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JAK/STAT SignalingProtein Tyrosine Kinase/RTK-

CNX-2006?????????????????????EGFR???????????????????????????IC50< 20 nM???????????????EGFR??????????????????

EGFR

相关产品

AZD-9291-Gefitinib-Lapatinib-Afatinib-Erlotinib-AG-490-Genistein-AG-1478-Neratinib-EGF816-Olmutinib-AZD3759-Dacomitinib-Irbinitinib-CO-1686-

生物活性

Description

CNX-2006 is a novel irreversible mutant-selective EGFR inhibitor with IC50 of < 20 nM, with very weak inhibition at wild-type EGFR.IC50 value: <20 nMTarget: Mutant EGFRCNX-2006 is a novel irreversible EGFR tyrosine kinase inhibitor, specifically inhibits activating mutations of EGFR as well as the T790M mutation while having very weak inhibition at wild-type EGFR. In in vitro modeling of acquired resistance, continuous CNX-2006 treatment on drug-sensitive EGFR mutant cells leads to resistance more slowly than erlotinib. Dose escalation with CNX-2006 leads to differential effects in different lines, but does not select for T790M-mediated resistance. CNX-2006 resistent cells shows increased expression of EMT markers and MMP9. CNX-2006 is effective in H1975 (EGFR L858R/T790M) xenograft model.

References

[1].1. Kadoaki Ohashi, et al. CNX-2006, a novel irreversible epidermal growth factor receptor (EGFR) inhibitor, selectively inhibits EGFR T790M and fails to induce T790M-mediated resistance in vitro. Cancer Res April 15, 201373; 2101A

[2].Kadoaki Ohashi, et al. CNX-2006, a Novel Irreversible Epidermal Growth Factor Receptor (EGFR) Inhibitor,  Selectively Inhibits EGFR T790M and Fails to Induce T790M-Mediated Resistance In Vitro

[3].Elena Galvani, et al. Role of epithelial-mesenchymal transition (EMT) in sensitivity to CNX-  2006,a novel mutant-selective EGFR inhibitor which overcomes in vitro  T790M-mediated resistance in NSCLC