Abstract
The third-generation tyrosine kinase inhibitors (TKI), AZD9291 (osimertinib) and CO-1686 (rociletinib) of epidermal growth factor receptor (EGFR) are highly active against T790M positive non-small cell lung cancer (NSCLC). However, resistance develops rapidly. EGFR C797S mutation was reported to be a leading mechanism of resistance to the third-generation inhibitors. The C797S mutation appears to be an ideal target for overcoming the acquired resistance to the third-generation inhibitors. This review summarizes the latest development on the discovery of a fourth-generation EGFR TKI, EAI045.3.
Keywords:
AZD9291; EAI045; EGFR; NSCLC; Rociletinib; TKI; epidermal growth factor receptor; non-small cell lung cancer; tyrosine kinase inhibitor.
Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.
MeSH terms
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Animals
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Antineoplastic Agents / therapeutic use*
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Benzeneacetamides / therapeutic use*
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Carcinoma, Non-Small-Cell Lung / drug therapy*
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Carcinoma, Non-Small-Cell Lung / enzymology
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Carcinoma, Non-Small-Cell Lung / genetics
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Carcinoma, Non-Small-Cell Lung / pathology
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Drug Design*
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Drug Resistance, Neoplasm* / genetics
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ErbB Receptors / antagonists & inhibitors*
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ErbB Receptors / genetics
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ErbB Receptors / metabolism
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Humans
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Lung Neoplasms / drug therapy*
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Lung Neoplasms / enzymology
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Lung Neoplasms / genetics
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Lung Neoplasms / pathology
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Molecular Targeted Therapy
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Mutation
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Protein Kinase Inhibitors / therapeutic use*
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Signal Transduction / drug effects
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Thiazoles / therapeutic use*
Substances
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Antineoplastic Agents
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Benzeneacetamides
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EAI045
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Protein Kinase Inhibitors
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Thiazoles
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EGFR protein, human
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ErbB Receptors