Afatinib

An irreversible, dual EGFR/HER2 inhibitor with IC50 of 0.5/0.4/10/14 nM for wt EGFR/EGFR L858R/EGFR L858R+T790M/HER2 respectively; shows high selectivity over HGFR, c-Src, β-InsRK, VEGFR2; suppresses transformation in isogenic cell-based assays, inhibits survival of cancer cell lines and induces tumor regression in xenograft and transgenic lung cancer models.Lung Cancer Approved (In Vitro) :Afatinib (100 nM) sufficiently prevents heregulin-stimulated HER3 phosphorylation.Afatinib (0-10000 nM) effectively inhibits anchorage-independent proliferation of NIH-3T3 cells ectopically expressing EGFR mutants, and inhibits cell proliferation of H1666, H3255, and NCI 1975 cells.Afatinib (48-72 h) shows growth inhibition in HKESC-1, HKESC-2, SLMT-1 and EC-1 cells.Afatinib (0-1 μM, 24-48 h) inhibits AKT and MAPK pathways, and inhibits EGFR and AKT phosphorylation in ESCC cell lines.Afatinib (0-1 μM, 16-48 h) induces G0/G1 cell cycle arrest in HKESC-2 and EC-1.Afatinib (0-1 μM, 24-48 h) effectively induces apoptotic cell death in HKESC-2 and EC-1. (In Vivo) :Afatinib (0-20 mg/kg, Orally, daily for 25 days) shows dramatic tumor regression and downregulation of EGFR, HER2, HER3 and AKT phosphorylation.Afatinib (15 mg/kg, Orally, in a schedule of 5 days on plus 2 days off, for two weeks) strongly inhibits the growth of HKESC-2 tumor.

850140-72-6

BIBW-2992 | BIBW2992 | BIBW 2992

Pharmacology & Drug Discovery

>98% (HPLC)

10 mM in DMSO

CN (C) CC=CC (=O) NC1=C (C=C2C (=C1) C (=NC=N2) NC3=CC (=C (C=C3) F) Cl) OC4CCOC4

C24H25ClFN5O3

485.9384

Storage temperature: -20°C. Stability: ≥ 2 years

For research use only.