Cardio Lab · DeCure for X

DeCure for Atrial septal defect 3

DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for atrial septal defect 3 — 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
All cures
CardioDOID:0110108$DeCureCardio

The disease map

Disease moduleAtrial septal defect 3 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 atrial septal defect 3 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

Two kindreds with secundum-type atrial septal defect were traced to common ancestors in the 18th century. Among 16 cases with certain diagnosis (nine verified at operation, one at autopsy, two by catheterisation), the distribution in the combined pedigree satisfied criteria for dominant inheritance. Four additional cases were strongly suspected. The authors note this does not contradict the general view that most atrial septal defects and other cardiovascular malformations are due to multifactorial mechanisms. A separate 1997 report describes a family in which a mother, her two children, and two other relatives all had ostium secundum atrial septal defect; the index case and her mother also had prolonged atrioventricular conduction, and the defect was considered inherited as a mendelian dominant trait.

Atrial septal defect occurs in about 25% of children with congenital heart defects. There are five types: patent foramen ovale, ostium secundum defect, ostium primum defect, sinus venosus defect, and coronary sinus defect. Small defects usually close spontaneously in childhood. Large defects that do not close may require percutaneous or surgical intervention to prevent stroke, dysrhythmias, and pulmonary hypertension. Many ASDs go undiagnosed until adulthood, so treatment of large defects is often delayed. Untreated large defects can cause exercise intolerance, cardiac dysrhythmias, palpitations, increased incidence of pneumonia, pulmonary hypertension, and increased mortality.

A 1994 journal article on secundum atrial septal defect repair is listed but no results, sample sizes, or outcomes are provided in the abstract. A 2020 review states that even though atrial septal defects are treatable, the underlying cause is not clear and research must continue.

What is still missing is a clear molecular or genetic mechanism for most cases, prospective data on how often familial dominant inheritance actually explains the defect in unselected populations, and any trial comparing long-term outcomes of early versus delayed closure in adults. No drug therapy is mentioned in any of these abstracts.

Evidence

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

Clinical Genetics · 1971 · 22 citations

Dominant mode of inheritance in atrial septal defect

AbstractTwo kindreds showing an accumulation of secundum‐type atrial septal defects have been traced back to common ancestors in the 18th century. The distribution of affected individuals in the combined pedigree satisfies the criteria of a dominant mode of inheritance. The diagnosis is considered certain in 16 cases (verified at operation in nine, at autopsy in one, and by heart catheterization in two) and more or less strongly suggested in four. Evidence from this and some additional reports gives support to the hypothesis that in exceptional cases atrial septal defect may be inherited as an autosomal dominant character showing high or even complete penetrance and little variation in expressivity. This does not contradict the generally accepted view that, in most cases, atrial septal defect as well as other cardiovascular malformations must be due to multifactorial mechanisms.

https://doi.org/10.1111/j.1399-0004.1971.tb00259.x
Postgraduate Medical Journal · 1994 · 1 citations · open access

Secundum atrial septal defect repair

AbstractJournal Article Secundum atrial septal defect repair Get access M I Khalid M I Khalid Regional Cardiothoracic Centre, Freeman Hospital, Newcastle upon Tyne NE7 7DN, UK Search for other works by this author on: Oxford Academic Google Scholar Postgraduate Medical Journal, Volume 70, Issue 825, July 1994, Pages 522–523, https://doi.org/10.1136/pgmj.70.825.522 Published: 01 July 1994

https://doi.org/10.1136/pgmj.70.825.522
Pediatrics International · 1997 · 1 citations

Familial atrial septal defect with prolonged atrioventricular conduction

AbstractA family is described in which a mother, her two children and another two relatives all had atrial septal defect of the ostium secundum type. The index case and her mother also had prolonged atrioventricular conduction. It is considered that the defect is the familial type and inherited as a mendelian dominant trait.

https://doi.org/10.1111/j.1442-200x.1997.tb03657.x
Frontiers in Medical Science Research · 2020 · 0 citations

Etiology of Atrial Septal Defect: Review

AbstractAtrial septal defect is caused by malformation of the septum between left and right atrium. This paper will firstly review the embryology and classification of atrial septal defect, then the etiology of atrial septal defect will be discussed according to various studies. Even atrial septal defects are treatable, the underlying cause of such defects is not clear, therefore, the research into them must be continued.

https://doi.org/10.25236/fmsr.2020.020202
Radiološke tehnologije · 2024 · 0 citations · open access

Atrial septal defect (ASD), trans-catheter closure – case report

AbstractAtrial septal defect (ASD) is one of the most common types of congenital heart defects, occurring in about 25% of children. An atrial septal defect occurs when there is a failure to close the communication between the right and left atria. It encompasses defects involving both the true septal membrane and other defects that allow for communication between both atria. There are five types of atrial septal defects ranging from most frequent to least: patent foramen ovale, ostium secundum defect, ostium primum defect, sinus venosus defect, and coronary sinus defect. Small atrial septal defects usually spontaneously close in childhood. Large defects that do not close spontaneously may require percutaneous or surgical intervention to prevent further complications such as stroke, dysrhythmias, and pulmonary hypertension. This activity describes the evaluation, diagnosis, and management of atrial septal defect and highlights the role of team-based interprofessional care for affected patients. Atrial septal defects are frequently asymptomatic. The characteristic murmur is a soft, systolic ejection murmur over the pulmonic area (second intercostal space) combined with a wide, fixed splitting of S2. Many ASDs go undiagnosed until adulthood; therefore, treatment, especially of large defects, is often delayed. Untreated large defects can cause exercise intolerance, cardiac dysrhythmias, palpitations, increased incidence of pneumonia, pulmonary hypertension and increased mortality.

https://doi.org/10.48026/issn.26373297.2024.1.15.6

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.