Real-World Multicenter Experience with Mepolizumab and Benralizumab in the Treatment of Uncontrolled Severe Eosinophilic Asthma Over 12 Months.

Treatment of severe eosinophilic asthma (SEA) has been revolutionized by the development of monoclonal antibodies targeting underlying immunological pathways of eosinophilic asthma. Two of the most frequently used antibodies in clinical practice are mepolizumab, targeting interleukin (IL) 5 and benralizumab, targeting the IL5 receptor alpha. The comparative treatment efficacy of these antibodies remains unclear, particularly regarding long-term outcomes. In this multicenter, retrospective study, we included 123 patients treated with mepolizumab and 64 patients treated with benralizumab for 12 months at one of three study sites in Germany. Data were collected at baseline and after 6 and 12 months of therapy. Endpoints were changes in pulmonary function (PF), exacerbation rate, oral corticosteroid (OCS) use and dose, asthma control test (ACT) score and fractional exhaled nitric oxide (FeNO) levels. Both mepolizumab and benralizumab led to significant improvements in PF with an increase in median forced expiratory volume (FEV1) after 12 months from 59% to 74% for mepolizumab and 63% to 72% for benralizumab. Treatment also led to significant improvements in ACT scores after 12 months (mepolizumab: 13 [interquartile range (IQR) 9-17] to 19 [IQR 15-23]; benralizumab: 12 [IQR 9-16] to 22 [IQR 16-25]) as well as a reduction of mean OCS dose (mepolizumab 8 mg [IQR 5-12.5 mg] median prednisolone equivalent at baseline to 5 mg [IQR 3-7.5 mg]; benralizumab 7.5 mg [IQR 5-15 mg] to 5 mg [IQR 2-10 mg]). The exacerbation rates were reduced significantly, irrespective of the treatment. Overall, changes were similar after 6 and 12 months of therapy. Both mepolizumab and benralizumab are highly effective in the long-term treatment of SEA, with no clinically relevant differences in outcomes after 12 months of therapy. In both groups, improvements were similar after 6 and 12 months of therapy, underlining the feasibility of early treatment evaluation.

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© 2021 Kayser et al.

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Katrin Milger reports personal fees/speaker honoraria from AstraZeneca, GSK, Novartis, Sanofi, outside the submitted work. Nikolaus Kneidinger reports personal fees from AstraZeneca outside the submitted work. Stephanie Korn reports grants, personal fees from AstraZeneca, grants, personal fees from GSK, personal fees from Novartis, personal fees from Sanofi, personal fees from Teva, during the conduct of the study. Roland Buhl received grants to his institution and/or personal fees from Boehringer Ingelheim, GSK, Novartis, and Roche, as well as personal fees from AstraZeneca, Berlin-Chemie, Chiesi, Cipla, Sanofi, and Teva, outside the submitted work. Tobias Welte and/or his institution received grants and advisory/lecture/clinical trial fees from AstraZeneca, Basilea, Biotest, Bayer, Boehringer, Berlin Chemie, GSK, Infectopharm, MSD, Novartis, Pfizer, Roche, AstraZeneca, Basilea, Biotest, Bayer, Boehringer, Gilead, GSK, Janssen, Novartis, Pfizer, Roche, all outside the submitted work. Hendrik Suhling reports personal fees/speaker honoraria from AstraZeneca, GSK, Novartis and Sanofi, outside the submitted work. The authors report no other conflicts of interest in this work.