The rationale for designing the anti-IgE therapeutic antibodies and the pharmacological mechanisms of anti-IgE therapy have been summarized in review articles by the inventor of the anti-IgE therapy, Tse Wen Chang, and his colleagues. Perhaps the most dramatic effect, which was not foreseen at the time when the anti-IgE therapy was designed and which was discovered during clinical trials, is that as the free IgE in patients is depleted by<unk> , the FcεRI receptors on basophils, mast cells, and dendritic cells are gradually down-regulated with somewhat different kinetics, rendering those cells much less sensitive to stimulation by allergens. Thus, therapeutic anti-IgE antibodies such as<unk>  represent a new class of potent mast cell stabilizers. This is now thought to be the fundamental mechanism for<unk> 's effects on allergic and non-allergic diseases involving mast cell degranulation. Many investigators have identified or elucidated a host of pharmacological effects, which help bring down the inflammatory status in<unk> -treated patients. IgE in allergic diseases In conjunction with achieving the practical goal to investigate the applicability of the anti-IgE therapy as a potential treatment for allergic diseases, the many corporate-sponsored clinical trials of TNX-901 and<unk>  on asthma, allergic rhinitis, peanut allergy, chronic idiopathic urticaria, atopic dermatitis, and other allergic diseases, have helped define the role of IgE in the pathogenesis of these prevalent allergic diseases. For example, the clinical trial results of<unk>  on asthma have unambiguously settled the long debate whether IgE plays a central role in the pathogenesis of asthma. Numerous investigator-initiated case studies or small-scale pilot studies of<unk>  have been performed on various allergic diseases and several non-allergic diseases, especially inflammatory skin diseases. These diseases include atopic dermatitis, various subtypes of physical urticaria (solar, cold-induced, local heat-induced, or delayed pressure-induced), and a spectrum of relatively less prevalent allergic or non-allergic diseases or conditions, such as allergic bronchopulmonary aspergillosis, cutaneous or systemic mastocytosis, bee venom sensitivity (anaphylaxis), idiopathic anaphylaxis, eosinophil-associated gastrointestinal disorder, bullous pemphigoid, interstitial cystitis, nasal polyps, and idiopathic angiodema. Roles in non-allergic diseases Several groups have reported clinical trial results that<unk>  may be effective in patients with non-allergic asthma. This seems to be contrary to the general understanding of the pharmacological mechanisms of the anti-IgE therapy discussed above. Furthermore, among the diseases in which<unk>  has been studied for efficacy and safety, some are not allergic diseases, because hypersensitivity reactions toward external antigens is not involved. For example, a portion of the cases of chronic idiopathic urticaria and all cases of bullous pemphigoid are clearly autoimmune diseases. For the remaining cases of chronic idiopathic urticaria and those of the different subtypes of physical urticaria, the internal abnormalities leading to the disease manifestation have not been identified. Notwithstanding these developments, it is apparent that many of those diseases involve inflammatory reactions in the skin and the activation of mast cells. An increasing series of papers have shown that IgE potentiates the activities of mast cells and<unk>  can function as a mast cell-stabilizing agent, rendering these inflammatory cells to be less active.
Omalizumab
Crizanlizumab
Reslizumab
Lirentelimab
Tildrakizumab
Risankizumab
Bebtelovimab
Brolucizumab