Respiratory Lab · DeCure for X

DeCure for Postinflammatory pulmonary fibrosis

DeCure's autonomous Respiratory AI scientist is researching a drug-repurposing hypothesis for postinflammatory pulmonary fibrosis — screening already-approved drugs against its 20-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.

Disease module20 genesLead labRespiratory
All cures
RespiratoryDOID:12123$DeCureResp

The disease map

Disease modulePostinflammatory pulmonary fibrosis maps to a 20-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 postinflammatory pulmonary fibrosis 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

pleckstrin homology and RUN domain containing M1 (PLEKHM1)PLEKHM1 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.

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helix sheet gtpdrag to rotate · scroll to zoom

RCSB Protein Data Bank · entry 8JC5 · 2.01 Å · ligand GUANOSINE-5'-TRIPHOSPHATE (GTP). Experimental structure, not a prediction.

What the evidence adds up to

A 2011 review of epidemiological and basic research argues that diabetes is an independent risk factor for pulmonary dysfunction and that diabetes induces pulmonary fibrosis, though it notes that earlier epidemiological studies were inconclusive. The review calls diabetic pulmonary fibrosis a potential complication warranting more attention, but provides no patient-level data on any treatment.

A 2024 meta-analysis of 7 trials with 496 participants examined anti-fibrotic drugs for post-COVID-19 pulmonary fibrosis. It found no significant differences between anti-fibrotic and standard treatment in chest CT score, length of hospital stay, or mortality. Improvements in pulmonary function were observed with anti-fibrotic drugs: forced expiratory volume in one second as a percentage of predicted increased by a mean difference of 23.95, and the FEV1/FVC ratio increased by a mean difference of 18.17. The authors state that the use of anti-fibrotic medications in these patients is currently based more on theory than on solid medical evidence and remains empirical.

A 2022 review of lung transplantation for idiopathic pulmonary fibrosis notes that antifibrotic therapies are generally effective in delaying disease progression, but some patients continue to progress despite treatment. Lung transplantation is described as a surgical option that increases overall survival and quality of life for selected patients with advanced disease. The review provides no numerical survival or response data from any specific trial.

What is still missing are large, randomised trials that test specific anti-fibrotic drugs in postinflammatory pulmonary fibrosis with adequate follow-up and patient stratification by aetiology, severity, and diabetic status. Funding for such trials, rather than for further reviews of existing weak evidence, is needed.

Evidence

Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.

Diabetes/Metabolism Research and Reviews · 2011 · 43 citations

Pulmonary fibrosis: a possible diabetic complication

AbstractDiabetic complications affect many organs in diabetic patients. Emerging evidence indicates that diabetes can increase the risk of pulmonary dysfunction. Early epidemiological studies from different populations on whether diabetes was an independent risk for pulmonary dysfunction were inconclusive. Recent epidemiological studies and systematic reviews clearly indicate that diabetes is an independent risk factor for pulmonary dysfunction. Given that pulmonary fibrosis is an important predictor of mortality in people with this chronic disease, whether diabetes directly causes pulmonary fibrosis is an important unresolved clinical question. This review combines recent epidemiological data with findings from basic research to indicate that diabetes induces pulmonary fibrosis. We then discuss the possible underlying mechanisms for the histological and biochemical pathology. At the end of this review, we emphasize that diabetic pulmonary fibrosis as a potential diabetic complication warrants more attention.

https://doi.org/10.1002/dmrr.1175
International Journal of Infectious Diseases · 2024 · 8 citations · open access

Impact of anti-fibrotic medications on post-COVID-19 pulmonary fibrosis: A systematic review and meta-analysis

AbstractOBJECTIVES: The impact of anti-fibrotic medications on pulmonary fibrosis caused by COVID-19 remains inconclusive and lacks systematic investigation. This study assessed the efficacy of anti-fibrotic drugs in addressing post-COVID-19 lung fibrosis. METHODS: statistic, and publication bias was assessed via funnel plots. RESULTS: The study (CRD42024552847) included 7 trials with 496 participants. No significant differences were observed in chest CT score (SMD = -0.60, 95% CI: -1.33 to 0.12, P = 0.10), length of hospital stay (MD = -1.34, 95% CI: -4.39 to 1.70, P = 0.39), and mortality (OR = 0.91, 95% CI: 0.50 to 1.64, P = 0.75) between anti-fibrosis and standard treatment groups. Notable improvements in pulmonary function were observed with anti-fibrotic drugs, as indicated by FEV1%pred (MD = 23.95, 95% CI: 12.24 to 35.67, P < 0.0001) and FEV1/FVC (MD = 18.17, 95% CI: 11.96 to 24.38, P < 0.00001). CONCLUSIONS: Anti-fibrotic medications may help reduce fibrotic lesions and improve pulmonary function in post-COVID-19 pulmonary fibrosis, but their practical use is currently based more on theory than on solid medical evidence. Currently, in clinical practice, the use of anti-fibrotic drugs in these patients primarily relies on empirical treatment. Further clinical studies are imperative to bolster its credibility for future applications.

https://doi.org/10.1016/j.ijid.2024.107193
IntechOpen eBooks · 2022 · 0 citations · open access

Lung Transplantation in Idiopathic Pulmonary Fibrosis

AbstractIdiopathic pulmonary fibrosis (IPF) is a progressive lung disease associated with a high degree of morbidity and mortality in its more advanced stages. Antifibrotic therapies are generally effective in delaying the progression of disease; however, some patients continue to progress despite treatment. Lung transplantation is a surgical option for selected patients with advanced pulmonary fibrosis that increases their overall survival and quality of life. Changes in the Lung Allocation Score (LAS) in 2005 have resulted in increased transplants and decreased waitlist mortality in this population. Indications for transplant evaluation and listing include the clinical progression of the disease and related mortality risk ≥50% at 2 years without a transplant. Patients with clinically rapid deterioration or acute flares needing hospitalization can be bridged to transplant on extracorporeal support while remaining ambulatory and free from mechanical ventilation.

https://doi.org/10.5772/intechopen.105725

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.