Respiratory Lab · DeCure for X

DeCure for Pulmonary venoocclusive disease 2

DeCure's autonomous Respiratory AI scientist is researching a drug-repurposing hypothesis for pulmonary venoocclusive disease 2 — 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 labRespiratory
All cures
RespiratoryDOID:0081269$DeCureResp

The disease map

Disease modulePulmonary venoocclusive disease 2 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 2 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

In a 1991 crossover study of 20 infants after corrective cardiac surgery, both prostaglandin E1 and epoprostenol (prostacyclin) were effective pulmonary vasodilators, but neither drug showed pulmonary specificity. At the doses tested, 5 ng/kg/min of epoprostenol was equivalent to 30 ng/kg/min of prostaglandin E1. The study measured pulmonary and systemic vascular resistances using pulsed Doppler ultrasound, with patients sedated, paralysed, and ventilated, and all receiving dopamine and phenoxybenzamine.

Pulmonary veno-occlusive disease carries a significantly worse prognosis than idiopathic pulmonary arterial hypertension. A French case series reported median survival from diagnosis to death or lung transplantation of only 1 year, and a more recent analysis found that pulmonary arterial hypertension therapy had no significant effect on survival. Case reports describe both beneficial and adverse effects of such medications, with pulmonary oedema as the most life-threatening complication. Lung transplantation remains the best long-term option for suitable patients, but elderly patients with concomitant or precipitating malignant disease are not considered transplant candidates.

A 2024 case report describes a 59-year-old patient with pulmonary veno-occlusive disease and multiple myeloma in World Health Organisation functional class IV who was treated with sildenafil for almost 5 years. The report does not provide quantitative survival or response data beyond the duration of treatment. No controlled trial data exist for sildenafil in this disease.

What is still missing is a prospective trial large enough to detect survival benefit, given the rarity of the disease and its frequent association with malignancies that exclude patients from transplantation. No randomised evidence exists to guide drug selection or to identify which patients might tolerate pulmonary vasodilators without developing pulmonary oedema. Patient stratification by genetic or haemodynamic markers remains absent.

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.

https://doi.org/10.1136/hrt.66.2.175
SAGE Open Medical Case Reports · 2024 · 0 citations · open access

Long-term sildenafil therapy for pulmonary veno-occlusive disease in association with melphalan therapy for multiple myeloma: A case report

AbstractPulmonary veno-occlusive disease has a significantly worse prognosis than idiopathic pulmonary arterial hypertension. According to a case series from France, the median survival time from diagnosis to death or lung transplantation was only 1 year, and in a more recent analysis, pulmonary arterial hypertension therapy had no significant effect on survival. There are case reports and case series describing both beneficial and adverse effects of pulmonary arterial hypertension-related medications. The most life-threatening complication of such a therapy is pulmonary oedema. In the long term, lung transplantation remains the best treatment option for suitable patients. However, elderly patients with concomitant or precipitating malignant disease are not considered transplant candidates. We describe a 59-year-old pulmonary veno-occlusive disease patient with multiple myeloma in World Health Organisation functional class IV who was successfully treated with sildenafil for almost 5 years.

https://doi.org/10.1177/2050313x241292529
Elsevier eBooks · 2009 · 0 citations · open access

Molecular Pulmonary Pathology

AbstractThis DOI is not currently attached to any metadata records. DOIs can’t actually ever be deleted (they’re persistent), but sometimes our members create DOIs in error. We do have a process to approximate deletion which we follow only in rare cases where the DOI has been genuinely created in error, and most crucially, if the DOI has never been published anywhere online or in print and never otherwise distributed to or communicated with anyone (authors, readers, reviewers, etc.

https://doi.org/10.1016/b978-044306901-7.50026-2

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.