Omalizumab and new therapeutic targets in chronic spontaneous urticaria
Abstract Chronic spontaneous urticaria (CSU) is a common and distressing skin disease characterized by itchy wheals, angioedema, or both. There is currently no cure for CSU and symptomatic treatment is often insufficient. Omalizumab, a humanized anti-immunoglobulin (Ig) E monoclonal antibody, remains the only biological drug licensed for CSU, almost a decade after its approval. However, growing knowledge of the pathophysiological mechanisms of this disease has led to recent advances in its treatment, with several drugs in investigation both in pre-clinical and clinical settings. These include biologicals, such as dupilumab (anti-IL-4Rα), secukinumab (anti-IL-17), tezepelumab (anti-TSLP), ligelizumab (anti-IgE), lirentelumab (anti-Siglet 8), and barzovolimab (anti-cKIT), as well as “small molecules,” such as Bruton tyrosine kinase (BTK) inhibitors (remibrutinib) and a Mas-related G protein-coupled receptor X2 (MRGPRX2) antagonist. Here, we review the current and future therapeutic options for CSU, based on what is known about the pathogenesis of the disease.
| Main Authors: | , , , |
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| Format: | Digital revista |
| Language: | English |
| Published: |
Permanyer Publications
2024
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| Online Access: | http://scielo.pt/scielo.php?script=sci_arttext&pid=S2795-50012024000100011 |
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| Summary: | Abstract Chronic spontaneous urticaria (CSU) is a common and distressing skin disease characterized by itchy wheals, angioedema, or both. There is currently no cure for CSU and symptomatic treatment is often insufficient. Omalizumab, a humanized anti-immunoglobulin (Ig) E monoclonal antibody, remains the only biological drug licensed for CSU, almost a decade after its approval. However, growing knowledge of the pathophysiological mechanisms of this disease has led to recent advances in its treatment, with several drugs in investigation both in pre-clinical and clinical settings. These include biologicals, such as dupilumab (anti-IL-4Rα), secukinumab (anti-IL-17), tezepelumab (anti-TSLP), ligelizumab (anti-IgE), lirentelumab (anti-Siglet 8), and barzovolimab (anti-cKIT), as well as “small molecules,” such as Bruton tyrosine kinase (BTK) inhibitors (remibrutinib) and a Mas-related G protein-coupled receptor X2 (MRGPRX2) antagonist. Here, we review the current and future therapeutic options for CSU, based on what is known about the pathogenesis of the disease. |
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