Molecular Weight(MW): 446.90
Gefitinib (ZD-1839) is an EGFR inhibitor for Tyr1173, Tyr992, Tyr1173 and Tyr992 in the NR6wtEGFR and NR6W cells with IC50 of 37 nM, 37nM, 26 nM and 57 nM, respectively.
Cited by 91 Publications
12 Customer Reviews
Perturbation of EGFR by its ligand EGF and gefitinib (ZD-1839 Iressat; inhibits EGFR) produces opposite responses in the predicted EGFR target genes SOCS2 and NR2E1.
Mol Syst Biol 2011 7, 486. Gefitinib (ZD1839) purchased from Selleck.
Effects of shRNA-mediated RECK depletion on EGFR signaling in MEFs. (a) Immunoblotting (IB) of the indicated proteins in wild-type MEFs transduced with the indicated shRNAs and cultured for 48 h in the presence of 0.1% dimethyl sulfoxide (DMSO; vehicle) or 1 mM gefitinib (S1025, Selleck Chemicals,Houston, TX, USA). (b) Immunoprecipitation from whole lysates of cells from panel a with an anti-phosphorylated tyrosine (pTyr) antibody. Precipitates from 500 mg protein in whole cell lysates (upper) or 20 mg protein in whole cell lysates (lower) were analyzed by IB with anti-EGFR antibody.
Oncogene 2010 30, 737-750. Gefitinib (ZD1839) purchased from Selleck.
(B–C) LNCaP (B) and LNCaP-AI (C) cells were transiently transfected with sPLA2-IIa(-800)-Luc (0.5 μg). The cells were then treated with Erlotinib (20 μM), Gefitinib (20 μM), Lapatinib (20 μM), CI-1033 (8 μM), LY294002 (20 lM) and Bortezomib (20 μM) without or with EGF (100 ng/ml) for 24 h. Luciferase assay was performed according to a standard protocol with Renilla luciferase as an internal control. Data are presented as the mean (±SD) of duplicate values of a representative experiment that was independently repeated for five times.
Carcinogenesis 2010 31, 1948–1955 . Gefitinib (ZD1839) purchased from Selleck.
LNCaP-AI cells were starved in 1% stripped medium for 24 h. The cells were then treated with Erlotinib (20 μM), Gefitinib (20 μM), Lapatinib (20 μM), CI-1033 (8 μM), LY294002 (20 μM) and Bortezomib (20 μM) for 24 h. Cell culture medium was collected from each sample and subjected to ELISA for sPLA2-IIa. The condition medium samples were diluted 10 times for ELISA. Average of duplicate samples was converted to nanogram per milliliter against standard curve. The data represent one of five repeated experiments.
Carcinogenesis 2010 31, 1948–1955. Gefitinib (ZD1839) purchased from Selleck.
Susceptibility of lung cancer cells to cytolytic activity of NK-92 cells after treatment with EGFR inhibitors. Three lung cancer cells were untreated (open circle) or treated with 10 μM erlotinib or gefitinib (black filled square or black filled triangle) for 24 hours. The lung cancer cells were cocultured with NK-92 cells at indicated effector to target ratio (E:T ratio). To determine the specificity of NKG2D-mediated cytolysis of lung cancer cells, NK-92 cells were preincubated with blocking mAb against NKG2D before the assay (gray filled square and triangle) and correspond-ing isotype mAb (open square and triangle).
J Immunother 2011 34(4), 372-81. Gefitinib (ZD1839) purchased from Selleck.
Suppression of EGFR signaling by Gefitinib is dose dependent and non- toxic at millimolar concentrations.Results from plaque reduction tests of Hep2 cells infected with VACV(12.5pfu/well) treated with a serial dilution of Gefitinib (1000-0.01 m) and analyzed for (A)proliferation as indicator of cytotoxicity,(B) IC50 of plaque size inhibition, (C)dose dependent inhibition of EGFR-ERK1/2signaling and VACV proteins by Western blot analysis (pEGFR detection was obtained from a different experiment with identicals ettings) and (D)dose dependent inhibition of orthopoxvirus genome replication by real-time PCR.Untreated VACV infectedcells and uninfected cells are shown as controls in the right panel.
Antiviral Res 2010 89, 64-70. Gefitinib (ZD1839) purchased from Selleck.
