Table 1 Monoclonal antibodies for the management of severe asthma

Omalizumab

Human monoclonal antibody IgG1κ, subcutaneous.

It binds to free IgE by inhibiting its binding to high- and low-affinity IgE receptors (FcεRI and CD23). This reduces the expression of the aforementioned receptors in mast cells, basophils, and dendritic cells, limiting the type 2 immune response mediated by IgE. It also modulates the production of interferon-alpha (IFN-α) dendritic cells, reducing virus-induced exacerbations.

Mepolizumab

Humanized monoclonal antibody IgG1κ, subcutaneous.

It inhibits the maturation, activation, proliferation, and recruitment of eosinophils. It binds to a specific epitope of IL-5, preventing its interaction with the IL-5 receptor (IL-5Rα).

Reslizumab

Humanized monoclonal antibody IgG4κ, intravenous.

It inhibits the maturation, activation, proliferation, and recruitment of eosinophils. It binds to IL-5, preventing its binding to IL-5Rα. It’s in vitro affinity for IL-5 and its ability to suppress proliferation is greater than that of mepolizumab.

Benralizumab

Humanized monoclonal antibody IgG1κ, subcutaneous.

It binds to the alpha subunit of the receptor (IL-5Rα) avoiding the transduction of eosinophil survival signals. In addition, there is an amplified apoptosis mechanism induced by the activation of the FcyRIIIa (CD16a) receptor, mediated by natural killer cells and macrophages through a process called antibody-dependent cellular cytotoxicity. It reduces eosinophils and basophils.

Dupilumab

Human monoclonal antibody IgG4, subcutaneous.

It binds to the alpha subunit of the IL-4 receptor (IL-4Rα) shared by IL-4 and IL-13, thereby inhibiting the type 2 immune response. Simultaneous receptor blockade occurs in hematopoietic and nonhematopoietic cells.