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编 号：F230508
分子式：C22H26Cl3FN4O3
分子量：519.82
分子式：C22H26Cl3FN4O3
分子量：519.82
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CAS No: 184475-56-7
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生物活性：
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 .
体内研究：
Gefitinib dihydrochloride (Oral administration, 75 mg/kg/d, 21 days) inhibits the M2-like polarization of macrophages in LLC mice metastasis model.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.Gefitinib dihydrochloride (Oral gavage, 150 mg/kg, daily) enhances the anti-tumor effect of Cisplatin in H358R xenograft.Animal Model:LLC mice metastasis model
Dosage:75 mg/kg/d, for 21 days.
Administration:Oral administration
Result:Reduced the number of lung metastasis nodules, down-regulated the expression of M2 marker genes and the percentages CD206+ and CD68+ macrophages in tumor tissues.
Animal Model:BALB-NeuT transgenic mouse model
Dosage:75 mg/kg for the initial week, and increased by 15 mg/kg every other week, daily for 5 consecutive days per week, followed by 2 days without treatment and repeated for 8–9 weeks.
Administration:Oral administration
Result:Reduced tumor multiplicity from 9.6 to 0.58 (83%), and reduced the number and size of lobules and lobular nodules in treated mice.
体外研究：
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.Gefitinib dihydrochloride (1-2 μM, 72 h) significantly decreases EGFRvIII phosphotyrosine load, EGFRvIII-mediated proliferation and anchorage-independent growth.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.Gefitinib dihydrochloride (0.62 μM, 72 h) inhibits M2-like macrophage-promoted invasion and migration.Gefitinib dihydrochloride (0-10 μM, 72 h) induces apoptosis (induction of BIM protein) in NSCLC Cell Lines (H3255 and HCC827 cells).Gefitinib dihydrochloride (100 nM, 24 h) suppresses macropinocytosis and increases the cellular uptake of extracellular vesicles( EVs) in HCC827 and A549 cells.Gefitinib dihydrochloride (1.5-60 μM, 48 h) increases inhibition of proliferation in H358R and A549R cells (Cisplatin-resistant wtEGFR NSCLC cell lines).
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 .
体内研究：
Gefitinib dihydrochloride (Oral administration, 75 mg/kg/d, 21 days) inhibits the M2-like polarization of macrophages in LLC mice metastasis model.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.Gefitinib dihydrochloride (Oral gavage, 150 mg/kg, daily) enhances the anti-tumor effect of Cisplatin in H358R xenograft.Animal Model:LLC mice metastasis model
Dosage:75 mg/kg/d, for 21 days.
Administration:Oral administration
Result:Reduced the number of lung metastasis nodules, down-regulated the expression of M2 marker genes and the percentages CD206+ and CD68+ macrophages in tumor tissues.
Animal Model:BALB-NeuT transgenic mouse model
Dosage:75 mg/kg for the initial week, and increased by 15 mg/kg every other week, daily for 5 consecutive days per week, followed by 2 days without treatment and repeated for 8–9 weeks.
Administration:Oral administration
Result:Reduced tumor multiplicity from 9.6 to 0.58 (83%), and reduced the number and size of lobules and lobular nodules in treated mice.
体外研究：
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.Gefitinib dihydrochloride (1-2 μM, 72 h) significantly decreases EGFRvIII phosphotyrosine load, EGFRvIII-mediated proliferation and anchorage-independent growth.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.Gefitinib dihydrochloride (0.62 μM, 72 h) inhibits M2-like macrophage-promoted invasion and migration.Gefitinib dihydrochloride (0-10 μM, 72 h) induces apoptosis (induction of BIM protein) in NSCLC Cell Lines (H3255 and HCC827 cells).Gefitinib dihydrochloride (100 nM, 24 h) suppresses macropinocytosis and increases the cellular uptake of extracellular vesicles( EVs) in HCC827 and A549 cells.Gefitinib dihydrochloride (1.5-60 μM, 48 h) increases inhibition of proliferation in H358R and A549R cells (Cisplatin-resistant wtEGFR NSCLC cell lines).
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