On April 22, 2026 Nurix Therapeutics, Inc. (Nasdaq: NRIX), a clinical-stage biopharmaceutical company developing targeted protein degradation therapies, reported new preclinical data from multiple oncology programs at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026.
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The presentations highlight continued progress across Nurix’s oncology pipeline, including programs targeting pan-mutant BRAF, CBL-B and Aurora Kinase A (AURKA), as well as a featured AACR (Free AACR Whitepaper) Advances session presentation highlighting the broader scientific progress and clinical translation of targeted protein degradation. Collectively, these data provide additional mechanistic validation of Nurix’s approach to CBL-B, Aurora kinase A (AURKA) and mutant BRAF to address key limitations of traditional approaches, including resistance, incomplete pathway suppression, and inability to target non-enzymatic protein functions.
"These data, together with our participation in the AACR (Free AACR Whitepaper) Advances session, highlight the growing clinical and scientific validation of targeted protein degradation as a new therapeutic modality," said Arthur T. Sands, M.D., Ph.D., president and chief executive officer. "Across multiple programs, we are seeing consistent evidence that these therapies can drive deeper and more durable biological responses, supporting their potential to deliver meaningful benefit for patients."
AACR Advances Session
Later today, April 22, 2026, Gwenn Hansen, Ph.D., chief scientific officer of Nurix, will present "Designing Effective Degrader Therapeutics: What Early Clinical Experience Has Taught Us" as part of the AACR (Free AACR Whitepaper) Advances session "Induced Proximity Pharmacology: Degraders and Beyond." Dr. Hansen’s remarks will provide a broad perspective on recent advances in targeted protein degradation, including insights from early clinical experience and the evolving potential of induced proximity approaches to expand the druggable target space and improve therapeutic outcomes.
Pan-Mutant BRAF Degrader Program
In a poster presentation titled "NRX-0305, an orally bioavailable, CNS penetrant pan-mutant BRAF degrader demonstrates robust efficacy in intracranial models of melanoma brain metastasis and primary glioma," Nurix reported that NRX-0305 achieves dose-proportional pharmacokinetics across plasma, tumor, and brain, enabling robust degradation of mutant BRAF and downstream pathway inhibition. These properties translate into potent antitumor activity in intracranial glioma and melanoma models while selectively sparing wildtype BRAF and avoiding paradoxical MAPK pathway activation. In a clinically relevant BRAF inhibitor–resistant melanoma brain metastasis patient-derived xenograft (PDX) model, NRX-0305 significantly extended survival versus both vehicle and dabrafenib, delivering a 142% increase in lifespan, compared with approximately 12% for the approved BRAF inhibitor.
Additional data were presented in a poster titled "NRX-0305 is an orally bioavailable, pan-mutant BRAF degrader that exhibits single-agent and combination efficacy with MEKi or anti-EGFR across Class 1/2/3 BRAF-mutant cancers." In preclinical tumor models, NRX-0305 demonstrates broad activity across mutant BRAF classes, including activity across 14 PDX models spanning Class 1 treatment-resistant, Class 2, and Class 3 BRAF mutations. Combination of NRX-0305 with MEK inhibitors or anti-EGFR therapy enhanced tumor regressions in Class 2 and drove complete responses in Class 1 and 3 models. Notably, the complete regressions are achieved at lower MEK inhibitor dose levels, supporting the potential for an improved therapeutic window relative to current treatment approaches.
CBL-B Program
In an oral presentation titled "Discovery and characterization of CBL-B intramolecular glue inhibitors that increase T cell activation and suppress tumor growth," Nurix reported the discovery and characterization of novel intramolecular glue inhibitors targeting CBL-B, an E3 ubiquitin ligase that negatively regulates T, B, and NK cell activation. Using mechanism-agnostic screening assays guided by CBL-B biology, Nurix identified a novel series of intramolecular glue inhibitors that stabilize the closed, inactive conformation of CBL-B, representing a first-in-class mechanism of action. Through structure-guided optimization, this series was advanced to NX-1607, a potent and selective CBL-B inhibitor with sub-nanomolar binding affinity. In preclinical studies, NX-1607 enhanced T cell activation, as evidenced by increased IL-2 and IFN-γ secretion in response to TCR stimulation, and demonstrated single-agent anti-tumor activity across multiple syngeneic tumor models, including colorectal, triple-negative breast cancer, and B cell lymphoma. NX-1607 also synergized with anti-PD-1 therapy to significantly enhance survival across multiple models. Early clinical data demonstrated dose-dependent pharmacokinetics and modulation of the proximal pharmacodynamic biomarker pHS1 in CD8 T cells, providing initial evidence of target engagement in patients.
Aurora Kinase A (AURKA) Degrader Program
In a poster presentation titled "NRX-4972, a selective, oral, Aurora kinase A degrader, demonstrates increased efficacy in an SCLC tumor model, and greater in vitro synergy than an AURKA inhibitor," Nurix reported new data demonstrating that targeted degradation of AURKA enables more complete biological modulation compared to inhibition alone. NRX-4972 exhibits central nervous system penetration and a favorable pharmacokinetic and pharmacodynamic profile, translating into superior antitumor activity in aggressive small cell lung cancer models, particularly with an optimized twice-daily dosing regimen. In the H82 SCLC model, twice-daily administration of NRX-4972 resulted in 60% of mice surviving to the end of the study, whereas none of the mice treated with AURKA inhibitors alisertib or LY3295668 survived. Mechanistically, degradation of AURKA results in downregulation of MYC and enhanced induction of DNA damage, apoptosis, and G2/M arrest. NRX-4972 also demonstrated broader and more potent synergy than an AURKA inhibitor in an in vitro screen of combination agents across triple-negative breast cancer, SCLC, and NSCLC cell lines, further supporting its therapeutic potential.
About NRX-0305
NRX-0305 is a potent, selective, and orally bioavailable central nervous system (CNS)-penetrant pan-mutant 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 1, Class 2, and Class 3 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 NX-1607
NX-1607 is an investigational first-in-class oral inhibitor of the E3 ligase Casitas B-lineage lymphoma proto-oncogene B (CBL-B) being developed for immuno-oncology indications, including a range of solid tumor types. CBL-B is a cytoplasmic E3 ubiquitin ligase that negatively regulates T cell activation, making it an attractive target for immuno-oncology and offering a novel therapeutic approach to treat solid tumors. Inhibition of CBL-B in preclinical studies reverses T cell exhaustion, alleviates tumor induced immunosuppression, and may also exert direct antitumor effects. Nurix is evaluating NX-1607 in an ongoing Phase 1 trial in adults in a range of oncology indications. This study includes a thorough investigation of both dose and schedule in the Phase 1a portion. Additional information on the NX-1607 clinical trial can be accessed at www.clinicaltrials.gov (NCT05107674).
About NRX-4972
NRX-4972 is a CNS-penetrant, orally bioavailable and highly selective degrader of Aurora A kinase (AURKA). 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.
(Press release, Nurix Therapeutics, APR 22, 2026, View Source [SID1234664694])