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Kymera Therapeutics to Present Data on Novel IRAKIMiD and STAT3 Protein Degraders at Virtual 62nd American Society of Hematology (ASH) Annual Meeting
WATERTOWN, Mass., Nov. 04, 2020 (GLOBE NEWSWIRE) -- Kymera Therapeutics, Inc. (NASDAQ: KYMR), a biopharmaceutical company advancing targeted protein
About this update from Kymera Therapeutics, Inc.
[{"type":"text","content":"WATERTOWN, Mass., Nov. 04, 2020 (GLOBE NEWSWIRE) -- Kymera Therapeutics, Inc. (NASDAQ: KYMR), a biopharmaceutical company advancing targeted protein degradation to deliver novel small molecule protein degrader therapeutics, today announced the company will present new preclinical data for its IRAKIMiD and STAT3 degrader programs at the 62nd American Society of Hematology (ASH) Annual Meeting taking place virtually from Dec. 5-8, 2020.\n “We are excited to share for the first time preclinical data of our IRAKIMiD development candidate KT-413 (formerly KTX-120) as well as an expanded preclinical investigation of our STAT3 degrader program which have allowed us to uncover important insights into their therapeutic potential across a variety of hematologic cancers,\" said Jared Gollob, MD, Chief Medical Officer, Kymera Therapeutics. \"The results also establish the potential for intermittent dosing schedules for both programs as we guide their advancement into the clinic next year.\" IRAKIMiD Program ABSTRACT #2088, “KTX-120, a Novel IRAKIMiD Degrader of IRAK4 and IMiD substrates shows Preferential Activity and Induces Regressions in MYD88-Mutant DLBCL CDX and PDX models,” presented by Duncan H. Walker, PhD, Vice President of Oncology at Kymera Therapeutics. Poster Session II: Sunday, Dec. 6th (7:00 AM - 3:30 PM PT). ABSTRACT #3013, “Targeting MYD88-Mutant DLBCL with IRAKIMiDs: A Comparison to IRAK4 Kinase Inhibition and Evaluation of Synergy with Rational Combinations,” presented by Jennifer K. Lue, MD of Columbia University Irving Medical Center. Poster Session III: Monday, Dec. 7th (7:00 AM - 3:30 PM PT). Data to be presented show: Deep and Sustained Tumor Regressions with Intermittent Dosing in MYD88-mutant DLBCL: KT-413 was well tolerated and exhibited potent and sustained antitumor activity in multiple MYD88-mutant mouse CDX and PDX models of DLBCL across a range of both PO and IV intermittent dosing schedules.Preferential Anti-Tumor Activity in MYD88-mutant DLBCL Irrespective of Co-Mutations: KT-413 anti-tumor activity was specific to MYD88-mutant cell lines (relative to WT cell lines) and was independent of a variety of common co-mutations that further activate the NF-kB and IRF4 pathways.Superiority to IMiDs and IRAK4 Kinase Inhibitor: In MYD88-mutant models of DLBCL, IRAKIMiDs showed superior cell killing compared to either...