DeCure's autonomous Respiratory AI scientist is researching a drug-repurposing hypothesis for pneumonia — screening already-approved drugs against its 36-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease modulePneumonia maps to a 36-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 pneumonia 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
interleukin 1 beta (IL1B) — IL1B 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 2sdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 5R8Q · 1.23 Å · ligand 1-methyl-N-{[(2S)-oxolan-2-yl]methyl}-1H-pyrazole-3-carboxamide (JGY). Experimental structure, not a prediction.
What the evidence adds up to
In a retrospective study of 12 children with severe refractory Mycoplasma pneumoniae pneumonia, methylprednisolone pulse therapy (30 mg/kg) was given a mean of 5.4 days after admission, after all children had deteriorated despite appropriate antibiotics. After the steroid pulse, clinical symptoms improved in all patients with no adverse events reported; fever subsided within 0–2 hours, abnormal radiological findings resolved within a mean of 2.6 days, and C-reactive protein fell from a mean of 6.7 mg/dL to 1.3 mg/dL within 3.0 days. The sample is small, uncontrolled, and retrospective, so these results cannot be taken as proof of efficacy.
A 2021 study in a mouse model of pneumonia investigated the cytokine oncostatin M (OSM). Transcriptional profiling of whole-lung tissue after 6 hours of infection with OSM neutralisation revealed 241 differentially expressed genes, many linked to STAT1, STAT3 and interferon signalling. By 24 hours, OSM neutralisation led to upregulation of STAT1 and STAT3 activation, suggesting that interrupting OSM dysregulates these pathways. Neutrophils and, to a lesser extent, macrophages were identified as the primary sources of OSM, indicating a positive feedback loop. The authors concluded that OSM from recruited neutrophils tunes early innate immune signalling and improves pneumonia outcomes in this model.
A 1948 report from Philadelphia General Hospital noted that pneumonia mortality had declined sharply in the preceding decade but that the hospital still saw a serious problem, with an impression that response to specific therapy had become less dramatic than in earlier years. The study was designed to verify that impression, but no quantitative results from that verification are given in the abstract.
A 2008 letter responding to a previous article defended the concept of switching from intravenous to oral antibiotics in severe community-acquired pneumonia, citing the 2007 ATS/IDSA guidelines which give a strong recommendation with level II evidence for that strategy. The letter does not present new data.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Allergy Asthma and Immunology Research · 2013 · 90 citations · open access
Effects of Methylprednisolone Pulse Therapy on Refractory<i>Mycoplasma pneumoniae</i>Pneumonia in Children
AbstractPURPOSE: Mycoplasma pneumoniae (M. pneumoniae) is one of the most common causes of community-acquired pneumonia in children. The clinical course is typically self-limited and benign; however, rare cases of severe pneumonia can develop despite appropriate antibiotic therapy. We studied the effects of methylprednisolone pulse therapy on severe refractory M. pneumoniae pneumonia in children. METHODS: The clinical effects of methylprednisolone therapy were evaluated retrospectively in 12 children with severe refractory M. pneumoniae pneumonia, which was diagnosed serologically. All patients developed respiratory distress, high fever, and initial lobar pneumonic consolidation based on radiological findings. All clinical symptoms deteriorated despite appropriate antibiotic therapy. Thus, children were treated with intravenous methylprednisolone pulse therapy in addition to antibiotics. RESULTS: The average febrile period before admission was 4.9±1.7 days, and fever persisted in all children until steroid administration. Methylprednisolone pulse therapy (30 mg/kg) was given 5.4±2.5 days after admission. After methylprednisolone pulse therapy, clinical symptoms improved in all patients without adverse events. The fever subsided 0-2 h after initiation of corticosteroid therapy. The abnormal radiological findings resolved within 2.6±1.3 days, and the high C-reactive protein levels (6.7±5.9 mg/dL) on admission decreased to 1.3±1.7 mg/dL within 3.0±1.1 days after starting corticosteroid therapy. CONCLUSIONS: Three-day methylprednisolone pulse therapy could be applied to treatment of refractory M. pneumoniae pneumonia despite appropriate antibiotic therapy and appeared to be efficacious and well-tolerated.
New England Journal of Medicine · 1948 · 14 citations
Pneumonia at the Philadelphia General Hospital, 1936–1946
AbstractIN RECENT years pneumonia has rapidly become less important as a cause of death. There has been a sharp decline in admission of patients with pneumonia in most hospitals and recent studies on the effectiveness of modern therapy of pneumonia have indicated a low case mortality. Nevertheless, at the Philadelphia General Hospital, pneumonia remains a serious problem, and the impression has been obtained that in late years the response of patients with pneumonia to specific therapy has not been so dramatic as that observed in earlier years. The present study was projected to verify this impression, and to determine if . . .
Infection and Immunity · 2021 · 12 citations · open access
Neutrophil-Derived Oncostatin M Triggers Diverse Signaling Pathways during Pneumonia
AbstractPneumonia is a major public health concern, causing significant morbidity and mortality annually despite the broad use of antimicrobial agents. Underlying many of the severe sequelae of acute lung infections is dysfunction of the immune response, which remains incompletely understood yet is an attractive target of adjunct therapy in pneumonia. Here, we investigate the role of oncostatin M (OSM), a pleiotropic cytokine of the interleukin-6 (IL-6) family, and how its signaling modulates multiple innate immune pathways during pneumonia. Previously, we showed that OSM is necessary for neutrophil recruitment to the lungs during pneumonia by stimulating STAT3-driven CXCL5 expression. In this study, transcriptional profiling of whole-lung pneumonia with OSM neutralization revealed 241 differentially expressed genes following only 6 h of infection. Many downregulated genes are associated with STAT1, STAT3, and interferon signaling, suggesting these pathways are induced by OSM early in pneumonia. Interestingly, STAT1 and STAT3 activation was subsequently upregulated with OSM neutralization by 24 h, suggesting that OSM interruption dysregulates these central signaling pathways. When we investigated the source of OSM in pneumonia, neutrophils and, to a lesser extent, macrophages appear to be primary sources, suggesting a positive feedback loop of OSM production by neutrophils. From these studies, we conclude that OSM produced by recruited neutrophils tunes early innate immune signaling pathways, improving pneumonia outcomes.
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.
