 257: 529, 1957. CrossrefMedlineGoogle Scholar2. TedeschiWagnerPani CGBMDC: Studies in rheumatic fever, Arch. Path. 60: 408, 1955. MedlineGoogle Scholar3. PentonMillerLevine GBHSA: Some clinical features of complete heart block, Circulation 13: 801, 1956. CrossrefMedlineGoogle Scholar4. Place EH: Heart in diphtheria and scarlet fever, New England J. Med. 207: 864, 1932. CrossrefGoogle Scholar5. HoyneWelford ANT: Diphtheritic myocarditis, J. Pediat. 5: 642, 1934. CrossrefGoogle Scholar6. White PD: Acute heart block occurring as the first sign of rheumatic fever, Am. J. M. Sc. 152: 589, 1916. CrossrefGoogle Scholar7. Stern VS: Stokes-Adams attacks in the child, Brit. Heart J. 6: 66, 1944. CrossrefMedlineGoogle Scholar8. WarshawskyAbramson HW: Complete heart block in calcareous aortic stenosis, Ann. Int. Med. 27: 1040, 1947. LinkGoogle Scholar9. Leys DG: Heart block following diphtheria, Brit. Heart J. 7: 57, 1945. CrossrefMedlineGoogle Scholar10. PeacockLippschultzLukas RAEJA: Myocardial sarcoidosis, Circulation 16: 67, 1957. CrossrefMedlineGoogle Scholar11. LongcopeFreiman WTDG: A study of sarcoidosis, Medicine 31: 1, 1952. CrossrefMedlineGoogle Scholar12. YatesLeamanCornell WMWGVH: Congenital heart block; report of third case of complete heart block studied by serial sections through conduction system, J. A. M. A. 102: 1660, 1934. CrossrefGoogle Scholar13. WendkosStudy MHRS: Familial congenital complete A-V heart block, Am. Heart J. 34: 138, 1947. CrossrefMedlineGoogle Scholar14. Lillehei CW, discussion of Kirklin, J. W., Harshbarger, H. G., Donald, D. E., and Edwards, J. E.: Surgical correction of ventricular septal defect: anatomic and technical considerations, J. Thoracic Surg. 33: 45, 1957. CrossrefGoogle Scholar15. Lillehei CW: Present status of open cardiotomy for correction of congenital and acquired cardiac disease, Mod. Concepts Cardiovas. Dis. 27: 441, 1958. MedlineGoogle Scholar16. Nelson CT: Kveim reaction in sarcoidosis, J. Chron. Dis. 6: 158, 1957. CrossrefMedlineGoogle Scholar17. RicherClark WM: Sarcoidosis: a clinical pathologic review of three hundred cases including twenty-two autopsies, Am. J. Clin. Path. 19: 725, 1949. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Cleveland, Ohio*Received for publication June 2, 1958.From the Departments of Medicine, University Hospitals and the Institute of Pathology, Western Reserve University, Cleveland, Ohio.†Supported in part by training grant of the U. S. Public Health Service.Requests for reprints should be addressed to Frank E. Young, M.D., Institute of Pathology, Western Reserve University, Cleveland, Ohio. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byCardiac sarcoidosis: Diagnostic, prognostic, and therapeutic considerationsAnatomie und pathologische Anatomie des spezifischen Reizbildungs- und Erregungsleitungssystems sowie des kontraktilen MyokardsInfiltrative cardiomyopathy with conduction disease and ventricular arrhythmia: Electrophysiologic and pathologic correlationsSarcoidosis of the cardiac conducting systemClinicopathologic correlations. De subitaneis mortibus. XXV. Sarcoid heart disease.Sarcoidosis of the heartMorphologische Befunde beim kompletten HerzblockCase 42-1965UNUSUAL GIANT CELL LESIONS IN BIOPSY SPECIMENS OF LEFT ATRIAL APPENDAGES IN MITRAL STENOSISAnatomic basis for atrioventricular blockThe pathology of complete atrioventricular blockBILATERAL ADRENAL CALCIFICATION WITH NORMAL ADRENOCORTICAL FUNCTIONSarcoid of the myocardial septum with complete heart block Report of two casesAdams-Stokes syndromeSarcoid Heart DiseaseSarcoidosis Cordis 1 October 1959Volume 51, Issue 4Page: 811-820KeywordsCardiovascular therapyElectrocardiographyHeartHospital medicineIsoproterenolMedical servicesMyocarditisStenosisSyncopeYoung adults ePublished: 1 December 2008 Issue Published: 1 October 1959 PDF downloadLoading ...
Current Opinion in Cardiology · 2010 · 15 citations
Genetic testing in cardiovascular diseases
AbstractPURPOSE OF REVIEW: To review the current state and different aspects, including the yield, of genetic counseling and genetic testing in inherited heart disease. RECENT FINDINGS: The number of counselees is growing rapidly all over the world, and the first studies about patients' perspectives and follow-up have been published. Progress has been made by gene-specific studies on long QT syndrome to judge the relevance of detected mutations in the specific domains. SUMMARY: With the increasing identification of associated genes and available techniques in molecular testing of the inherited heart diseases, the diagnostic yield of mutation analysis is growing rapidly. To determine the relevance of all these mutations, ongoing research is needed. Furthermore, the process of genetic counseling can be optimized and extended with cascade screening, which leads to identifying patients at risk and timely treatment.
Cardiology Research · 2020 · 9 citations · open access
Heart Rate Changes Following the Administration of Sugammadex to Infants and Children With Comorbid Cardiac, Cardiovascular, and Congenital Heart Diseases
AbstractBACKGROUND: Sugammadex is a novel, rapidly-acting pharmacologic agent to reverse steroidal neuromuscular blocking agents with demonstrated advantages over acetylcholinesterase inhibitors. However, anecdotal reports have noted rare instances of bradycardia and even cardiac arrest. The current study examined heart rate (HR) changes in infants and children with comorbid cardiac, cardiovascular, and congenital heart diseases. METHODS: Patients less than 18 years of age, who had a comorbid cardiac, cardiovascular, or congenital heart disease and were to receive sugammadex, were included in this prospective observational study. After sugammadex administration, HR was continuously monitored and recorded every minute for the first 15 min, and then every 5 min for the next 15 min or until the patient was transferred from the operating room. The primary outcome, bradycardia, was defined as HR below the fifth percentile for age. Secondary outcomes included greatest decrease in HR from baseline for each patient and interventions required for bradycardia. RESULTS: The study cohort included 99 patients (58 male and 41 female) with a median age of 3 years. Bradycardia was noted in 20 of 99 patients (20%); however, six of these patients were bradycardic prior to the administration of sugammadex. Older patients, male patients, and patients with higher body weight were the most likely to experience bradycardia. None of the patients required treatment for bradycardia. CONCLUSIONS: The incidence of bradycardia following the administration of sugammadex was low, even in patients with congenital heart disease. Bradycardia was not associated with clinically significant hemodynamic changes and no treatment was required.
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.
