Journal of medicinal chemistry · 2026
Leveraging Kinase Drugs for Neurosciences: Discovery of Selective, CNS-Penetrant Reversible Bruton's Tyrosine Kinase Inhibitors as Therapeutics for Neuroinflammation.
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Hopkins Brian T, Marx Isaac E, Vandeveer Harlod George, Nevalainen Marta, Basile Rebecca, Bajrami Bekim, Choi Colin K, Grater Richard J, Gu Chungang, Hoemberger Marc, Kadakia Ekta, Kapadnis Sudarshan K, Liu Ying, Ma Bin, Magee Tom, Metrick Claire M, Mingueneau Michael, Muste Cathy A, Parker Harp Chelsea R, Prince Robin J, Santoro Joseph C, Schulz Jurgen, Sciabola Simone, Tang Hao, Wang Ti, Meissner Robert, Bohnert Tonika
Аннотация
Bruton's tyrosine kinase (BTK) is a nonreceptor tyrosine kinase clinically validated to impact B-cell development. Molecules designed to target BTK, through either covalent or reversible inhibition, have transformed the treatment of hematopoietic malignancies. Wen, T.; Wang, J.; Shi, Y.; Qian, H.; Liu, P. Inhibitors targeting Bruton's tyrosine kinase in cancers: drug development advances. Leukemia 2021, 35(2), 312-332.10.1038/s41375-020-01072-6. These advancements are paving the way for new therapeutics to treat nononcology indications, De Bondt, M.; Renders, J.; Struyf, S.; Hellings, N. Inhibitors of Bruton's tyrosine kinase as emerging therapeutic strategy in autoimmune diseases. Autoimmun. Rev. 2024, 23(5), 103532.10.1016/j.autrev.2024.103532 such as multiple sclerosis (MS), and provide benefits to patients with progressive disease. In this context, we describe the discovery of a highly selective, CNS-penetrant, reversible BTK inhibitor designed to sequester Tyr-551, the critical phosphorylation site, into an inactive conformation, thereby blocking B-cell receptor (BCR) signaling. While this class of molecules demonstrated excellent safety when administered at doses that fully inhibited B-cell activity in the periphery, increasing exposure to achieve similar efficacy in the CNS led to adverse findings. This raises the question of whether it was a molecule-specific off-target toxicity or a consequence of blocking BTK function in microglia.