BRISBANE, Calif. — Nurix Therapeutics, Inc. (Nasdaq: NRIX), a clinical-stage biopharmaceutical company focused on the discovery, development and commercialization of targeted protein degradation medicines in oncology and autoimmune disease, today presented new clinical data from patients with relapsed or refractory Waldenström macroglobulinemia (WM) treated in the Phase 1 clinical trial of its Bruton’s tyrosine kinase (BTK) degrader bexobrutideg (NX-5948). These data will be presented by Scott Huntington M.D., MPH, Associate Professor of Internal Medicine (Hematology), Yale School of Medicine, and a clinical investigator on the trial, on December 8, 2025, at 6 p.m. ET at the 67th American Society of Hematology (ASH) Annual Meeting and Exposition being held in Orlando, FL.
“The data presented at ASH in this older and heavily pre-treated WM population that includes patients with MYD88 and CXCR4 mutations continue to demonstrate encouraging activity of bexobrutideg with durable and deepening responses with longer time on treatment,” said Paula G. O’Connor, M.D., chief medical officer of Nurix. “Bexobrutideg was well tolerated, consistent with the overall study population and previous disclosures.”
“Collectively, these clinical data and recent data highlighting the unique properties of our potent and highly selective BTK degrader contribute to a growing body of evidence that support bexobrutideg’s potential to be the best-in-class and an important new therapeutic option for patients,” said Arthur T. Sands, M.D., Ph.D., president and chief executive officer of Nurix. “We believe bexobrutideg is an innovative therapy with the potential to transform care in CLL, WM, and additional NHL indications, while supporting long-term value creation as its development expands into inflammatory and autoimmune settings.”
The data presented at the 2025 ASH Annual Meeting include patients with WM (n=31) treated with bexobrutideg at doses ranging from 200 mg to 600 mg once daily by oral administration from both the Phase 1a dose escalation and Phase 1b cohort expansions. Among the 31 WM patients, the median age was 71.0 years (range 49–88 years), and the median number of prior lines of therapy was 3 (range 1-7). All 31 patients previously had been treated with a BTK inhibitor (100%), 28 had received prior chemotherapy/chemo-immunotherapy (90.3%), four had received prior non-covalent BTK inhibitor (12.9%), and four patients had received prior treatment with a BCL2 inhibitor (12.9%). Twenty-four patients (77.4%) had mutations in MYD88, and six patients (19.4%) had mutations in CXCR4. Three patients (9.7%) had central nervous system (CNS) involvement at baseline.
Bexobrutideg was well tolerated in patients with WM, consistent with the overall study population and previous disclosures. Adverse events (AEs) were predominantly low grade with the most common being neutropenia (29.0%), petechiae (29.0%), diarrhea (25.8%), anemia (22.6%), purpura/contusion (22.6%), and thrombocytopenia (19.4%). There were no dose limiting toxicities observed and no grade 5 AEs. Two treatment emergent AEs led to drug discontinuation. No new onset atrial fibrillation was observed.
As of the September 19, 2025 data cut, 28 patients were evaluable for response. Bexobrutideg demonstrated an objective response rate (ORR) of 75.0%, including very good partial responses (VGPR) in three patients (10.7%), partial responses (PR) in 14 patients (50.0%), and minor responses (MR) in four patients (14.3%). Six patients (21.4%) had a best response of stable disease (SD). In a subgroup analysis of patients with 2 or more disease assessments (n=23), ORR was 82.6% and disease control rate (DCR) was 100.0%.
Responses were observed in patients regardless of their baseline mutations in MYD88 and CXCR4. Out of three patients with CNS involvement (2 with systemic disease), two have responded and none progressed. Overall, responses were durable. With a median follow up of 8.1 months, median duration of response and median progression-free survival were not reached. As of the September 19, 2025 data cut, fourteen patients had continued on treatment for more than six months, and six patients had remained on treatment for more than one year.
About Bexobrutideg (NX-5948)
Bexobrutideg is an investigational, orally bioavailable, brain penetrant, highly selective small molecule degrader of BTK currently being evaluated in the DAYBreak CLL-201 clinical trial (NCT07221500), a pivotal single-arm Phase 2 study of bexobrutideg in patients with relapsed or refractory chronic lymphocytic leukemia. Nurix also continues enrollment in the NX-5948-301 Phase 1a/1b clinical trial (NCT05131022) of bexobrutideg in patients with relapsed or refractory B cell malignancies.
About Nurix Therapeutics, Inc.
Nurix Therapeutics is a clinical stage biopharmaceutical company focused on the discovery, development and commercialization of targeted protein degradation medicines, the next frontier in innovative drug design aimed at improving treatment options for patients with cancer and inflammatory diseases. Nurix’s wholly owned, clinical stage pipeline includes degraders of Bruton’s tyrosine kinase (BTK), a B-cell signaling protein, and inhibitors of Casitas B-lineage lymphoma proto-oncogene B (CBL-B), an E3 ligase that regulates activation of multiple immune cell types including T cells and NK cells. Nurix also is advancing multiple potentially first-in-class or best-in-class degraders and degrader antibody conjugates (DACs) in its preclinical pipeline. Nurix’s partnered drug discovery pipeline consists of preclinical stage degraders of IRAK4 and STAT6, as well as multiple additional programs under collaboration agreements with Gilead Sciences, Inc., Sanofi S.A. and Pfizer Inc., within which Nurix retains certain options for co-development, co-commercialization and profit sharing in the United States for multiple drug candidates. Powered by a fully AI-integrated discovery engine capable of tackling any protein class, and coupled with unparalleled ligase expertise, Nurix’s dedicated team has built a formidable advantage in translating the science of targeted protein degradation into clinical advancements. Nurix aims to establish degrader-based treatments at the forefront of patient care, writing medicine’s next chapter with a new script to outmatch disease. Nurix is headquartered in San Francisco, California. For additional information visit http://www.nurixtx.com.
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Nurix Therapeutics, Inc.
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