On March 25, 2025 Nurix Therapeutics, Inc. (Nasdaq: NRIX), a clinical-stage biopharmaceutical company focused on the discovery, development and commercialization of targeted protein degradation medicines, reported that company scientists will present preclinical data from its proprietary DEL-AI platform and several degrader programs in two oral presentations and two poster presentations at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) 2025 Annual Meeting, which will be held from April 25-30, 2025, in Chicago, IL (Press release, Nurix Therapeutics, MAR 25, 2025, View Source [SID1234651409]).

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Oral Presentation Details:

Title: DEL-AI: Proteome-wide in silico screening of multi-billion compound libraries using machine learning foundation models
Presenting author: Paul Novick, Ph.D.
Session title: Innovative Approaches in Drug Discovery: Novel Leads, Degraders, and AI-Driven Solutions
Session date and time: Monday, April 28, 2025, 2:30 PM – 4:30 PM CST
Abstract ID: 3762

Title: Identification of selective, orally bioavailable Aurora A degraders for treatment of pediatric and adult cancers
Presenting author: Ryan Rountree, Ph.D.
Session title: Degraders and Glues
Session date and time: Tuesday, April 29, 2025, 2:30 PM – 4:30 PM CST
Abstract ID: 6379

Poster Presentation Details:

Title: NRX-0305: a pan-mutant BRAF degrader with broad preclinical efficacy, brain penetrance, and synergistic potential with MEKi across class 1/2/3 BRAF-mutant cancers
Presenting authors: Alexandra ‘Sasha’ Borodovsky, Ph.D.
Session title: Degraders and Glues 2
Session date and time: Monday, April 28, 2025, 9:00 AM – 12:00 PM CST
Abstract ID: 1651

Title: NX-5948 is a CNS-penetrant catalytic Bruton’s tyrosine kinase (BTK) degrader that breaks established design rules for CNS drugs
Presenting authors: Wylie Palmer, Ph.D.
Session title: Targeted Protein Degradation
Session date and time: Wednesday, April 30, 2025, 9:00 AM – 12:00 PM CST
Abstract ID: 7003

About DEL-AI
DEL-AI is Nurix’s discovery platform which employs advanced machine learning to enable all aspects of Nurix’s discovery engine, starting with DNA encoded library (DEL) hit-finding and degrader design, followed by automated chemistry synthesis and direct-to-biology screening and optimization, to rapidly generate degraders and degrader antibody conjugates (DACs) as new chemical entity drug candidates. By leveraging hundreds of billions of DEL compound binding signatures derived from thousands of DEL affinity screens collected from a diverse set of highly validated protein targets, our DEL-AI platform can prospectively identify binders as starting points for drug discovery for virtually any pharmaceutically relevant target.

About Bexobrutideg (NX-5948)
Bexobrutideg is an investigational, orally bioavailable, brain penetrant, small molecule degrader of BTK. Bexobrutideg is currently being evaluated in a Phase 1 clinical trial in patients with relapsed or refractory B cell malignancies. Additional information on the ongoing clinical trial can be accessed at clinicaltrials.gov (NCT05131022).

About NRX-0305
NRX-0305 is a potent, selective, and orally bioavailable mutant-specific BRAF degrader that Nurix is exploring for use in oncology. Nurix has reported preclinical data demonstrating potent anti-tumor activity in multiple cell line-derived and patient-derived xenograft disease models representing Class I, Class II and Class III B-RAF mutations. Anti-tumor activity was also observed in the setting of CNS disease and treatment-resistance, suggesting the potential for utility across a broad range of solid tumor types

About Aurora A Kinase
Aurora A kinase (AURKA) is an oncogene frequently overexpressed in adult solid tumors, hematologic malignancies, and pediatric cancers. Several AURKA inhibitors are effective in preclinical tumor models, but this activity has failed to translate into clinical efficacy. To address the limitations of inhibitors, Nurix has designed bifunctional targeted protein degraders of AURKA that enable removal of both enzymatic and scaffolding functions.