In a recent study, Bruton's tyrosine kinase (BTK) inhibitor Remibrutinib suppressed hives effector cells aroused by serum from chronic urticaria-affected people independent of Omalizumab clinical responsiveness and FcεR1 (high-affinity IgE receptor) expression level. Researchers wanted to know how Remibrutinib affected human blood basophils and CD34+-derived mast cells activation triggered by serum procured from individuals suffering from hives.

The study comprised a sex-matched control group, 22 subjects having chronic spontaneous urticaria (mean age, 52 years; 27% females), and 22 subjects having chronic inducible urticaria (mean age, 46 years; 27% females). Based on total IgE levels, clinical data, and expression of FcεR1a on blood basophils, volunteers were categorized as non-responders or responders to anti-IgE treatment.

Mast cells and basophils were tested in vitro for their responses to serum exposure and for the inhibitory effects of Remibrutinib using alterations in CD63 expression, which is an activation marker.

Remibrutinib blocks the arousal brought on by factors found in the serum of individuals with inducible and spontaneous chronic urticaria, as well as the degranulation aroused by IgE cross-linking in basophils and mast cells. Compared to controls, the patient's serum induced more effector cells to degranulate. As found, serum from chronic urticaria patients exhibited a higher ability to stimulate mast cell and basophil degranulation compared to sera procured from healthy controls.

Mast cells and basophils arousal by patient sera was not associated with Omalizumab response. In spite of how well individuals with chronic urticaria respond to Omalizumab, Remibrutinib suppressed the activation of human mast cells and basophils that is elicited in vitro by exposure to the serum.