Abstract

IgE is a central molecule in type I hypersensitivity reactions. Currently, there is one approved anti-IgE therapeutic antibody, omalizumab. Next generation anti-IgE antibodies have primarily focused on improved affinity within the FceRI binding region. However, depending on the disease type, blocking IgE binding to both FceRI and FceRII may be important when treating atopy. We sought to create a therapeutic candidate which could neutralize soluble IgE and remove IgE bound to both FceRI and FceRII.

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