Omalizumab binds free IgE in the serum, forming trimers and hexamers. The drug binds to IgE at the same site that the high-affinity IgE receptor (Fc-epsilon-RI) binds, so IgE bound to drug cannot bind its receptor on mast cells and basophils. Omalizumab does not bind IgE that is already bound to Fc-epsilon-RI and so should not result in cross-linking of receptors. As a result of the binding of free IgE, the number of IgE receptors on the surface of mast cells and basophils declines over time, which is believed to be a critical component of the clinical effect of the drug. Omalizumab also blocks binding of IgE to the low-affinity IgE receptor (Fc-epsilon-RII or CD23, not shown), although the therapeutic relevance of this is not known.
