Kymera Therapeutics to Present New Clinical Data from the Ongoing Phase 1 Trial of STAT3 Degrader KT-333 at EHA Annual Meeting

Abstract released today highlights safety, pharmacodynamic and clinical response data collected through February 6, 2024 cut-off date

Updated data to be presented at the European Hematology Association (EHA) Annual Meeting

KT-333 Phase 1 study ongoing with additional data expected in the second half of 2024

WATERTOWN, Mass., May 14, 2024 (GLOBE NEWSWIRE) --  Kymera Therapeutics, Inc. (NASDAQ: KYMR), a clinical-stage biopharmaceutical company advancing a new class of small molecule medicines using targeted protein degradation (TPD), today announced that new Phase 1 data for KT-333, a first-in-class degrader of STAT3, highlighting safety, pharmacokinetics (PK), pharmacodynamics (PD) and clinical responses will be presented at the European Hematology Association (EHA) Annual Meeting, taking place from June 13-16, 2024, in Madrid, Spain. Results released in an EHA abstract today, which include a data cut-off as of February 6, 2024, demonstrate that KT-333 is a potent and selective STAT3 degrader that has demonstrated clinically significant responses in specific patient populations. The poster presentation is expected to include additional data, including PK/PD, safety and results of disease response assessments from additional patients subsequent to the abstract cut-off date.

“We’re encouraged by the Phase 1 data generated to date. We have demonstrated clinically significant responses in specific patient populations, including cHL and CTCL, at tolerated doses. We have also achieved substantial target knockdown and pathway activation,” said Jared Gollob, MD, Chief Medical Officer, Kymera Therapeutics. “We look forward to completing the Phase 1 study and sharing additional updates on this first-in-class program across a range of indications later this year.”

Highlights of the KT-333 Clinical Abstract

The abstract reported Phase 1 data from 39 patients enrolled through six dose levels (DL) with a mean of 8.7 doses, including patients with classic Hodgkin’s lymphoma (cHL), B-cell non-Hodgkin’s lymphoma, cutaneous T-cell lymphoma (CTCL), peripheral T-cell lymphoma (PTCL), large granular lymphocytic leukemia (LGL-L), T-cell prolymphocytic leukemia (T-PLL) as well as solid tumors. Highlights include:

• Two complete responses in two cHL patients at DL4, three partial responses in CTCL patients at DL2, 4 and 5, and stable disease in four solid tumor patients at DL3-4.
• KT-333 achieved maximum degradation up to 97.5% in peripheral blood mononuclear cells at DL1-5 in Cycle 1 with evidence of STAT3 pathway inhibition and downregulation of inflammatory biomarkers in whole blood. Notably, KT-333 resulted in robust reduction of STAT3, pSTAT3, and SOCS3 expression in a CTCL tumor biopsy in DL4.
• Induction of an IFN-γ stimulated gene signature predictive of sensitivity to anti-PD1 was seen in both peripheral blood and tumor, suggestive of favorable immunomodulatory response in the tumor microenvironment following KT-333 treatment.
• Dose dependent increases in KT-333 plasma exposure were observed, achieving levels predicted to be efficacious.
• KT-333 was generally well-tolerated with the most common adverse events being stomatitis, nausea, ALT increase, constipation and fatigue. Two dose-limiting toxicities (DLTs) were observed at DL5 including Grade 3 stomatitis and arthralgia in two separate LGL-L patients. No DLTs were observed in lymphoma or solid tumor patients at the time of the cut-off. Grade 3 stomatitis was also the only KT-333 related serious adverse event.