The epidermal growth factor receptor (EGFR; ErbB-1; HER1 in humans) is a transmembrane protein. And it is a receptor for members of the epidermal growth factor family (EGF family) of extracellular protein ligands. In many cancer types, mutations affecting EGFR expression or activity could result in cancer.

Gefitinib is an Orally Active EGFR Tyrosine Kinase Inhibitor for Cancers Research

Gefitinib (ZD1839) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. And it selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib also induces autophagy and cell apoptosis, which can be used for cancer related research, such as Lung cancer and breast cancer.

In Vitro, Gefitinib (0.01-0.1  μM, 72 h) results in increased phosphotyrosine load of the receptor, increased signalling to ERK and stimulation of proliferation and anchorage-independent growth. What’s more, Gefitinib (1-2 μM, 72 h) significantly decreases EGFRvIII phosphotyrosine load, EGFRvIII-mediated proliferation and anchorage-independent growth. Morever, Gefitinib (0.62 μM, 24-72 h) inhibits IL-13-induced M2-like polarization of RAW 264.7 cells through the STAT6-dependent signaling pathway. It also (0.62 μM, 72 h) inhibits M2-like macrophage-promoted invasion and migration. Gefitinib (0-10 μM, 72 h) induces apoptosis (induction of BIM protein) in NSCLC Cell Lines (H3255 and HCC827 cells). In addition, Gefitinib (100 nM, 24 h) suppresses macropinocytosis and increases the cellular uptake of extracellular vesicles( EVs) in HCC827 and A549 cells. Gefitinib (1.5-60 μM, 48 h) increases inhibition of proliferation in H358R and A549R cells (Cisplatin-resistant wtEGFR NSCLC cell lines).

In Vivo, Gefitinib (Oral administration, 75 mg/kg/d, 21 days) inhibits the M2-like polarization of macrophages in LLC mice metastasis model. Gefitinib (Oral administration, 75 mg/kg for the initial week, daily for 5 consecutive days per week) eliminates phosphorylation of HER2 and HER3 and signaling through MAPK and Akt in lobular hyperplasias and carcinomas, increases MAPK activity and cytokine production in splenocytes and lymph nodes. Gefitinib (Oral gavage, 150 mg/kg, daily) enhances the anti-tumor effect of Cisplatin in H358R xenograft.

In conclusion, Gefitinib is a potent, selective and orally active EGFR tyrosine kinase inhibitor for cancers research.


[1] Cancer Res. 2002 Oct 15;62(20):5749-54.

[2] Br J Cancer. 2005 Oct 17;93(8):915-23.