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News
Bexobrutideg is turning heads in CLL/SLL treatment. The novel BTK degrader achieved response rates above 83% across multiple treatment lines — including in treatment-naive patients — in a phase 1 trial. Its ability to degrade both wild-type and mutant BTK makes it a promising option for patients who've stopped responding to standard BTK inhibitors, and a pivotal phase 3 trial is now on the horizon.
A new BTK degrader is showing strong results in hard-to-treat blood cancers
Bexobrutideg (NX-5948), a novel BTK protein degrader, is demonstrating impressive response rates across treatment lines in chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL). Updated data from the phase 1a/b NX-5948-301 trial, presented at the 2026 SOHO Annual Meeting, showed an overall response rate (ORR) of 83% in heavily pretreated relapsed/refractory patients — with responses holding up even in those with high-risk genetic features like TP53 mutations and unmutated IGHV.
Unlike standard BTK inhibitors, bexobrutideg works by triggering the complete destruction of BTK protein — including resistant mutant forms — through a cereblon-mediated degradation pathway. This mechanism addresses both the kinase and scaffolding functions of BTK, potentially overcoming resistance that sidelines current therapies. A phase 3 trial (DAYBreak CLL-306) is now planned to pit bexobrutideg head-to-head against pirtobrutinib in approximately 620 patients with relapsed/refractory CLL/SLL.
By the Numbers
Why it matters: BTK resistance mutations affect more than half of patients who progress on current therapies, leaving a significant unmet need. Bexobrutideg's ability to degrade — not just inhibit — BTK could be a meaningful advance for patients who've exhausted standard options.
