DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for pulmonary valve stenosis — 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 modulePulmonary valve stenosis 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 pulmonary valve stenosis 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
Pulmonary valve stenosis with an intact ventricular septum is a congenital condition where the only notable abnormality is fusion of the pulmonary valve cusps, causing obstruction. The severity of symptoms is determined by the degree of fusion, and many patients are asymptomatic. The prognosis is generally good, depending on the severity of obstruction and the pressure produced in the right ventricle. Poststenotic dilatation of the pulmonary artery is practically always present even though pressure in the pulmonary artery is low. In one 2012 case report, a 21-year-old woman with previously diagnosed mild pulmonary valve stenosis presented with breathlessness, reduced exercise tolerance, intermittent palpitations, and chest pain, and was found to have an aneurysm of the pulmonary artery.
The available abstracts do not report any drug treatment or clinical trial for pulmonary valve stenosis. The 1951 paper describes surgical treatment, and the 1970 paper states that an angiocardiogram can help plan the surgical approach if operation is necessary. No medical therapy is mentioned for this condition in these sources.
The remaining abstracts concern aortic valve stenosis, a different disease. One 2007 review describes aortic valve stenosis as an active atheroinflammatory process with activated inflammatory cells, lipid deposits, and calcific nodules. In experimental animals, hypercholesterolaemia induced calcification that could be inhibited by statin treatment, and the potential of statins to retard progression was recognised in clinical studies, but the review states further prospective trials are needed. A 2025 dataset abstract reports that patients undergoing aortic valve replacement had significantly higher levels of immature surfactant protein B (proSP-B) compared to control subjects, and that proSP-B may serve as a marker of alveolar capillary membrane damage in valvular heart disease. These findings do not apply to pulmonary valve stenosis.
What is still missing for pulmonary valve stenosis is any evidence from prospective clinical trials testing drug therapy, any identified molecular target for medical treatment, and any patient stratification beyond severity of obstruction. No randomised trial, no repurposed drug, and no biomarker-guided approach has been reported in these abstracts for this specific disease.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Current Opinion in Lipidology · 2007 · 132 citations
Aortic valve stenosis: an active atheroinflammatory process
AbstractPURPOSE OF REVIEW: To summarize the current understanding of the pathobiology of aortic valve stenosis and portray the major advances in this field. RECENT FINDINGS: Stenotic aortic valves are characterized by atherosclerosis-like lesions, consisting of activated inflammatory cells, including T lymphocytes, macrophages, and mast cells, and of lipid deposits, calcific nodules, and bone tissue. Active mediators of calcification and cells with osteoblast-like activity are present in diseased valves. Extracellular matrix remodeling, including collagen synthesis and elastin degradation by matrix metalloproteinases and cathepsins, contributes to leaflet stiffening. In experimental animals, hypercholesterolemia induces calcification and bone formation in aortic valves, which can be inhibited by statin treatment. The potential of statins to retard progression of aortic valve stenosis has also been recognized in clinical studies; however, further prospective trials are needed. Angiotensin II-forming enzymes are upregulated in stenotic valves. Angiotensin II may participate in profibrotic progression of aortic valve stenosis and may serve as a possible therapeutic target. SUMMARY: Recent findings regarding the interaction of inflammatory cells, lipids, mediators of calcification, and renin-angiotensin system in stenotic valves support the current opinion of aortic valve stenosis being an actively regulated disease, potentially amenable to targeted molecular therapy. Evidence from prospective clinical studies is eagerly awaited.
SURGICAL TREATMENT OF PULMONARY STENOSIS WITH INTACT INTERVENTRICULAR SEPTUM
AbstractSTENOSIS of the pulmonary valve is the only abnormality of note in a small but significant number of patients with cyanosis due to congenital heart disease. The pathologic process in such patients differs from that seen in typical tetralogy of Fallot in that the interventricular septum is intact and consequently there can be no overriding of the aorta. Instead of stenosis in the infundibular region as usually seen in the tetralogy of Fallot, stenosis in these cases is caused by fusion of the cusps of the pulmonary valve (fig.<i>2D</i>). The degree of this fusion, varying from negligible to complete, determines the severity of the symptoms. Immediately distal to the stenosis marked dilatation of the pulmonary artery is usually seen. It is mysterious that poststenotic dilatation of the pulmonary artery is practically always present although pressure in the pulmonary artery is low. In fact, patients with the severest pulmonary stenosis,
AbstractA 21-year-old female previously diagnosed as having mild pulmonary valve stenosis (PS) presented with breathlessness, reduced exercise tolerance, intermittent palpitations and chest pain. There were no cardiovascular risk factors or family history of significance. Examination revealed normal second heart sound, an ejection systolic and a diastolic murmur in the pulmonary area. Electrocardiogram showed incomplete right bundle branch block and …
AbstractThe clinical manifestations of pulmonary valve stenosis with an intact ventricular septum are determined by its severity.Often the patient is asymptomatic. The prognosis is generally good, depending on the severity of obstruction and pressure produced in the right ventricle. An angiocardiogram will delineate the morphology and, if operation is necessary, help to plan the surgical approach.
Zenodo (CERN European Organization for Nuclear Research) · 2025 · 0 citations · open access
Dataset related to the article " Immature surfactant proteins B increases in the plasma of pa-tients with calcific severe aortic stenosis"
Abstract<p>This record contains row data related to the article "<span><strong>Immature surfactant proteins B increases in the plasma of patients with calcific severe aortic stenosis</strong>"</span></p> <p><strong><span>Abstract: </span></strong><span>Valvular disease is a complex pathological condition that impacts countless individuals around the globe. </span><span>Due to limited treatments, it is crucial to understand its mechanisms to identify new targets.</span></p> <p><span>Valve disease may result in pulmonary venous hypertension, which is linked to compromised functioning of the alveolar and capillary membranes, and hindered gas exchange. Nonetheless, the correlation between surfactant proteins (SP) and valve disease remains unexplored. </span></p> <p><span>A total of 44 patients were enrolled, out of which 36 underwent aortic valve replacement, and 8 underwent a second aortic valve substitution due to bioprosthetic valve degeneration. Ten healthy subjects were also included in the study. The results showed that patients who underwent both the first valve replacement and the second surgery had significantly higher levels of immature SP-B (proSP-B) compared to control subjects</span>. The levels of the extra-lung collectin SP-D were higher in patients who needed a second surgery due to bioprosthetic valve degeneration, while SP-A levels remained unchanged. The research also showed that there was no reciprocal relationship between inflammation and SP-D as the levels of inflammatory mediators did not differ between groups.</p> <p>The present demonstrates that circulating proSP-B serves as a reliable marker of alveolar capillary membrane damage in patients with valvular heart disease.</p>
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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