Authors
Ozge Sevil Karstarli Bakay, Emek Kocaturk
Published in
Expert opinion on pharmacotherapy. Aug 19, 2026. Epub Aug 19, 2026.
Abstract
Chronic spontaneous urticaria (CSU) results from multiple interacting pathogenic mechanisms. Despite available treatments, a proportion of patients remain inadequately controlled, supporting the need for therapeutic options.
This review examines the role of Bruton's tyrosine kinase (BTK) in CSU and summarizes the development of BTK inhibitors. Data on fenebrutinib, remibrutinib, rilzabrutinib, TAS5315, and other emerging agents are reviewed, focusing on mechanisms of action, efficacy, safety, and their potential place in practice. TAS5315 remains at an earlier stage of development, with CSU findings available from conference abstracts and registry data. The literature search included PubMed-indexed articles, clinical trial reports, regulatory documents, and congress presentations relevant to BTK inhibition in CSU.
BTK inhibitors act on intracellular pathways involved in mast-cell activation, basophil signaling, and B-cell mediated immune responses. Studies have shown reductions in disease activity across multiple BTK inhibitors, with benefit observed early after treatment initiation in several studies. Remibrutinib is the first BTK inhibitor approved for CSU and has the most extensive phase 3 evidence. Oral administration may provide a treatment option for patients. Defining the place of BTK inhibitors within treatment algorithms and identifying patients most likely to benefit from this approach remain areas for future research.
PMID:
42615080
Bibliographic data and abstract were imported from PubMed on 20 Aug 2026.
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