DeCure's autonomous Respiratory AI scientist is researching a drug-repurposing hypothesis for pulmonary venoocclusive disease — 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 venoocclusive disease 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 venoocclusive 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
bone morphogenetic protein receptor type 2 (BMPR2) — BMPR2 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 adpdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 6UNP · 2.3 Å · ligand ADENOSINE-5'-DIPHOSPHATE (ADP). Experimental structure, not a prediction.
What the evidence adds up to
No abstract in this set directly studies pulmonary venoocclusive disease. The 1991 crossover trial in 20 infants after cardiac surgery found that both prostaglandin E1 and epoprostenol lowered pulmonary vascular resistance, but neither drug was pulmonary-specific: 5 ng/kg/min of epoprostenol was equivalent to 30 ng/kg/min of prostaglandin E1, and systemic vasodilation occurred with both. The 2010 review of pulmonary arterial hypertension notes that eight FDA-approved drugs exist across three classes (prostacyclins, endothelin-receptor antagonists, PDE-5 inhibitors) but states plainly that morbidity and mortality remain high and that there is a great unmet medical need for more efficacious therapies. No data from that review apply specifically to pulmonary venoocclusive disease.
The 1986 case report describes interstitial lung disease and pulmonary fibrosis after vindesine plus radiation in one patient with squamous cell lung cancer; clinical improvement followed drug cessation and corticosteroids. The 2019 retrospective analysis of 29 COPD patients treated with endoscopic lung volume reduction using nitinol coils found no significant long-term changes in lung function or six-minute walk distance over 6 to 12 months, and the authors conclude that the procedure should be considered critically. Neither of these abstracts concerns pulmonary venoocclusive disease or any drug therapy for it.
What is missing for pulmonary venoocclusive disease specifically: no prospective trial data, no validated animal model for drug screening, no dedicated funding for a rare disease that is often excluded from pulmonary hypertension trials, and no clear patient stratification strategy to distinguish it from other forms of pulmonary hypertension before treatment begins.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Heart · 1991 · 41 citations · open access
Comparison between prostaglandin E1 and epoprostenol (prostacyclin) in infants after heart surgery.
AbstractOBJECTIVE: To study the dose response characteristics of prostaglandin E1 and epoprostenol (prostacyclin) and directly to compare their effectiveness as pulmonary vasodilators in infants with pulmonary hypertension. DESIGN: A crossover design with each patient receiving both drugs in random order. SETTING: Infants were studied in the intensive care unit while they were sedated, paralysed, and ventilated. PATIENTS: Twenty infants who had undergone corrective cardiac surgery and who were in sinus rhythm, had stable haemodynamic function, and had a pulmonary artery catheter in place. All infants were receiving dopamine and phenoxybenzamine. INTERVENTIONS: Baseline haemodynamic measurements were taken and an infusion of the first drug was started at the lowest dose: after 20 minutes the measurements were repeated and the dose increased. This protocol was repeated for all doses of both drugs: 10, 30, and 100 ng/kg/min of prostaglandin E1 and 5, 10, and 25 ng/kg/min of epoprostenol. Cardiac output was measured by the pulsed Doppler ultrasound method. MAIN OUTCOME MEASURES: Pulmonary and systemic vascular resistances were calculated from the cardiac output and compared by the Wilcoxon signed ranks test. RESULTS: Both prostaglandin E1 and epoprostenol were effective vasodilators: 5 ng/kg/min of epoprostenol was equivalent to 30 ng/kg/min of prostaglandin E1. CONCLUSIONS: Neither drug showed pulmonary specificity.
Expert Opinion on Emerging Drugs · 2010 · 12 citations
Emerging drugs for pulmonary hypertension
AbstractIMPORTANCE OF THE FIELD: Pulmonary arterial hypertension (PAH) is a clinical syndrome characterized by structural narrowing of the small pulmonary arteries that often culminates in fatal right heart failure. AREAS COVERED IN THIS REVIEW: PubMed was searched for PAH and treatment. Data from scientific meetings and pharmaceutical websites are also included. There are currently eight FDA approved drugs for PAH that fall into one of three classes: prostacyclins, endothelin-receptor antagonists and PDE-5 inhibitors. All have important limitations and morbidity and mortality remain high. Several new agents with similar mechanisms of action are in clinical development. Multiple novel therapeutic targets are being explored. New applications for PAH therapies, such as pulmonary hypertension due to left heart and lung disease, are also being investigated. WHAT THE READER WILL GAIN: An understanding of currently available drugs and those in clinical development for pulmonary hypertension. TAKE HOME MESSAGE: Drugs targeting the pulmonary vasculature have been an extremely active area of basic and clinical research for the past 20 years and will continue to be so for the foreseeable future. Considerable progress has been made, and yet there continues to be a great unmet medical need for developing more efficacious therapies.
Interstitial Lung Disease Associated With Vindesine and Radiation Therapy for Carcinoma of the Lung
AbstractDiffuse interstitial lung disease and pulmonary fibrosis occurred after the use of vindesine and radiation therapy in a patient with squamous cell carcinoma of the lung. Clinical improvement occurred after the drug was discontinued and corticosteroid therapy was initiated. Review of the literature reveals no previously reported cases of pulmonary toxicity due to vindesine when used alone or in combination with other therapeutic modalities.
AbstractIntroduction: Patients with chronic obstructive pulmonary disease (COPD), which is the fourth most common cause of death worldwide, usually suffer very much of a concomitant pulmonary emphysema. \nMethodes like endoscopic lung volume reduction (eLVR) should reduce symptoms and upgrade the quality of life. Previous studies have shown an improvement in lung function following lung volume reduction. \nThis study analyzes, if these results can be reproduced in clinical routine. \n \nMethods: This study is a retrospective analysis of all patients treated with endoscopic lung volume reduction using coils in our center between 03.09.2013 and 25.11.2014. \nParticular attention was paid to lung function data and six-minutes walk test. \nFurthermore, the CT analysis softwares for CT-based target lung lobe selection was tested compered to visual target lobe selection. \n \nResults: 41 medical interventions on 29 patients were analyzed. \nOver a period of 6 to 12 months no significant changes were observed in the data of lung function testing. \nOnly right after treatment there was a statistically relevant decrease in the percentage of residual volume to total lung capacity at 2.32% ± 6.24% and moreover a significant increase in vital capacity at 0.14L ± 0.39L. \nConsidering residual volume and one-second capacity immediately after the medical intervention, 41.38% respectively 48.28% could be denoted as responders, \nbut none of the positive effects could be kept over a period of 6 to 12 months. In the six-minutes walk test no significant changes were observed. \nIn 70% respectively 81.25% of the cases, the CT analysis softwares chose the same lung lobes as the attending physican. \n \nConclusion: Endoscopic lungvolume reduction with Nitinol Coils for the treatment of lung emphysema should be considered critically. \nOn the long term, there was no significant improvement of symptom burden. \nA wrong target lobe selection by visual evaluation is improbable, because this analysis showed a good correlation between analysis softwares and treating physican. \nBased on these results, other opportunities for lung volume reduction should be considered.
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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