Tozorakimab now has three phase 3 COPD wins in 2026. AstraZeneca’s IL-33 inhibitor has done what two rivals couldn’t, and the question has shifted from whether the target works to why competitors got it wrong.
The Miranda study enrolled 1,451 COPD patients still experiencing moderate-to-severe exacerbations on inhaled standard of care. Patients received 300 mg tozorakimab or placebo every two weeks for a year. The trial met its primary endpoint with statistical significance, cutting annualized moderate-to-severe exacerbation rates among former smokers, and hit its secondary endpoint in the overall population.
Miranda follows a pair of phase 3 COPD wins for tozorakimab last month, giving AstraZeneca three clean readouts in a row. Two other drugs targeting IL-33 signaling, Sanofi and Regeneron’s itepekimab and Roche’s astegolimab, both failed their COPD trials. AstraZeneca’s argument has always been mechanism: tozorakimab completely blocks both the ST2 and RAGE/EGFR signaling cascades. RAGE/EGFR affects mucus production, which drives exacerbations, and the epithelial remodeling that decreases lung function in COPD patients, a piece of the pathway those drugs don’t address.
If regulators accept that mechanistic distinction, tozorakimab doesn’t just win a COPD indication. It validates differentiated IL-33 inhibition as a viable regulatory path and could open the door for tozorakimab’s late-stage program in severe viral lower respiratory tract disease and its phase 2 asthma study.
AstraZeneca has projected peak sales of $3 billion to $5 billion. Miranda data will be shared with regulators; public presentation at a future medical meeting, date unset.
— Sarah Chen