4 Results for "

EGFR-TKI resistance

" in MedChemExpress (MCE) Product Catalog:
Products (4)

4 Results for "EGFR-TKI resistance" in MCE Product Catalog:

1
1 Cited Publications
Cat. No.: HY-139920
CAS No.: 2035089-28-0
Purity:  99.59%
Synonyms: SH-1028
Target:  

EGFR

Research Areas:  

Cancer

Oritinib (SH-1028), an irreversible third-generation EGFR TKI, overcomes T790M-mediated resistance in non-small cell lung cancer. Oritinib (SH-1028), a mutant-selective inhibitor of EGFR kinase activity, inhibits EGFR WT, EGFR L858R, EGFR L861Q, EGFR L858R/T790M, EGFR d746-750 and EGFR d746-750/T790M kinases, with IC50s of 18, 0.7, 4, 0.1, 1.4 and 0.89 nM, respectively .
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Cat. No.: HY-19815
CAS No.: 1660963-42-7
Synonyms: CK-101; RX518
Target:  

EGFR

Research Areas:  

Cancer

Olafertinib (CK-101) is an orally available, third generation and irreversible epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI). Olafertinib selectively inhibits both EGFR-TKI-sensitizing and resistance mutations with minimal activity on wild-type EGFR. Olafertinib can be used in research for non-small cell lung cancer (NSCLC) with EGFR mutations and other advanced malignancies .
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Cat. No.: HY-175839
Target:  

PROTACs EGFR ATP Synthase

Research Areas:  

Inflammation/Immunology Cancer

PROTAC EGFR degrader 15 is a Pomalidomide (HY-10984)-based Gefitinib (HY-50895) EGFR PROTAC degrader. PROTAC EGFR degrader 15 triggers EGFR degradation via ubiquitin-proteasome-dependent proteolysis and autophagy-lysosome activation pathways. PROTAC EGFR degrader 15 targets ETFA to enhance ATP production. PROTAC EGFR degrader 15 significantly suppresses tumor growth in a Gefitinib-acquired resistant HCC-827 xenograft model. PROTAC EGFR degrader 15 can be used for the study of non-small cell lung cancer (NSCLC) .
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Cat. No.: HY-163006
CAS No.: 3020728-68-8
Target:  

EGFR c-Met/HGFR

Research Areas:  

Cancer

EGFR/c-Met-IN-1 (compound TS-41) is a dual-target inhibitor of EGFR/c-Met. The IC50 for inhibiting EGFR L858R and c-Met is 68.1 nM and 0.26 nM respectively. . EGFR/c-Met-IN-1 induces apoptosis and cell cycle arrest in A549-P cells, downregulating the phosphorylation of EGFR, c-Met, and downstream AKT. EGFR/c-Met-IN-1 inhibits tumor growth in vitro and in vivo .
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