Nurix Therapeutics Announces Bexobrutideg Oral Presentation at the 2026 European Hematology Association Congress
Clinical Trial Updates

Nurix Therapeutics Announces Bexobrutideg Oral Presentation at the 2026 European Hematology Association Congress

Published : 13 May 2026

At a Glance
IndicationChronic lymphocytic leukemia
DrugBexobrutideg
Mechanism of ActionBTK degrader
CompanyNurix Therapeutics, Inc.
Trial PhasePhase 1a/b
Trial AcronymNX-5948-301
NCT IDNCT05131022
CategoryClinical Trial Event
Sub CategoryInterim Analysis
Conference NameEuropean Hematology Association (EHA2026) Congress
Presentation TypeOral Presentation
Presentation TitleUpdated efficacy and safety data from an ongoing phase 1a/b trial of the BTK degrader bexobrutideg (NX-5948) in patients with CLL across lines of therapy
PresenterTahla Munir, MBChB, Ph.D.
Session Titles449 Novel therapies in relapsed/refractory CLL
Presentation DateJune 14, 2026
Presentation Time11:00 – 12:15 CEST
Conference LocationStockholm, Sweden
Abstract IDS150
Patient PopulationPatients with chronic lymphocytic leukemia (CLL) across lines of therapy

Nurix to Present Updated Bexobrutideg Phase 1a/b CLL Data at EHA2026

Nurix Therapeutics announced that updated efficacy and safety data from its ongoing Phase 1a/b trial of BTK degrader bexobrutideg (NX-5948) in patients with chronic lymphocytic leukemia (CLL) across lines of therapy has been accepted for an oral presentation. This presentation will take place at the 31st Congress of the European Hematology Association (EHA2026), scheduled for June 11-14, 2026, in Stockholm, Sweden. Bexobrutideg is an investigational, orally bioavailable, brain penetrant, highly selective small molecule degrader of Bruton’s tyrosine kinase (BTK). The company is also evaluating bexobrutideg in the pivotal single-arm Phase 2 DAYBreak CLL-201 study (NCT07221500) for relapsed or refractory CLL.

  • Nurix Therapeutics is set to present updated efficacy and safety data for its BTK degrader, bexobrutideg (NX-5948), at the EHA2026 Congress. The oral presentation, titled "Updated efficacy and safety data from an ongoing phase 1a/b trial of the BTK degrader bexobrutideg (NX-5948) in patients with CLL across lines of therapy," will be delivered by Tahla Munir, MBChB, Ph.D., on June 14, 2026, during the 'Novel therapies in relapsed/refractory CLL' session.
  • Bexobrutideg (NX-5948) is an investigational, orally bioavailable, brain penetrant, and highly selective small molecule degrader of Bruton’s tyrosine kinase (BTK). As a targeted protein degradation medicine, it represents a novel approach in drug design, aiming to improve treatment options for patients suffering from cancer and autoimmune diseases by specifically degrading disease-driving proteins.
  • The data to be presented at EHA2026 originates from the ongoing Phase 1a/b clinical trial (NCT05131022) of bexobrutideg in patients with relapsed or refractory B cell malignancies, including CLL. In addition to this study, Nurix is also advancing bexobrutideg in the pivotal single-arm Phase 2 DAYBreak CLL-201 clinical trial (NCT07221500), which is designed to support accelerated approval in relapsed/refractory chronic lymphocytic leukemia.

Addressing Unmet Needs in Relapsed/Refractory CLL

Chronic lymphocytic leukemia (CLL) continues to present significant therapeutic challenges despite advances in targeted therapies. The disease remains largely incurable, with drug resistance and treatment relapse representing persistent obstacles that affect patient outcomes across all treatment lines.

Drug resistance and relapse patterns: CLL patients inevitably develop resistance to current therapies, with drug resistance remaining a major cause of treatment failure, particularly in high-risk patients with TP53 defects who experience early disease progression and fail to benefit from standard chemoimmunotherapy approaches.

Limited treatment durability: Despite achieving high complete response rates with modern targeted agents, all patients eventually relapse, and current treatments struggle to attain deep remissions with high complete response rates, especially in patients with unfavorable biological characteristics such as unmutated immunoglobulin heavy chain (UM-IGHV) and TP53 aberrations.

Therapeutic selectivity challenges: Treatment approaches are limited by the nonselectivity of therapeutic agents toward normal residual immune cells, leading to immunosuppression and compromised immune function that affects both treatment tolerability and long-term patient outcomes.

