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CNX-2006, a structural analog of CO-1686, is a selective and irreversible inhibitor of mutant-EGFR with IC50 value of < 20 nM.

The epidermal growth factor receptor (EGFR) is the cell-surface receptor for epidermal growth factor and plays an important role in tumor invasion and cancer cell proliferation.

CNX-2006 is a novel and irreversible mutant-selective EGFR inhibitor with very weak inhibition of wild-type EGFR. In non-small cell lung cancer (NSCLC) models expressing mutant EGFR-T790M, CNX-2006 inhibited EGFR signaling. CNX-2006 acquired resistance which was drove by NF-κB. So NF-κB activation might replace the EGFR signaling. These results suggested that inhibition of NF-κB pathway was a promising therapy method for patients who progressed after treatment with mutant-selective EGFR inhibitors [1].

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