Bruton’s tyrosine kinase (BTK)

Bruton’s tyrosine kinase (BTK) is a non-receptor tyrosine kinase encoded by the BTK gene, classified within the Tec family of kinases[3][5]. It plays a central role in mediating signal transduction from the B-cell antigen receptor and is essential for B-cell development, proliferation, and survival[1][3][5][7]. BTK is also expressed in multiple hematopoietic lineages, contributing to immune cell activation, especially within the myeloid lineage[1][7]. BTK inhibitors selectively target the kinase activity of BTK, thereby blocking downstream signaling pathways central to both malignant and autoimmune pathologies. Clinically, BTK inhibition has transformed the management of B-cell malignancies and is expanding into autoimmunity and chronic inflammation[1][2][4]. Important drugs in this class include ibrutinib, acalabrutinib, zanubrutinib, and others, with mechanisms ranging from irreversible (covalent) inhibition to reversible blockade of ATP binding[3][4][5][6]. Safety concerns focus on bleeding risk, cardiac events, infection, and development of resistance mutations, particularly in patients under long-term therapy[1][6].

Other names

Tyrosine-protein kinase BTKBtkBruton's kinase

Inhibition of BTK leads to blockade of B-cell receptor signaling Suppression of B cell proliferation and survival Modulation of myeloid cell activation Reduction of autoantibody production in autoimmune disorders