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Dave Singh, MD, discusses IL-33 inhibition for non-type 2 COPD, 2027 GOLD report refinements, and how to view biologics not yet in the GOLD algorithm.
Targeting the alarmin interleukin (IL)-33 may extend biologic therapy to patients with chronic obstructive pulmonary disease (COPD) who lack evidence of type 2 inflammation, according to Dave Singh, MD. Singh is professor of clinical pharmacology and respiratory medicine at the University of Manchester, medical director of the Medicines Evaluation Unit and a member of the GOLD Science Committee. He discussed IL-33 inhibition and the 2027 GOLD report with HCPLive at the 2026 GOLD COPD International Conference in Philadelphia, Pennsylvania.
Singh described non-type 2 COPD, marked by low eosinophil counts, as an area of clear unmet need. IL-33 is released by epithelial and endothelial cells and drives a broad range of inflammatory pathways, which makes it a candidate target beyond eosinophilic disease.
In the replicate phase 3 OBERON and TITANIA trials, tozorakimab 300 mg every 4 weeks reduced moderate to severe exacerbations by 30% and 29%, respectively, across former and current smokers.¹˒² In a pooled analysis, the reduction was 23% among patients with blood eosinophil counts below 150 cells/µL and 43% among those with counts of 300 cells/µL or higher.²
Singh expects responses to vary among patients. Until clinicians can predict who will benefit, he said, treatment decisions may depend on assessing response after a trial of therapy.
Singh described the 2027 GOLD update as a refinement rather than a major advance, adding detail on issues clinicians see often in practice.³ The report expands its discussion of the evidence on mucus plugging. It also adjusts the language around early, mild and pre-COPD, terms Singh acknowledged often cause confusion.
He linked the focus on earlier disease to clinical trial design. Most COPD trials enroll patients late in the course of the disease. Singh emphasized the value of studying younger, higher-risk individuals before substantial lung damage develops, both to support earlier diagnosis and to build a stronger evidence base.
GOLD discusses published trial data for investigational biologics such as tozorakimab and astegolimab but leaves them out of its treatment algorithm until they are licensed.³ Singh noted that tozorakimab has 2 positive phase 3 trials. Roche has reported that astegolimab’s phase 3 results were less consistent.⁴
He advised clinicians to follow their local licensing framework. Once a biologic is approved in a given country, clinicians there can prescribe it according to its label.
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.
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