Article

The novel MET inhibitor, HQP8361, possesses single agent activity and enhances therapeutic efficacy of osimertinib, against NSCLC cells with acquired resistance to osimertinib due to MET amplification

2020-04-29

Abstract excerpt

<title>Abstract</title> <p>Background The oncogenic protein, MET (or c-MET), is involved in the positive regulation of cell survival and proliferation and in mediating acquired resistance to EGFR-TKIs including AZD9291 (osimertinib). Thus, MET inhibition is a promising strategy for overcoming acquired EGFR-TKI resistance due to MET amplification. HQP8361 (MK8033) is a novel and selective MET kinase inhibitor that...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: 4cc27f38-8fee-5134-a3d0-259111e67d27
DOI: 10.21203/rs.3.rs-25317/v1

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

The novel MET inhibitor, HQP8361, possesses single agent activity and enhances therapeutic efficacy of osimertinib, against NSCLC cells with acquired resistance to osimertinib due to MET amplificationDOI 10.21203/rs.3.rs-25317/v1Read

MET inhibitors for targeted therapy of EGFR TKI-resistant lung cancerSemantic proximity Read

Overcoming Acquired Resistance to AZD9291, A Third-Generation EGFR Inhibitor, through Modulation of MEK/ERK-Dependent Bim and Mcl-1 Degradation.Semantic proximity Read

Preclinical Study of a Biparatopic METxMET Antibody-Drug Conjugate, REGN5093-M114, Overcomes MET-driven Acquired Resistance to EGFR TKIs in EGFR-mutant NSCLC.Semantic proximity Read

Emerging MET tyrosine kinase inhibitors for the treatment of non-small cell lung cancer.Semantic proximity Read

Acquired resistance to AZD9291 as an upfront treatment is dependent on ERK signaling in a preclinical model.Semantic proximity Read

Diverse Mechanisms of Resistance against Osimertinib, a Third-Generation EGFR-TKI, in Lung Adenocarcinoma Cells with an EGFR-Activating Mutation.Semantic proximity Read

MET Dependence Oversteps EGFR Dependence via Balancing Dimerization of the Receptor Tyrosine Kinases in Osimertinib-Resistant MET-Amplified, EGFR-Mutated Non-Small Cell Lung Cancer.Semantic proximity Read

Met gene amplification and protein hyperactivation is a mechanism of resistance to both first and third generation EGFR inhibitors in lung cancer treatment.Semantic proximity Read

Impact of MET alterations on targeted therapy with EGFR-tyrosine kinase inhibitors for EGFR-mutant lung cancerSemantic proximity Read

The clinical efficacy of combinatorial therapy of EGFR-TKI and crizotinib in overcoming MET amplification-mediated resistance from prior EGFR-TKI therapy.Semantic proximity Read

Activation of AXL as a Preclinical Acquired Resistance Mechanism Against Osimertinib Treatment in EGFR -Mutant Non–Small Cell Lung Cancer CellsSemantic proximity Read

The Combined Therapy of Cabozantinib, Crizotinib, and Osimertinib in a Lung Cancer Patient with Acquired MET Amplification and Resistance Mutations.Semantic proximity Read