Adverse effects and treatment discontinuation: Patients frequently suffer from adverse effects that mandate treatment discontinuation, while long-duration treatments create additional problems including cost burden, progressive drug resistance development, and cumulative toxicity profiles.

Mechanism-specific limitations: Targeted therapies face inherent limitations, such as mTOR-specific inhibitors having limited efficacy due to positive feedback loops via mTOR complex 2 resulting in activation of prosurvival signaling pathways.

High-risk population outcomes: Real-world outcomes for high-risk CLL patients remain inferior to those reported in clinical trials, with median overall survival for high-risk patients at 47.1 months after first-line treatment, underscoring persistent unmet medical needs in this population.

Bexobrutideg's EHA Update: Reshaping CLL Treatment Paradigms

The upcoming oral presentation of updated Phase 1a/b data for bexobrutideg (NX-5948) at EHA2026 marks a significant moment for Nurix Therapeutics and the broader chronic lymphocytic leukemia (CLL) treatment landscape. Bexobrutideg, an orally bioavailable and brain-penetrant Bruton’s tyrosine kinase (BTK) degrader, is poised to address a critical unmet need for patients with relapsed or refractory CLL, particularly those who have become resistant to both covalent BTK inhibitors and BCL2 inhibitors.

BTK degraders represent a novel therapeutic class, leveraging the cell's natural machinery for targeted protein degradation (TPD). This mechanism allows them to overcome common resistance mutations, such as C481S, by actively degrading both wild-type and mutant BTK proteins, rather than merely inhibiting them. This distinct approach offers a promising avenue for patients who currently have limited effective options, often facing poor prognoses. The progression of bexobrutideg into a pivotal Phase 2 study underscores the confidence in its potential to provide durable clinical benefit in this challenging patient population.

However, the path forward is not without considerations. The emerging field of BTK degraders is becoming increasingly competitive, with several agents like BGB-16673, NX-2127, and AC676 also in early clinical development. Establishing optimal sequencing and combination strategies for bexobrutideg within the evolving CLL treatment paradigm will be crucial for its market positioning. Furthermore, while potent BTK degradation is observed, studies suggest that the catalytic rate of degradation is a more accurate predictor of optimal activity, necessitating a nuanced evaluation of efficacy data. There is also a need for vigilance regarding potential class-effect risks, such as invasive fungal infections, as highlighted by a case of mucormycosis in a patient receiving another BTK degrader. As clinical trials progress, the ability of bexobrutideg to demonstrate a favorable safety profile alongside its potent efficacy will be key to its success in enhancing treatment outcomes for patients with multiply relapsed CLL.

Frequently Asked Questions

Is CLL affected by stress?
Chronic psychological stress can influence neuroendocrine pathways and immune function, potentially impacting Chronic Lymphocytic Leukemia (CLL) progression. Elevated stress hormones like cortisol and catecholamines have been shown to affect B-cell survival, proliferation, and apoptosis resistance in vitro. While direct clinical evidence definitively linking stress to accelerated CLL progression in all patients remains an area of ongoing research, these biological mechanisms suggest a potential modulatory role.
What is the role of Bruton's tyrosine kinase inhibition in chronic lymphocytic leukemia?
BTK inhibitors have revolutionized CLL treatment by targeting a crucial signaling pathway essential for B-cell survival and proliferation. These oral agents provide effective therapy, particularly for patients with high-risk features or those unsuitable for chemoimmunotherapy. However, continuous use can lead to acquired resistance or tolerability challenges over time.
How might novel BTK inhibitors like Bexobrutideg improve outcomes for CLL patients?
Next-generation BTK inhibitors are designed to overcome limitations of earlier agents, such as acquired resistance mutations (e.g., C481S) or off-target toxicities. Bexobrutideg, as a novel agent, aims to provide sustained efficacy and an improved safety profile. This could broaden treatment options for patients who have progressed on or are intolerant to existing therapies, including those with specific resistance mechanisms.
What are the key considerations for selecting therapy in relapsed or refractory chronic lymphocytic leukemia?
Treatment selection for relapsed/refractory CLL depends on prior therapies, disease characteristics, and patient comorbidities. Factors such as the presence of specific genetic mutations, prior exposure to BTK or BCL-2 inhibitors, and patient fitness guide therapeutic decisions. Emerging agents like Bexobrutideg offer new mechanisms of action to address these complex patient populations and optimize sequencing strategies.

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