Nurix Therapeutics Releases New Translational Data From Its Ongoing Phase 1 Study Of NX-1607 Showing Dose-Dependent Pharmacologic Activity, Increased Peripheral T-Cell Activation And Proliferation, And Evidence Of Immune Engagement, Particularly In Patients With Stable Disease

Nurix Therapeutics, Inc. (NASDAQ:NRIX), a clinical-stage biopharmaceutical company developing targeted protein modulation therapies to treat cancer and immune disorders, today announced the presentation of new translational data from its ongoing Phase 1 study of NX-1607, an oral, first-in-class inhibitor of Casitas B-lineage lymphoma proto-oncogene B (CBL-B), at the Society for Immunotherapy of Cancer (SITC) 2025 Annual Meeting which is being held November 5–9, 2025, in National Harbor, MD.

The poster, titled Translational Insights from a First-in-Human Study of an Oral CBL-B Inhibitor in Advanced Solid Tumors, expands upon data presented at the recent European Society for Medical Oncology (ESMO) Congress from heavily pretreated patients with a variety of tumor types who were treated with NX-1607 in an ongoing Phase 1a clinical trial. The new data presented at SITC demonstrate that treatment with NX-1607 resulted in dose dependent pharmacologic activity consistent with target engagement and downstream immune modulation. Treatment with NX-1607 led to increased peripheral T cell activation and proliferation, which were statistically significantly greater in patients with stable disease (SD) compared with those with progressive disease (PD), indicative of active T-cell receptor (TCR) engagement and immune responsiveness to treatment.

The poster also highlights a case study of a patient with metastatic castration-resistant prostate cancer (mCRPC) who achieved a best response of stable disease while receiving NX-1607. Treatment was associated with expansion of activated peripheral memory T cell subsets, an increase in CD8+ tumor infiltrating lymphocyte (TIL) density and enhanced immune activation gene signatures in paired metastatic lymph node tumor biopsies. Collectively, these findings indicate that NX-1607 induced peripheral immune activation is associated with remodeling of the tumor microenvironment (TME), linking systemic immune activation to local tumor control.

"These translational findings further support the biological rationale for CBL-B inhibition as a novel immune-oncology therapy," said Arthur T. Sands, M.D., Ph.D., president and chief executive officer of Nurix Therapeutics. "NX-1607 has demonstrated encouraging signs of immune activation and disease control in heavily pretreated patients, supporting its potential as a novel next generation checkpoint inhibitor therapy and its continued development as a monotherapy and in combination with other anticancer agents for the treatment of advanced solid tumors."

Key Findings

• Dose-dependent pharmacology and immune activation: NX-1607 demonstrated dose-dependent pharmacokinetics and pharmacodynamic modulation of the proximal biomarker pHS1, confirming target engagement and inhibition of CBL-B–mediated signaling.
• Peripheral immune activation linked to clinical benefit: Patients with stable disease exhibited a greater enrichment of circulating PD-1⁺ CD8⁺ T cells expressing Ki67⁺ (proliferation) and ICOS⁺(activation) markers compared with those with progressive disease, demonstrating active TCR engagement and antitumor immune responsiveness.
• Remodeling of the tumor microenvironment: In a case study of a heavily pretreated mCRPC patient (5 prior therapies), NX-1607 treatment achieved a best response of stable disease. Paired pre and post treatment metastatic lymph node tumor biopsy analyses showed an increase in CD8⁺ TIL density, upregulation of cytotoxic and interferon-response pathways, and reduced regulatory T-cell signatures, consistent with enhanced effector activity and immune activation within the TME.
• Transcriptomic evidence of immune pathway engagement: RNA sequencing analyses demonstrated dose-dependent enrichment of immune signaling pathways, including interferon response, antigen presentation, and effector T cell activation, further supporting a mechanistic link between NX-1607 exposure and immune activation.