Exhibit 99.1
![LOGO](https://capedge.com/proxy/8-K/0001193125-21-179209/g152875g91s63.jpg)
Nurix Therapeutics Announces Presentation of Preclinical Data from NX-5948 Program Demonstrating Significant Reduction of Inflammation in a Model of Autoimmune Disease
Orally available NX-5948 is a potent selective degrader of Bruton’s Tyrosine Kinase (BTK) without IMiD activity
Data were presented at the European Alliance of Associations for Rheumatology (EULAR) 2021 Virtual Congress
SAN FRANCISCO, June 2, 2021 (GLOBAL NEWSWIRE) — Nurix Therapeutics, Inc. (Nasdaq: NRIX), a biopharmaceutical company developing targeted protein modulation drugs, today announced the presentation of preclinical data from its NX-5948 program, demonstrating that daily oral dosing of NX-5948 resulted in a robust resolution of symptoms and inflammation in an animal model of arthritis. The data, which support further investigation of NX-5948 for clinical development as a potential treatment for autoimmune disorders, were presented at the EULAR 2021 Virtual Congress which is being held June 2-5, 2021.
“NX-5948 demonstrates highly selective, complete and durable BTK degradation activity resulting in profound reduction in inflammation in models of severe arthritis,” said Robert J. Brown, M.D., Nurix’s senior vice president of clinical development. “We remain on track to initiate clinical trials of NX-5948 in B cell malignancies in the second half of this year and, based on our recent findings, will consider the potential for future expansion of indications into selected autoimmune diseases in 2022.”
“The data presented at this year’s EULAR congress highlight the power of Nurix’s DELigase platform to generate differentiated products that have the potential to address challenging diseases such as autoimmune disorders,” said Arthur T. Sands, M.D., Ph.D., Nurix’s chief executive officer. “The unique activities of NX-5948 include its ability to cross the blood-brain barrier in animal models. We plan to further explore this property in models of multiple sclerosis and other central nervous system diseases.”
Aberrant activation of B cells and autoantibody-mediated tissue damage are hallmarks of autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus. In B cells and myeloid cells, BTK transduces signals downstream of the B cell receptor (BCR), toll-like receptors, and Fc receptors and its overexpression in B cells leads to hyperactive BCR signaling, plasma cell generation, and autoantibody secretion. This makes degradation of BTK a potentially powerful therapeutic strategy to address autoimmune disease.