Key asthma updates from EAACI 2026

In this video, Sebastian Riemann reviews selected asthma highlights from EAACI 2026, focusing on new clinical trial data, improved patient phenotyping, mechanisms of treatment response and the role of allergen immunotherapy.

An important clinical update concerned depemokimab, an ultra-long-acting anti-IL-5 antibody administered once every 26 weeks. The placebo-controlled SWIFT-1 and SWIFT-2 phase III trials had previously demonstrated a 54% reduction in annualised exacerbations in the pooled analysis.¹ At EAACI 2026, results from the phase III NIMBLE trial were discussed.² This study evaluated switching to depemokimab in almost 1,700 patients with severe asthma who had already experienced clinical benefit from mepolizumab or benralizumab for at least 12 months. At 52 weeks, annualised exacerbation rates were 0.57 with depemokimab and 0.49 with continued mepolizumab or benralizumab, corresponding to a rate ratio of 1.16. As the upper limit of the 95% confidence interval exceeded the predefined margin, non-inferiority was not formally demonstrated. Nevertheless, most patients in both groups remained free from clinically significant exacerbations, while asthma control, lung function, quality of life and safety outcomes remained comparable. Depemokimab has received FDA and EMA approval, adding a further option to the biologic armamentarium for severe eosinophilic asthma, although the missed non-inferiority endpoint should be considered when interpreting the NIMBLE results.

The congress also highlighted the value of more precise phenotyping when selecting biologic therapy. Age at asthma onset may help predict treatment response, with new data suggesting that dupilumab, like anti-IL-5 therapy, may be particularly effective in late-onset disease. Adding sputum biomarkers, including local cytokines, into treatment algorithms was associated with substantially higher rates of clinical remission than standard clinical assessment alone. Eosinophil peroxidase may provide further evidence on ongoing eosinophil activity and tissue damage, even when absolute sputum eosinophil counts are low. Polygenic risk scores combining large numbers of genetic variants are also being investigated as potential tools for predicting an individual’s future risk of developing asthma.

Regarding mechanisms of response and non-response to anti-T2 biologics, a population of intermediate type 2 innate lymphoid cells producing both type 2 cytokines and IL-17a was associated with poorer treatment responses. This finding suggests that mixed inflammatory pathways may contribute to biologic non-response and could support the future development of combined or broader therapeutic strategies. Obesity was highlighted as another key treatable trait, with a bidirectional relationship with asthma: asthma and corticosteroid exposure may contribute to weight gain, while obesity independently increases the risk of developing asthma and, once asthma is present, worsens symptoms and exacerbation risk. Trials of metabolic interventions, including GLP-1 receptor agonists, are awaited to clarify whether treating obesity can improve asthma outcomes.

Finally, allergen immunotherapy may be considered in selected patients whose severe asthma is well controlled with biologic therapy, although it remains contraindicated in uncontrolled disease. Multidisciplinary collaboration, including input from allergologists where available, is recommended, and prior non-adherence to pharmacotherapy should be considered a predictor of non-adherence to immunotherapy.