1. JAK/STAT Signaling
    Protein Tyrosine Kinase/RTK
    Autophagy
    Apoptosis
  2. EGFR
    Autophagy
    Apoptosis
  3. Gefitinib dihydrochloride

Gefitinib dihydrochloride (Synonyms: ZD 1839 dihydrochloride)

Cat. No.: HY-50895B
Handling Instructions

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 .

For research use only. We do not sell to patients.

Gefitinib dihydrochloride Chemical Structure

Gefitinib dihydrochloride Chemical Structure

CAS No. : 184475-56-7

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Top Publications Citing Use of Products

79 Publications Citing Use of MCE Gefitinib dihydrochloride

    Gefitinib dihydrochloride purchased from MCE. Usage Cited in: Breast Cancer Res. 2017 Aug 4;19(1):90.

    The effect of Gefitinib-FTY720 treatment on CD44 expression in TNBC cell lines. HCC1806, Hs578T, and MDA-MB-468 TNBC cell lines at ~40% confluence in 12-well plates are exposed for 24 h to Gefitinib (Gef: 0.1 to 10 μM), with or without the addition of 1.5 μM FTY720.

    Gefitinib dihydrochloride purchased from MCE. Usage Cited in: Theranostics. 2018 Jul 30;8(15):4262-4278.

    BV2 cells are pretreated with 0.1% DMSO (Ctrl), JuA (25 µM) or JuA (25 µM) with the indicated antagonist of RTKs (Dovitinib at 1 µM, Gefitinib at 2.5 µM, SU 11248 at 2.5 µM and LDC1267 at 1 µM) for 30 min, followed by administration of Aβ42 (5 μM) for 12 h.

    Gefitinib dihydrochloride purchased from MCE. Usage Cited in: Chem Pharm Bull (Tokyo). 2017 Aug 1;65(8):768-775.

    Changes in Bcl-2 protein expression in MCF-7 cells after treatment with 2CdA, BMS-354825 or Gefitinib alone or in combination for 12 h. Expression of Bcl-2 protein is analyzed by western blotting analysis.

    Gefitinib dihydrochloride purchased from MCE. Usage Cited in: Exp Cell Res. 2017 Dec 15;361(2):246-256.

    Western blot analysis for p21, p-p21, Cyclin D1. Bcl-2, Caspase 3, Cleaved Caspase 3, Caspase 9, Cleaved Caspase 9 and Bax in HCC827-GR and PC-9-GR cells treated with control, Efatutazone alone, Gefitinib alone, or Efatutazone combined with gefitinib for 48 h.

    Gefitinib dihydrochloride purchased from MCE. Usage Cited in: Oncogene. 2018 Aug;37(31):4300-4312.

    Western blot analysis of E-cadherin and vimentin in HCC827 xenograft tumors treated with Gefitinib daily for 6-8 weeks until tumors regrown (resistant) or saline for 1 week (sensitive) (left panel).

    Gefitinib dihydrochloride purchased from MCE. Usage Cited in: Cancer Cell. 2018 Jun 11;33(6):1061-1077.e6.

    WT mice are either treated with vehicle or Gefitinib (100 mg/kg/day) starting one day prior to DEN injection (100 mg/kg). Livers are collected at 3 and 48 hr after DEN injection and subjected to IB analyses with the indicated antibodies.

    Gefitinib dihydrochloride purchased from MCE. Usage Cited in: Cell Death Dis. 2018 Feb 15;9(3):269.

    WB is used to detect the effect of EGF treatment for 4 h on the expression of YAP with the inhibitors of EGFR or its downsream members, including Gefitinib, LY294002, Wortmannin, GSK2334470, BX-795, MK-2206, GSK1120212, and U0126 in the Si RhoA transfected HepG2 and SMMC7721 cells for 48 h in HepG2 and SMMC7721 cells.

    Gefitinib dihydrochloride purchased from MCE. Usage Cited in: Oncol Rep. 2018 Oct;40(4):2242-2250.

    Effects of Gefitinib(G) and SC 58635 (Cel) on ABCB1 (MDR1), FOXM1 and Bcl 2 protein levels in PC3/DR and DU145/DR cell lines. The effects of Gefitinib, SC 58635 and their combination on ABCB1 (MDR1), FOXM1 and Bcl 2 expression in the PC3/DR and DU145/DR cell lines are determined by a western blot assay.

    Gefitinib dihydrochloride purchased from MCE. Usage Cited in: Mol Med Rep. 2017 Sep;16(3):3475-3481.

    Cyclin B1 and Cdk1 protein expression levels are significantly downregulated in NCI-H1975 cells treated with the combination of DHA (5 µM) and Gefitinib (10 µM).
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    Description

    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 [1][2][5].

    IC50 & Target

    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].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Western Blot Analysis[2]

    Cell Line: NR6wtEGFR, NR6W and NR6M
    Concentration: 1, 10, 100 μM
    Incubation Time: 5 h
    Result: Inhibited EGFR tyrosine phosphorylations.

    Cell Migration Assay [3]

    Cell Line: LLCs cell
    Concentration: 0.62 μM
    Incubation Time: 72 h
    Result: Abrogated M2-like macrophage promoted invasion and migration of LLCs.
    In Vivo

    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].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Model: LLC mice metastasis model[3]
    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[5]
    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.
    Molecular Weight

    519.82

    Formula

    C22H26Cl3FN4O3

    CAS No.
    SMILES

    COC1=CC2=NC=NC(NC3=CC=C(F)C(Cl)=C3)=C2C=C1OCCCN4CCOCC4.[H]Cl.[H]Cl

    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage

    Please store the product under the recommended conditions in the Certificate of Analysis.

    References
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