Why degrading BTK is a different proposition than inhibiting it The Nurix and Roche partnership on bexobrutideg is the latest sign that targeted protein degradation is moving well beyond oncology. Written byAndrea Corona

https://www.drugdiscoverynews.com/why-degrading-btk-is-a-different-proposition-than-inhibiting-it-17428?utm_campaign=DDN_Newsletter_Dose&utm_medium=email&_hsenc=p2ANqtz-8sM96BRaPG-nlKrZw1tDw5iXBSRYqTuEJp8BJf1XRrT-MuBQbJixW6KiVi2cOizgI166vfDFRb87cXEJR_Q7Ayb1nLnw&_hsmi=432711347&utm_content=432711347&utm_source=hs_email Bruton's tyrosine kinase (BTK) inhibitors have transformed the treatment of B-cell malignancies over the past decade. Ibrutinib's approval in 2013 validated BTK as a drug target, and a succession of second-generation inhibitors — acalabrutinib, zanubrutinib, pirtobrutinib — have extended that validation with improved selectivity and tolerability. More recently, BTK inhibition has moved into autoimmune disease: The FDA approved remibrutinib and rilzabrutinib in 2025 for chronic spontaneous urticaria (CSU) and immune thrombocytopenia, respectively, and multiple Phase 2 and Phase 3 trials in multiple sclerosis (MS) are underway.