DeCure's autonomous Respiratory AI scientist is researching a drug-repurposing hypothesis for pulmonary edema — screening already-approved drugs against its 24-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease modulePulmonary edema maps to a 24-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 edema 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
MYCN proto-oncogene, bHLH transcription factor (MYCN) — MYCN 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 5G1X · 1.72 Å · ligand ADENOSINE-5'-DIPHOSPHATE (ADP). Experimental structure, not a prediction.
What the evidence adds up to
Acute pulmonary edema has been described as a syndrome that can arise from cardiovascular, renal, cerebral, or pulmonary diseases, as well as trauma, infections, and shock. A 1956 review distinguished two main clinical types based on differing responses to therapy, and recommended antifoaming agents as an initial symptomatic measure while further treatment is selected. No drug was shown to resolve the underlying cause.
A 2018 review of specialised pro-resolving mediators (SPMs) in acute respiratory distress syndrome (ARDS) reported that these molecules upregulated epithelial sodium channels, Na,K-ATPase, cystic fibrosis transmembrane conductance regulator, and aquaporins, and improved Na,K-ATPase activity in experimental models. The review also stated that SPMs inhibited inflammatory cytokine expression and promoted alveolar epithelial repair. These findings are based on pre-clinical studies; no human trial data were presented.
In a 2022 rat model of lipopolysaccharide-induced acute lung injury, ulinastatin (UTI) reduced pulmonary oedema compared to the LPS-only group. The treated animals showed lower concentrations of TNF-α, IL-1β, and IL-6 in bronchoalveolar lavage fluid, and increased expression of α1Na,K-ATPase, β1Na,K-ATPase, α-ENaC, β-ENaC, γ-ENaC, and tight junction proteins ZO-1, Occludin, and Claudin-5 in lung tissue. The mechanism was linked to promotion of PI3K/Akt signalling and suppression of TLR4/MyD88/NF-κB pathways. All results are from a single rodent study; no human data exist for ulinastatin in pulmonary oedema.
What remains missing is any randomised controlled trial in patients with pulmonary oedema, whether from heart failure, ARDS, or other causes. The proposed mechanisms from animal and cell work have not been tested in humans, and no drug has been shown to improve alveolar fluid clearance or survival in a clinical setting. Funding for such trials, appropriate patient stratification, and validated endpoints for oedema resolution are all 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.
Circulation · 1956 · 62 citations · open access
Acute Pulmonary Edema
AbstractAcute pulmonary edema may be associated with the most varied clinical conditions including cardiovascular, renal, cerebral, and pulmonary diseases, trauma to the skull or chest, infections, and shock. Many drugs and physical means have been employed in the treatment of this syndrome. Two main clinical types of pulmonary edema may be differentiated because of the different effect of therapy in each of them. Antifoaming therapy, a purely symptomatic method of treatment, tends to break a vicious circle and may be lifesaving. It should be employed initially while the patient is being examined and drugs or other remedies are being selected for possible additional treatment.
AbstractOBJECTIVE: Acute respiratory distress syndrome (ARDS) is an acute and lethal clinical syndrome that is characterized by the injury of alveolar epithelium, which impairs active fluid transport in the lung, and impedes the reabsorption of edema fluid from the alveolar space. This review aimed to discuss the role of pro-resolving mediators on the regulation of alveolar fluid clearance (AFC) in ARDS. DATA SOURCES: Articles published up to September 2017 were selected from the PubMed, with the keywords of "alveolar fluid clearance" or "lung edema" or "acute lung injury" or "acute respiratory distress syndrome", and "specialized pro-resolving mediators" or "lipoxin" or "resolvin" or "protectin" or "maresin" or "alveolar epithelial cells" or "aspirin-triggered lipid mediators" or "carbon monoxide and heme oxygenase" or "annexin A1". STUDY SELECTION: We included all relevant articles published up to September 2017, with no limitation of study design. RESULTS: Specialized pro-resolving mediators (SPMs), as the proinflammatory mediators, not only upregulated epithelial sodium channel, Na,K-ATPase, cystic fibrosis transmembrane conductance regulator (CFTR), and aquaporins levels, but also improved Na,K-ATPase activity to promote AFC in ARDS. In addition to the direct effects on ion channels and pumps of the alveolar epithelium, the SPMs also inhibited the inflammatory cytokine expression and improved the alveolar epithelial cell repair to enhance the AFC in ARDS. CONCLUSIONS: The present review discusses a novel mechanism for pulmonary edema fluid reabsorption. SPMs might provide new opportunities to design "reabsorption-targeted" therapies with high degrees of precision in controlling ALI/ARDS.
Ulinastatin alleviates pulmonary edema by reducing pulmonary permeability and stimulating alveolar fluid clearance in a rat model of acute lung injury.
AbstractObjectives: Previous studies have shown that ulinastatin (UTI) alleviates pulmonary edema in acute lung injury (ALI) caused by lipopolysaccharide (LPS), although the mechanism behind this action is uncertain. This research aimed to identify the fundamental mechanism by which UTI alleviates pulmonary edema. Materials and Methods: We established a model of acute lung injury (ALI) in rats by using LPS as the inciting agent.The control, LPS, and LPS+UTI groups were each comprised of a specific number of randomly selected Wistar rats. We evaluated lung injury and determined pulmonary edema. The concentrations of TNF-α, IL-1β and IL-6 in BALF and the expression levels of α1Na, k-ATPase, β1Na, K-AtPase, α-ENaC, β-ENaC, γ-ENaC, Zonula occludens (ZO)-1, Occludin, Caludin-5, PI3K, Akt, TLR4, MyD88 and NF-ƘBwere identified in lung tissues. Results: <0.01) in lung tissues. Conclusion: Our results demonstrated that UTI attenuated pulmonary edema by reducing pulmonary permeability and promoting AFC through inhibiting the inflammatory response, and the mechanism is related to promoting PI3K/Akt signaling pathways and suppressing TLR4/MyD88/NF-ƘB signaling pathways.
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.
