Nurix Therapeutics Inc. (NASDAQ: NRIX) has announced preliminary data showing clinically significant Bruton’s tyrosine kinase inhibitor degradation in patients with refractory or relapsed B cell malignancies, including chronic lymphocytic leukemia patients having considerable BTK gene mutations related to the standard of care BTK inhibitors resistance.
The company’s CEO Arthur T. Sands and SVP clinical development Robert J. Brown will present the findings at the 4th Annual Targeted Protein Degradation Conference.
The study focused on protein degradation
Sands said, “The initial data from our study are the first proof-of-mechanism of targeted protein degradation in patients with hematologic malignancies. The concept of degrading BTK as a new therapeutic strategy in hematologic cancer has taken an important step forward, and the NX-2127 program has hit an exciting milestone in its clinical development.”
BTK levels in peripheral blood dramatically fell in all patients in the trial starting on day 1 and were suppressed throughout the dosing period, according to preliminary PK, and PD data from the first two completed 100 mg and 200 mg cohorts, which included six patients. In the first dose cohort, BTK degradation was greater than 80% at a steady-state, and in the second dose cohort, it was greater than 90%.In preclinical animal models, such levels of BTK degradation have been linked to anti-tumor benefits.
NX-2127 offers a way to block uncontrolled B cell signaling
Brown commented, “Patients with relapsed and refractory B cell malignancies continue to require new drugs and new modalities to address their unmet medical need, and we believe that NX-2127 may offer a novel mechanism to block uncontrolled B cell signaling and tumor growth with the further potential to overcome acquired resistance to current treatments. The safety profile of NX-2127 to date is encouraging and we look forward to completing the dose escalation portion of the study and moving into the expansion phase in selected cancers in the first half of 2022.”
