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Nurix Therapeutics Announces Presentation of NX-1607 Preclinical Data at AACR
CBL-B inhibitor NX-1607 mediates anti-tumor activity through both T cells and NK cellsPreclinical tumor models support clinical development of NX-1607 as
About this update from Nurix Therapeutics, Inc.
[{"type":"text","content":"CBL-B inhibitor NX-1607 mediates anti-tumor activity through both T cells and NK cellsPreclinical tumor models support clinical development of NX-1607 as monotherapy or in combination with PD-1 blockade SAN FRANCISCO, March 10, 2021 (GLOBE NEWSWIRE) -- Nurix Therapeutics, Inc. (Nasdaq: NRIX), a biopharmaceutical company developing targeted protein modulation drugs, today announced presentation of data from its NX-1607 program at the American Association for Cancer Research 2021 annual meeting which is being held virtually over two weeks, April 10-15 and May 17-21. NX-1607, an orally bioavailable, small-molecule inhibitor of Casitas B-lineage lymphoma B (CBL-B), demonstrated significant anti-tumor efficacy in animal models of both colorectal cancer and triple negative breast cancer. Importantly, the combination of NX-1607 and an anti-PD-1 antibody substantially increased the median overall survival and the frequency of long-lasting tumor rejection in these models compared to either single agent alone. The activity of NX-1607 is shown to be dependent on CD8+ T cells and NK cells. “The emerging data for our first-in-class CBL-B inhibitor demonstrate the unique potential of NX-1607 as an oral immuno-oncology agent with both T cell and NK cell activity,” said Gwenn M. Hansen, Ph.D., Nurix’s chief scientific officer. “The data that we will present at the AACR meeting support our plans to advance NX-1607, the lead program in our ligase inhibitor portfolio, into a clinical trial in patients with solid tumors in the second half of 2021.” Abstract Number: 2765Title: Small molecule inhibition of the ubiquitin ligase CBL-B results in potent T and NK cell mediated anti-tumor responseSession Title: Combination ImmunotherapiesPoster Number: 1595 The E3 ubiquitin ligase CBL-B is expressed in T cells where it functions as an important negative regulator of immune activation. CBL-B attenuates T-cell activation initiated by TCR engagement in part by mediating the requirement for CD28 co-stimulation, thus setting the threshold for T cell activation. CD4+ and CD8+ T cells from mice deficient in Cbl-b have 5 to 10-fold enhanced secretion of IL-2 and IFN-gamma when stimulated ex vivo with anti-CD3. Cbl-b deficient mice also demonstrate enhanced NK cell function. NX-1607 is an investigational, orally bioavailable, small molecule inhibitor of CBL-B. NX-...