Business
Erasca Announces Presentation of Preclinical Data on ERAS-801, a CNS-Penetrant EGFR Inhibitor with Broad Activity against Oncogenic EGFR Alterations, at AACR Conference on Brain Cancer
ERAS-801's CNS penetration: four times higher than approved EGFR inhibitorsComprehensive inhibition against oncogenic EGFR vIII and wildtype
About this update from Erasca, Inc.
[{"type":"text","content":"ERAS-801's CNS penetration: four times higher than approved EGFR inhibitorsComprehensive inhibition against oncogenic EGFR vIII and wildtype alterationsImproved outcomes in over 90% of EGFR-driven patient-derived glioblastoma modelsIND submission in refractory glioblastoma planned for Q1 2022 SAN DIEGO, Oct. 25, 2021 (GLOBE NEWSWIRE) -- Erasca, Inc. (Nasdaq: ERAS), a clinical-stage precision oncology company singularly focused on discovering, developing, and commercializing therapies for patients with RAS/MAPK pathway-driven cancers, today announced the presentation of preclinical data for ERAS-801, a small molecule epidermal growth factor receptor (EGFR) inhibitor specifically designed to have high central nervous system (CNS) penetration for the treatment of glioblastoma multiforme (GBM), at the American Association for Cancer Research (AACR) Special Virtual Conference on Brain Cancer. “While mutations in EGFR are common oncogenic drivers in glioblastoma, approved EGFR inhibitors lack both sufficient CNS penetration for primary brain tumors and clinical activity against oncogenic EGFR alterations that are prevalent in GBM,” said Jonathan E. Lim, M.D., Erasca’s chairman, CEO, and co-founder. “ERAS-801 is an EGFR inhibitor with four times the CNS penetrance of approved EGFR inhibitors, resulting in robust CNS enrichment while limiting systemic exposure. In more than 30 GBM patient-derived preclinical models, ERAS-801 demonstrated potent activity across mutant and wildtype oncogenic EGFR alterations, and we are highly encouraged by the extensive therapeutic potential of ERAS-801 for patients with this aggressive malignancy.” David A. Nathanson, Ph.D., Associate Professor of Molecular and Medical Pharmacology at the University of California, Los Angeles (UCLA), added, “About 60% of glioblastomas are driven by oncogenic alterations in EGFR that include amplifications and mutations such as the highly prevalent vIII deletion. Wildtype EGFR has a pathogenic role in glioblastoma and can drive disease following amplification or through heterodimerization with mutant EGFR. Effective disease control of glioblastoma ultimately requires comprehensive inhibition of both mutated and wildtype forms of EGFR, which approved EGFR inhibitors do not currently achieve. Our work demonstrates that ERAS-801 can improve outcomes in over 90% of diverse E...