Kymera Therapeutics to Present New Preclinical Data for its First-In-Class Oral IRAK4 Degrader in MYD88-Mutant Lymphoma at Late-Breaking Session of the American Association for Cancer Research Annual Meeting
CAMBRIDGE, Mass., March 29, 2019 /PRNewswire/ --Kymera Therapeutics Inc., a biotechnology company pioneering targeted protein degradation to create breakthrough medicines for patients, will present new preclinical data for its first-in-class oral IRAK4 protein degrader, KYM-001, in MYD88-mutant lymphoma. Data will be presented in a late-breaking research session at the American Association for Cancer Research Annual Meeting on April 3 from 8 a.m. – 12 p.m. (Poster #18, Session: Experimental and Molecular Therapeutics 2). The study showed that KYM-001 led to highly selective degradation of IRAK4 and tumor regression upon oral dosing, both alone and in combination with BTK inhibition.
"IRAK4 degraders offer an entirely new therapeutic approach to treat MYD88-driven B cell lymphomas, which are often aggressive and have a poor prognosis," said Nello Mainolfi, PhD, co-founder and Chief Scientific Officer, Kymera Therapeutics and study co-author. "IRAK4 kinase and scaffolding functions are critical to MYD88-driven Myddosome signaling. Unlike conventional kinase inhibitors, our novel degrader KYM-001 removes both the kinase and scaffolding function of IRAK4 to effectively block Myddosome signaling, resulting in tumor growth arrest and subsequent regression. The team has been able to very quickly identify orally active degraders that offer ease and flexibility of dosing. "
MYD88-activating mutations occur in 30-40% of patients with activated B cell-like (ABC) diffuse large B cell lymphoma (DLBCL). This study assessed the antitumor activity of Kymera's orally active small molecule degraders in human ABC DLCBL cell lines in vitro and in tumor xenograft models in vivo, alone and in combination with the BTK inhibitor ibrutinib.
Study Highlights "KYM-001, a first-in-class oral IRAK4 protein degrader, induces tumor regression in xenograft models of MYD88-mutant ABC DLBCL alone and in combination with BTK inhibition":
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