Category
- PI3K/Akt/mTOR
- Epigenetics
- Methylation
- Immunology & Inflammation
- Protein Tyrosine Kinase
- Angiogenesis
- Apoptosis
- Autophagy
- ER stress & UPR
- JAK/STAT
- MAPK
- Cytoskeletal Signaling
- Cell Cycle
- TGF-beta/Smad
- DNA Damage/DNA Repair
- Stem Cells & Wnt
- Hippo
- Ubiquitin
- Neuronal Signaling
- NF-κB
- GPCR & G Protein
- Endocrinology & Hormones
- Transmembrane Transporters
- Metabolism
- Proteases
- Microbiology
- Others
Archives
EGFR C797S as a Resistance Mechanism of Lazertinib in Non-small Cell Lung Cancer with EGFR T790M Mutation
The non-small cell lung cancer with activating epidermal growth factor receptor (EGFR) mutation eventually acquires resistant to either first or second-generation EGFR tyrosine kinase inhibitor (TKI). As the following option, targeting EGFR T790M with third-generation EGFR TKI is now established as a standard treatment option. In this study, we are reporting the first case of resistance mechanism to the novel third-generation EGFR TKI, lazertinib, which showed promising clinical efficacy in phase 1-2 study. The patients showed resistance to the treatment by acquiring the additional EGFR C797S mutation in cis which is also confirmed from the patient-derived cell lines.
Related Products
| Cat.No. | Product Name | Information | Publications | Customer Product Validation |
|---|---|---|---|---|
| S8724 | Lazertinib | Lazertinib (YH25448,GNS-1480) is a potent, highly mutant-selective and irreversible EGFR-TKI with IC50 values of 1.7 nM, 2 nM, 5 nM, 20.6 nM and 76 nM for Del19/T790M, L858R/T790M, Del19, L85R and Wild type EGFR respectively, showing much higher IC50 values aganist ErbB2 and ErbB4. | (1) |
