BRISBANE, Calif., May 14, 2026
Nurix Therapeutics presented new preclinical and Phase 1 translational data at the Society for Investigative Dermatology Annual Meeting 2026 highlighting the potential of bexobrutideg (NX-5948) as a next-generation treatment for chronic spontaneous urticaria (CSU) and other autoimmune diseases. The findings showed that the oral BTK degrader achieved rapid and robust Bruton’s tyrosine kinase (BTK) degradation in both blood and skin tissue, supporting continued clinical development in inflammation and immunology indications.
According to Nurix Therapeutics, bexobrutideg demonstrated potent BTK degradation across key immune cell types involved in CSU pathology, including B cells, basophils, and mast cells. The company reported that the degrader achieved significantly deeper suppression of FcεRI-driven immune signaling compared with the BTK inhibitor remibrutinib, showing approximately 25-fold greater potency in preclinical assays while maintaining a highly selective BTK-targeting profile across more than 8,700 proteins evaluated in proteomic analysis.
Bexobrutideg Shows Strong Tissue-Level BTK Suppression
Nurix stated that both single-ascending-dose and multiple-ascending-dose Phase 1 studies in healthy volunteers demonstrated rapid and near-complete degradation of BTK in blood and skin using the company’s new oral tablet formulation. Researchers emphasized that eliminating the BTK protein entirely may provide broader suppression of immune signaling compared with traditional BTK inhibitors, which only block enzymatic activity while leaving scaffolding functions intact.
Preclinical mouse models of passive cutaneous anaphylaxis further showed that bexobrutideg produced greater reductions in ear swelling and vascular permeability than remibrutinib, reinforcing its potential to control the inflammatory pathways driving CSU symptoms such as chronic itching, swelling, and allergic skin reactions.
Dr. Arthur T. Sands, President and CEO of Nurix Therapeutics, stated that targeted protein degradation may provide a fundamentally different level of disease control by catalytically removing BTK proteins rather than temporarily inhibiting them. The company believes this approach could lead to more durable suppression of pathogenic immune activity across multiple inflammatory and autoimmune diseases.
Targeted Protein Degradation Expands Autoimmune Pipeline
Bexobrutideg is part of Nurix’s broader targeted protein degradation platform, an emerging therapeutic strategy designed to eliminate disease-driving proteins through the body’s natural proteasomal degradation system. The therapy works by recruiting the cereblon E3 ligase complex, which tags BTK proteins for destruction, disrupting both kinase-dependent and scaffolding-mediated signaling pathways.
Beyond inflammation and immunology, bexobrutideg is also being evaluated in oncology indications, including chronic lymphocytic leukemia (CLL) and relapsed or refractory B-cell malignancies. Nurix continues to advance multiple degrader-based therapeutic programs targeting cancer and autoimmune disorders through both internal development and collaborations with companies including Sanofi, Gilead Sciences, and Pfizer.
The latest findings strengthen growing industry interest in targeted protein degradation medicines as a next-generation therapeutic class capable of addressing limitations associated with conventional small-molecule inhibitors.
Source: Nurix Therapeutics press release



