Treating IgE-mediated diseases via targeting IgE-expressing B cells using an anti-CεmX antibody

Targeting the IgE pathway is a clinically validated strategy for treating IgE-mediated diseases. Omalizumab, an anti-IgE antibody, which binds to free IgE and prevents the binding of IgE to Fc epsilon RI on mast cells and basophils has been approved for severe persistent allergic asthma and chronic spontaneous (idiopathic) urticaria. The therapeutic efficacy of anti-IgE has also been reported in allergic rhinitis, allergic bronchopulmonary aspergillosis, latex allergy, atopic dermatitis, allergic urticaria, anaphylaxis, and others. Anti-C epsilon mX, which binds to membrane-bound IgE (mIgE) on IgE-switched B cells, lyses mIgE-expressing B lymphoblasts and prevents the allergen-induced generation of IgE-producing plasma cells, offers an alternative mechanism of intervening with the IgE inflammatory pathway. Because anti-C epsilon mX does not bind to free IgE, it can modulate the IgE pathway regardless of the serum IgE levels in treated patients. These unique pharmacologic mechanisms potentially enable anti-C epsilon mX to provide different clinical utilities from anti-IgE and serve as a therapeutic and a prophylactic in some IgE-mediated diseases, which are not adequately treated with current medicine.