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Type 2 inflammation-targeted biologics have transformed asthma and chronic obstructive pulmonary disease (COPD) management within the past 2 years, with 2 agents now approved specifically for COPD's eosinophilic phenotype. Dupilumab (Dupixent) became the first COPD biologic in September 2024, when the FDA approved it based on the BOREAS (n = 468) and NOTUS (n = 470) trials, which showed 30% and 34% reductions, respectively, in annualized moderate or severe exacerbations among patients with blood eosinophil counts of 300 cells/µL or higher, alongside sustained gains in FEV1 and quality-of-life scores.1
Mepolizumab (Nucala) followed 8 months later, becoming the first COPD biologic approved for eosinophil counts as low as 150 cells/µL based on the MATINEE (rate ratio, 0.79; 95% CI, 0.66-0.94; P=.01) and METREX (rate ratio, 0.82; 95% CI, 0.68-0.98; P=.04) trials.2 The 2026 GOLD report further lowered the threshold for its highest-risk Group E classification to a single moderate exacerbation in the prior year and folded dupilumab and mepolizumab into its follow-up algorithm for eosinophilic, still-exacerbating patients, while the 2026 GINA update sharpened its push to minimize oral corticosteroid (OCS) exposure in favor of biologic therapy.3
Against that backdrop, a panel of pulmonary nurse practitioners gathered virtually, moderated by Mollie A. Chartoff, MSN, of the Vanderbilt Lung Institute and included APPs representing academic, community hospital, and private pulmonary practices across Tennessee, Louisiana, and Alabama.
The conversation landed at a moment when both diseases are increasingly reframed around biomarker-driven phenotyping rather than diagnostic labels alone, with guidelines asking clinicians to identify type 2 inflammation—elevated blood eosinophils or fractional exhaled nitric oxide (FeNO)—regardless of whether a patient carries an asthma or COPD diagnosis. The panel used that lens to work through new data on airway mucus plugging, cumulative steroid burden, and the access barriers shaping their day-to-day escalation decisions.
Much of the discussion centered on when to escalate beyond inhaled triple therapy. Panelists agreed recurrent OCS bursts—sometimes just 1 or 2 in a 6-month span—should trigger consideration of a biologic, citing data that cumulative prednisone doses of 500 to 1,000 mg over a lifetime meaningfully raise the risk of diabetes, cataracts, osteoporosis, and heart failure. For asthma, the panel weighed dupilumab, mepolizumab, and tezepelumab (Tezspire) against one another and agreed insurance coverage often dictates the choice as much as biomarker profile does; several panelists said tezepelumab, which targets thymic stromal lymphopoietin and carries no eosinophil threshold, has become their fallback when patients do not qualify for interleukin-4, interleukin-13, or interleukin-5-targeted options. Mucus plugging drew specific engagement: panelists cited VESTIGE trial data showing dupilumab significantly reduced airway mucus plug scores by week 24, correlating with lung function gains, and CASCADE trial findings that tezepelumab similarly reduced occlusive mucus plugs on CT imaging.4,5 Several panelists said they now actively look for mucus plugging on CT as a cue to consider a biologic in symptomatic patients.
On the COPD side, panelists described dupilumab and mepolizumab as having changed what they can offer patients who previously had little beyond inhalers and chronic steroids, citing BOREAS, NOTUS, MATINEE, and METREX data on exacerbation reduction and, for dupilumab, sustained FEV1 gains.1,2 One nurse practitioner on the panel described the effect on a patient who had cycled repeatedly through hospitalizations before starting dupilumab: “He has not been in the hospital since. He’s completely off of oxygen. He never has exacerbations anymore.” Panelists agreed biologics are still started too late in COPD, often only after patients are referred for advanced lung disease evaluation, and called for better workflow support, clearer patient-selection algorithms, and real-world data on whether biologics meaningfully reduce cumulative steroid exposure. Looking ahead, several panelists expressed interest in tozorakimab, an interleukin-33-targeted agent in development that would carry no eosinophil threshold, as a potential option for COPD patients without a clear type 2 signature.