Abstract
Abstract
Severe asthma carries a disproportionately high health burden and about half of adults with this pathology have an eosinophilic phenotype. In these patients, in addition to the production of eosinophils in bone marrow, local eosinopoiesis mechanisms are activated in lung tissue. Benralizumab is a humanized monoclonal antibody, which joins with high affinity and specificity to the alpha subunit of the IL-5 receptor (IL-5Rα) on the surface of eosinophils and other cells. The main differentiator of its mechanism of action is related to the removal of a fucose residue in Fc, which increases up to 50 times the affinity to NK cells with eosinophil apoptosis by antibody-dependent cell cytotoxicity (CCDA), that leads to a direct, rapid and nearly complete depletion in both peripheral blood and bone marrow. Additionally, benralizumab reduces >90% of eosinophils in lung tissue and sputum. Several controlled and real-life clinical studies have shown that this action over eosinophils is related to increased asthma control and decreased future risk. The safety profile is adequate without documenting parasitic infestations or long-term adverse effects related to the reduction of eosinophils.
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