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In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
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].
Reference:Galvani E, Sun J, Leon LG, et al. NF-κB drives acquired resistance to a novel mutant-selective EGFR inhibitor. Oncotarget, 2015.