Data demonstrate potent, synergistic anti-tumor activity in combination with multiple EGFR modulators in preclinical studies
Clinical development plan to include combination with the EGFR inhibitor, cetuximab; initiation of the QTX3034 clinical trial is on track for early 2024
October 11, 2023
Boston, Mass; October 11, 2023 — Quanta Therapeutics, a privately-held biopharmaceutical company pioneering targeted therapies to treat RAS-driven cancers, announced data from a late-breaking presentation at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics being held October 11-15, 2023, in Boston, Massachusetts. QTX3034 is a non-covalent multi-KRAS inhibitor with a favorable preclinical profile, including oral bioavailability and brain penetration. The combination of QTX3034 and EGFR (epidermal growth factor receptor) inhibitors, a class of drugs used to treat many commonly occurring cancers, demonstrated potent, synergistic anti-tumor activity in preclinical studies.
“The currently approved KRAS G12C inhibitors have shown enhanced anti-tumor activity in combination with EGFR inhibitors, enabling the development of novel treatment approaches to address difficult-to-treat tumor types, such as colorectal cancer,” said Perry Nisen, MD, PhD, Chief Executive Officer of Quanta Therapeutics. “Our goal is to apply this approach to the most prevalent drivers of these advanced cancers, KRAS G12D and G12V, leveraging the potent activity of QTX3034 against mutant KRAS and the synergistic drug mechanism demonstrated with the QTX3034/ EGFR inhibitor combination. These compelling data validate the potential of QTX3034 in combination with EGFR-targeted therapy across multiple cancer types and support the planned evaluation of this combination as part of our Phase 1 clinical development program, which is on track to begin in early 2024.”
Poster presentation details are as follows:
Title: QTX3034, a potent and selective multi-KRAS inhibitor, synergizes with EGFR inhibitors and enhances anti-tumor activity
Date and Time: Saturday, October 14, 2023 12:30 – 4:00 pm
Session Name: Poster Session C
Poster Number: LB-C09
The mitogen-activated protein kinase (MAPK) pathway is a chain of proteins that includes the signaling molecules RAS, RAF, MEK, and ERK. It is a central pathway that regulates cellular growth, proliferation, differentiation, and survival. When one of the proteins is mutated, it can drive tumor development and growth. RAS is the most frequently mutated oncogene in cancer, with KRAS mutations occurring in nearly one-quarter of all human cancers. RAS mutations impair the ability of RAS to convert from its active GTP-bound “ON” form into its inactive GDP-bound “OFF” state, leading to the sustained activation of the MAPK signaling pathway and ultimately driving tumorigenesis. KRAS mutations, especially G12D, G12V, and G12C, are highly prevalent in pancreatic, colorectal, and lung cancers. First-generation KRAS inhibitors have demonstrated clinical benefit, but their impact is limited to a subset of patients with a single type of KRAS mutation (G12C), and these tumors commonly develop resistance to treatment.
Quanta Therapeutics is a private biopharmaceutical company focused on the most prevalent and elusive target in oncology—RAS. Our vision is to develop novel small molecule cancer medicines by selectively targeting protein-protein interactions that are key to oncogenic RAS activity. Driving Quanta's success is our unique high-throughput platform that applies Second Harmonic Generation (SHG) optical technology to identify allosteric modulators of membrane-bound protein complexes. The Quanta team has extensive drug development expertise and substantial research experience in the RAS space. By applying innovative medicinal chemistry and its unique protein conformation detection technology, Quanta aims to advance differentiated, next-generation RAS programs that address the resistance paradigms of targeted therapy in oncology.
Find more information at https://www.quantatx.com/
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Quanta Therapeutics
Heather Meeks
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