Gefitinib dihydrochlorideGefitinib dihydrochloride
MedChemExpress (MCE)
HY-50895B
184475-56-7
ZD 1839 dihydrochloride
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Room temperature in continental US
may vary elsewhere.
Gefitinib (ZD 1839) dihydrochloride is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib dihydrochloride selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib dihydrochloride also induces autophagy and cell apoptosis, which can be used for cancer related research, such as Lung cancer and breast cancer .
Gefitinib dihydrochloride (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[2]. Gefitinib dihydrochloride (1-2 μM, 72 h) significantly decreases EGFRvIII phosphotyrosine load, EGFRvIII-mediated proliferation and anchorage-independent growth[2]. Gefitinib dihydrochloride (0.62 μM, 24-72 h) inhibits IL-13-induced M2-like polarization of RAW 264.7 cells through the STAT6-dependent signaling pathway[3]. Gefitinib dihydrochloride (0.62 μM, 72 h) inhibits M2-like macrophage-promoted invasion and migration[3]. Gefitinib dihydrochloride (0-10 μM, 72 h) induces apoptosis (induction of BIM protein) in NSCLC Cell Lines (H3255 and HCC827 cells)[4]. Gefitinib dihydrochloride (100 nM, 24 h) suppresses macropinocytosis and increases the cellular uptake of extracellular vesicles( EVs) in HCC827 and A549 cells[6]. Gefitinib dihydrochloride (1.5-60 μM, 48 h) increases inhibition of proliferation in H358R and A549R cells (Cisplatin-resistant wtEGFR NSCLC cell lines)[7].
Gefitinib dihydrochloride (Oral administration, 75 mg/kg/d, 21 days) inhibits the M2-like polarization of macrophages in LLC mice metastasis model[3]. Gefitinib dihydrochloride (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[5]. Gefitinib dihydrochloride (Oral gavage, 150 mg/kg, daily) enhances the anti-tumor effect of Cisplatin in H358R xenograft[7].
IC50: 37 nM (Tyr1173 site, in NR6wtEGFR cells), 37 nM (Tyr992 site, in NR6wtEGFR cells)[1]. In Vitro Gefitinib dihydrochloride (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[2]. Gefitinib dihydrochloride (1-2 μM, 72 h) significantly decreases EGFRvIII phosphotyrosine load, EGFRvIII-mediated proliferation and anchorage-independent growth[2]. Gefitinib dihydrochloride (0.62 μM, 24-72 h) inhibits IL-13-induced M2-like polarization of RAW 264.7 cells through the STAT6-dependent signaling pathway[3]. Gefitinib dihydrochloride (0.62 μM, 72 h) inhibits M2-like macrophage-promoted invasion and migration[3]. Gefitinib dihydrochloride (0-10 μM, 72 h) induces apoptosis (induction of BIM protein) in NSCLC Cell Lines (H3255 and HCC827 cells)[4]. Gefitinib dihydrochloride (100 nM, 24 h) suppresses macropinocytosis and increases the cellular uptake of extracellular vesicles( EVs) in HCC827 and A549 cells[6]. Gefitinib dihydrochloride (1.5-60 μM, 48 h) increases inhibition of proliferation in H358R and A549R cells (Cisplatin-resistant wtEGFR NSCLC cell lines)[7]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> Gefitinib dihydrochloride Related Antibodies Western Blot Analysis[2] Cell Line: NR6wtEGFR, NR6W and NR6M
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[1]. Wakeling AE, et al. ZD1839: an orally active inhibitor of epidermal growth factor signaling with potential for cancer therapy. Cancer Res. 2002 Oct 15
62(20):5749-54. [Content Brief]
[2]. Pedersen MW, et al. Differential response to gefitinib of cells expressing normal EGFR and the mutant EGFRvIII. Br J Cancer. 2005 Oct 17
93(8):915-23. [Content Brief]
[3]. Muhammad Tariq, et al. Gefitinib inhibits M2-like polarization of tumor-associated macrophages in Lewis lung cancer by targeting the STAT6 signaling pathway. Acta Pharmacol Sin. 2017 Nov
38(11):1501-1511. [Content Brief]
[4]. Mark S Cragg, et al. Gefitinib-induced killing of NSCLC cell lines expressing mutant EGFR requires BIM and can be enhanced by BH3 mimetics. PLoS Med. 2007 Oct
4(10):1681-89
discussion 1690. [Content Brief]
[5]. Marie P Piechocki, et al. Gefitinib prevents cancer progression in mice expressing the activated rat HER2/neu. Int J Cancer. 2008 Apr 15
122(8):1722-9. [Content Brief]
[6]. Tomoya Takenaka, et al. Effects of gefitinib treatment on cellular uptake of extracellular vesicles in EGFR-mutant non-small cell lung cancer cells. Int J Pharm. 2019 Dec 15
572:118762. [Content Brief]
[7]. Amin Li, et al. Gefitinib sensitization of cisplatin-resistant wild-type EGFR non-small cell lung cancer cells. J Cancer Res Clin Oncol. 2020 Jul
146(7):1737-1749. [Content Brief]
