For this reason, some patients with type 2 disease may simultaneously need broader biologic coverage, Singh explained. He identified anti-alarmin therapy as a potential answer, since this approach can act on both type 2 and non-type 2 inflammatory pathways.
The session closed with a discussion of how clinicians might identify responders. Singh described 2 approaches: empiric treatment followed by assessment of response, which takes time and depends on how response is judged, or prediction based on clinical characteristics and biomarkers. Prediction remains the favored approach in the field, and Singh emphasized it should stay central as new treatments emerge.
What Lessons from Asthma Apply to COPD?
Clinical trials of asthma biologics in COPD have produced both successes and failures, according to Singh. Effect sizes have generally been smaller in COPD, which he said signals a fundamental difference in underlying biology.
Type 2 inflammation is one component of COPD but the dominant process in most patients with asthma, Singh explained. This distinction helps explain why some type 2 biologics effective in asthma have failed in COPD trials.
The field is now working to refine the use of type 2 biologics in COPD, Singh said. Asthma specialists have learned to rely on clinical features and biomarkers to match each patient with the most appropriate biologic, and COPD clinicians are pursuing a similar strategy.
Editor’s Note: This summary of a session has been edited for grammar and clarity using artificial intelligence tools. Singh had no relevant financial disclosures of note.
References
Singh D, Uller L, Brusselle G, Wedzicha JA. Targeting pathways in COPD: a glimpse into the future? Presented at: GOLD 2026 COPD International Conference; November 6, 2026; Philadelphia, PA.
Bhatt SP, Rabe KF, Martinez FJ, et al. Dupilumab for COPD with blood eosinophil evidence of type 2 inflammation. N Engl J Med. 2024;390(24):2274-2283. doi:10.1056/NEJMoa2401304.
Sciurba FC, Criner GJ, Christenson SA, et al. Mepolizumab to prevent exacerbations of COPD with an eosinophilic phenotype. N Engl J Med. 2025;392(17):1710-1720. doi:10.1056/NEJMoa2413181.