ArticleTranslational lung cancer research2025
First case report of immune checkpoint inhibitor-related pneumonitis triggered by bispecific antibody (anti-PD-L1 and anti-CTLA-4) in a patient with non-small cell lung cancer: case report.
Article in Translational lung cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Monoclonal Antibodies and Derivatives: Therapeutic Tools for Cancer.Oncology research · 2026Review
- Application of corticosteroid therapy with esophageal cancer: a case report in the treatment of radiation-induced and immune-related pneumonia.AME case reports · 2026Article
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6 authors.
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Abstract
Background: Immune checkpoint inhibitors (ICIs) targeting programmed cell death-1 (PD-1) and cytotoxic T lymphocyte associated protein 4 (CTLA-4) have significantly improved the treatment of non-small cell lung cancer (NSCLC), offering new therapeutic options. However, immune-related adverse events (irAEs), particularly immune checkpoint inhibitor-related pneumonitis (ICI-P), remain a serious concern. Bispecific antibodies targeting both programmed death-ligand 1 (PD-L1) and CTLA-4 have recently emerged as promising alternatives to traditional dual ICI therapies, offering comparable efficacy with a potentially lower risk of irAEs. We report the first documented case of ICI-P induced by a bispecific antibody targeting PD-L1 and CTLA-4 in a patient with NSCLC, with a comprehensive account of the diagnostic process and therapeutic management. Case Description: A 64-year-old man with stage IV lung squamous cell carcinoma was enrolled in a clinical trial of KN046 combined with chemotherapy. After three treatment cycles, he developed symptoms of ICI-P, including cough and dyspnea, which were confirmed by chest computed tomography (CT) and laboratory testing. His symptoms worsened despite initial corticosteroid therapy. Tocilizumab and nintedanib were subsequently added, resulting in rapid clinical and radiologic improvement. This case highlights the potential role of nintedanib in managing corticosteroid-refractory ICI-P, a challenging complication of ICI therapy. Conclusions: This case represents the first reported instance of ICI-P induced by a bispecific antibody targeting PD-L1 and CTLA-4, with a comprehensive account of its clinical course and management. Compared to conventional dual ICI regimens, bispecific antibodies may offer a more favorable safety profile. The observed benefit of nintedanib in this corticosteroid-refractory case suggests a potential role for anti-fibrotic therapy in managing early fibrotic changes. Further clinical studies are needed to validate this approach.
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