DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for atrial septal defect 7 — 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 7 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 7 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
NK2 homeobox 5 (NKX2-5) — NKX2-5 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 6WC2 · 2.1 Å · ligand none (apo structure). Experimental structure, not a prediction.
What the evidence adds up to
In A/J mice, atrial septal defect occurs spontaneously and can be produced teratogenically, suggesting these mice are an animal homology of the human condition. The 1968 study proposed that such models allow investigation into how nongenetic factors push genetically predisposed individuals past a developmental threshold to produce a specific cardiac malformation. No drug was tested in that murine work; dextroamphetamine is mentioned only in the title as an influence, but the abstract gives no data on its effect.
A 1994 paper describes surgical repair of secundum atrial septal defect in humans at a UK cardiothoracic centre. No numbers of patients, survival rates, or outcomes are reported in the abstract. The 2020 review states that atrial septal defect is caused by malformation of the septum between the left and right atrium, that the defects are treatable, but that the underlying cause remains unclear.
What is missing is any controlled trial of a pharmacological agent for atrial septal defect, any molecular or genetic stratification of patients, and any funding directed at understanding the cause rather than just the surgical repair. The animal model exists but has not been translated into a drug target.
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 · 1995 · 413 citations · open access
A Comparison of Surgical and Medical Therapy for Atrial Septal Defect in Adults
AbstractBACKGROUND: The surgical closure of an atrial septal defect is frequently recommended for patients over 40 years of age. However, the prognosis for such patients with unrepaired defects is largely unknown, and the outcome for patients operated on after the fourth decade of life has not yet been compared with that for medically treated patients in a controlled follow-up study. METHODS: In a retrospective study, we examined the clinical course of 179 consecutive patients with isolated atrial septal defects diagnosed after the age of 40. The 84 patients (47 percent) who underwent surgical repair were compared with the 95 patients (53 percent) who were treated medically. The mean (+/-SD) follow-up period was 8.9 +/- 5.2 years (range, 1 to 26). RESULTS: Multivariate analysis revealed that surgical closure of the defect significantly reduced mortality from all causes (relative risk, 0.31; 95 percent confidence interval, 0.11 to 0.85). The adjusted 10-year survival rate of surgically treated patients was 95 percent, as compared with 84 percent for the medically treated patients. In addition, surgical treatment prevented functional deterioration, as measured by the New York Heart Association class (relative risk, 0.21; 95 percent confidence interval, 0.08 to 0.55). However, the incidence of new atrial arrhythmias or of cerebrovascular insults in the two groups was not significantly different. CONCLUSIONS: The surgical repair of an atrial septal defect in patients over 40 years of age, as compared with medical therapy, increases long-term survival and limits the deterioration of function due to heart failure. However, surgically treated patients should be followed closely for the onset of atrial arrhythmias so as to reduce the risk of thromboembolic complications.
Homologies for congenital heart diseases: Murine models, influenced by dextroamphetamine
AbstractAbstract The spontaneous occurrence and teratogenic production of atrial septal defect in A/J mice and ventricular septal defect in C57BL/6J mice lead to the proposal that these strains may represent animal homologies of these congenital heart diseases in human beings. Such models permit investigation into the mechanisms by which nongenetic factors cause genetically predisposed individuals to reach a particular threshold of developmental abnormality and develop a specific type of cardiac malformation.
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
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.
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.
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