DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for atrial septal defect 8 — 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 moduleAtrial septal defect 8 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 8 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
Cbp/p300 interacting transactivator with ED-rich tail 2 (CITED2) — CITED2 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 apo structuredrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 7LVS · 2.02 Å · ligand none (apo structure). Experimental structure, not a prediction.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Zenodo (CERN European Organization for Nuclear Research) · 2021 · 0 citations · open access
Pathophysiology, Investigations, and Management of Atrial Septal Defect
AbstractBackground: ASD (atrial septal defect) is one of the most prevalent types of congenital heart disorders, affecting around one-quarter of all children. When the link between the right and left atria is not closed, an atrial septal defect arises. It includes both real septal membrane abnormalities and additional anomalies that allow communication between the two atria. From most common to least common, there are five types of atrial septal defects: patent foramen ovale, ostium secundum defect, ostium primum defect, sinus venosus defect, and coronary sinus defect. In most cases, small atrial septal abnormalities close on their own throughout development. Large lesions that do not seal on their own may require percutaneous or surgical intervention to avoid consequences like stroke, dysrhythmias, and pulmonary hypertension. This exercise covers the assessment, diagnosis, and treatment of atrial septal defect, as well as the importance of team-based interprofessional care for individuals with the condition. Conclusion: The goal of this review article is to identify the etiology of the atrial septal defect, describe the presentation of a patient with atrial septal defect, describe the treatment and management options available for atrial septal defect, and explain interprofessional team strategies for improving care coordination and communication for patients with the atrial septal defect.
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.
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.
