Gefitinib hydrochloride (ZD-1839 hydrochloride) is an orally active selective and potent tyrosine kinase (EGFR) inhibitor. Gefitinib hydrochloride exhibits antitumor activity, selectively inhibits EGF-stimulated tumor cell growth, induces cellular autophagy, improves lung dysfunction, and inhibits inflammation. Gefitinib hydrochloride has antitumor activity, selectively inhibits EGF-stimulated tumor cell growth, induces cellular autophagy, ameliorates lung dysfunction, and inhibits the progression of inflammation and fibrosis.

GLC82 cells:2 μM, Calu3 (cells):2 μM, non-transformed cells:20 nM

Gefitinib hydrochloride (0.01-0.1 mM) increased phosphotyrosine loading of the receptor by inducing EGFRvIII dimerization, enhanced ERK signaling, and stimulated cell proliferation and anchorage-independent growth, especially upon prolonged exposure of EGFRvIII-expressing cells. In contrast, Gefitinib hydrochloride (1-2 mM) significantly reduced phosphotyrosine loading of EGFRvIII and inhibited EGFRvIII-mediated proliferation and anchorage-independent growth. [1]
Gefitinib hydrochloride inhibited monolayer growth of non-transformed cells driven by EGF with an IC50 of 20 nM. [2]
Gefitinib hydrochloride also inhibited the proliferation of CALU-3 and GLC82 cells with an IC50 of 2 μM. [3]

Gefitinib hydrochloride (150 mg/kg, orally) in combination with metformin significantly inhibited the growth of tumor xenografts formed by subcutaneous transplantation of H1299 or CALU-3 GEF-R cells in nude mice. [3]
In rats treated with radiation therapy, Gefitinib hydrochloride exacerbated the inflammatory response in the lungs, including the infiltration of inflammatory cells and the increase of pro-inflammatory factors, whereas Gefitinib hydrochloride served to slow down the fibrotic remodeling of the lungs by inhibiting the proliferation of lung fibroblasts. [4]

DMSO: < 0.1 mg/mL (insoluble)

H2O: 4 mg/mL (8.28 mM), Sonication is recommended.