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Afatinib

CAS No. : 850140-72-6

MCE 國際站：Afatinib

產品活性：Afatinib (BIBW 2992) 是一種口服有效且不可逆的 ErbB 家族 (EGFR 和 HER2) 雙特異性抑制劑，對 EGFR^wt, EGFR^L858R, EGFR^L858R/T790M 和 HER2 的 IC₅₀ 值分別為 0.5 nM、0.4 nM、10 nM 和 14 nM。Afatinib 可用于食管鱗狀細胞癌 (ESCC)、非小細胞肺癌 (NSCLC) 和胃癌的研究。

研究領域：JAK/STAT Signaling  |  Protein Tyrosine Kinase/RTK  |  Autophagy  |  Apoptosis  |  PI3K/Akt/mTOR  |  MAPK/ERK Pathway

作用靶點：EGFR  |  Autophagy  |  Apoptosis  |  c-Met/HGFR  |  Akt  |  p38 MAPK

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.

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