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*RHAPSIDO also inhibits the BTK-related kinases TEC and BMX. In a preclinical study, RHAPSIDO demonstrated high affinity and selectivity for BTK, with a subnanomolar binding constant (K_d) of 0.63 nM, and a selectivity of 175-fold against TEC (K_d of 110 nM) and 857-fold against BMX (K_d of 540 nM). RHAPSIDO did not show binding to ITK, EGFR, ERBB2, ERBB4, or JAK3 at concentrations of up to 10 µM. The clinical significance of this data has not been demonstrated.^1,2

BTK plays a key role in CSU³

CSU may be mediated by IgE and IgG inflammatory pathways⁴

BTK is expressed in select immune cells, including dermal mast cells, and can be activated by IgE (autoallergic) and IgG (autoimmune) pathways via FcεRI.³

Intracellular BTK signaling leads to mast cell degranulation and the release of histamine and other proinflammatory mediators.³

The pathogenesis of CSU has not been fully elucidated; however, it is believed to be primarily a mast cell–driven disease.^4,5

RHAPSIDO offers a unique approach to CSU¹

By inhibiting BTK in mast cells, RHAPSIDO blocks both IgE and IgG pathways, stopping mast cell degranulation and the release of histamine and proinflammatory mediators.¹