Gefitinib hydrochloride (ZD1839 hydrochloride) 是一种有效，选择性和具有口服活性的EGFR酪氨酸激酶抑制剂，IC50为 33 nM。Gefitinib hydrochloride 选择性抑制 EGF 刺激的肿瘤细胞生长 (IC50为 54 nM)，并阻断 EGF 刺激的肿瘤细胞中EGFR自磷酸化。Gefitinib hydrochloride 也诱导细胞Autophagy" style="display: inline; color: #c13a36">自噬 (Autophagy)，具有抗肿瘤活性。

Gefitinib hydrochloride (ZD1839 hydrochloride) is a potent and orally active EGFR tyrosine kinase inhibitor (EGFR-TKI) (IC 50 = 33 nM) that selectively inhibits EGF-stimulated tumor cell growth (IC 50 = 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib hydrochloride also induces autophagy, which has antitumour activity [1] [2].

Gefitinib (0.01-0.1 mM) causes increased phosphotyrosine load of the receptor, increased ERK signalling, and stimulation of proliferation and anchorage-independent growth, presumably by inducing EGFRvIII dimerisation in long-term exposure of EGFRvIII-expressing cells. On the other hand, gefitinib (1-2 mM) significantly decreases EGFRvIII phosphotyrosine load, EGFRvIII-mediated proliferation and anchorage-independent growth [1]. Gefitinib (ZD1839) inhibits the monolayer growth of these EGF-driven untransformed cells with IC 50 of 20 nM [2]. Gefitinib leads to an inhibition of CALU-3 and GLC82 cell proliferation, with an IC 50 of 2 μM [3].

Gefitinib (150 mg/kg, p.o.) in conbination with Metformin significant reduces in tumor growth in nude mice bearing H1299 or CALU-3 GEF-R cells that are grown subcutaneously as tumor xenografts [3]. In irradiated rats, Gefitinib treatment augmentes lung inflammation, including inflammatory cell infiltration and pro-inflammatory cytokine expression, while Gefitinib treatment reduces fibrotic lung remodeling due to the inhibition of lung fibroblast proliferation [4].

184475-55-6

C22H25Cl2FN4O3

483.36

Gefitinib hydrochloride

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years