A circular zone of EGFR activated but uninfected cells facilitate virus induced plaque development , efficiently blocked by Gefitinib. (A)Immun of luorescent staining of aplaque reduction tests with Hep2 cells 24,48,72 and 96 h after VACV infection (6.25pfu/chamber). VACV infected cells(green) were visualized by human IgG directed to orthopoxviruses (VIG) detected with a secondary FITC labelled antibody. Uninfected cells with activated EGFR signaling(red) are detected with a secondary Cy3labelled antibody. Positive cells for both , VACV and phosphorylated EGFR are shown in yellow(merge). Cellular nuclei are counterstained with DAPI. (B)Immunofluorescent staining of a plaque reduction test as described for (A) and treated with three different Gefitinib concentrations (1000 nM, 1 nM, and 0.01 nM) . The test was analyzed 96h afterVACV infection.Uninfected cells are shown as controls. Magnification100×.(For interpretation of the references to color in this figure legend , the reader is referred to the web version of the article.)
Antiviral Res 2010 89, 64-70. Gefitinib (ZD1839) purchased from Selleck.
Reduction of GPER expression in HCC1806 cells after treatment with gefitinib. (A) Concentration dependence. HCC1806 cells were treated with 50-500 nM gefitinib for 48 h. GPER was detected by western blotting. (B) Time dependence. HCC1806 cells were treated with 200 nM gefitinib for 24-96 h. ap<0.05 vs. control; bp<0.001 vs. control. Mean values and SE of three independent experiments are shown. (C) Representative western blotting of concentration dependence. (D) Representative western blotting of time dependence
Oncol Rep, 2017, 37(2):1212-1218. Gefitinib (ZD1839) purchased from Selleck.
Inhibition of signaling pathway activation in lung tumor cell lines by kinase inhibitors. Lung tumor cells were cultured in 10% FBS until reaching ∼80% confluence and then the cells were starved in serum-free medium for overnight, followed by 4-hour treatment with the inhibitors. Cell lysates were then prepared and used for determination of the pathway activation signals by the CEER assay.
Int J Proteomics 2011 215496. Gefitinib (ZD1839) purchased from Selleck.
Breast cancer cells were pretreated with 100ng/ml EGF for 15 min and then treated with the indicated concentrations of Gefitinib for 24 hours.
2010 Dr. Zhang of Tianjin Medical University. Gefitinib (ZD1839) purchased from Selleck.
Purity & Quality Control
Choose Selective EGFR Inhibitors
|Description||Gefitinib (ZD-1839) is an EGFR inhibitor for Tyr1173, Tyr992, Tyr1173 and Tyr992 in the NR6wtEGFR and NR6W cells with IC50 of 37 nM, 37nM, 26 nM and 57 nM, respectively.|
|Features||A potent EGFR tyrosine kinase inhibitor.|
Gefitinib effectively inhibits all tyrosine phosphorylation sites on EGFR in both the high and low-EGFR-expressing cell lines including NR6, NR6M and NR6W cell lines. The phosphorylation sites Tyr1173 and Tyr992 are less sensitive requiring higher concentrations of Gefitinib for inhibition. Gefitinib effectively blocks the phosphorylation of PLC-γ, with IC50 of 27nM, in NR6W cells. The NR6wtEGFR and NR6M cell lines has low levels of PLC-γ phosphorylation but the level in the NR6M cell line is more resistant to inhibition by Gefitinib with IC50 of 43 nM and 369 nM, respectively. Gefitinib inhibits Akt phosphorylations, with IC50 of 220 and 263nM, in the low-EGFR- and -EGFRvIII-expressing cell lines, respectively. Gefitinib in the dose range from 0.1 to 0.5μM significantly facilitates, rather than abrogates, colony formation of NR6M cells. However, at a concentration of 2 μM Gefitinib completely blocks NR6M colony formation. Gefitinib rapidly and in a dose-dependent manner inhibits EGFR and ERK phosphorylation up to 72 hours after EGF stimulation in both the high- and low-EGFR-expressing cell lines.  Gefitinib is the monolayer growth of these EGF-driven untransformed MCF10A cells with an IC50 of 20 nM.  The combination of Gefitinib (0.2 μM and 0.5 μM) with irradiation lead to a significant growth inhibition in LoVo cells, compared with radiation alone.. 
|In vivo||Gefitinib (100 mg/kg) improves the anti-tumor effect of radiotherapy in LoVo tumor xenografts.  Gefitinib treatment of nude mice bearing established human GEO colon cancer xenografts reveals a reversible dose-dependent inhibition of tumor growth because GEO tumors resumes the growth rate of controls at the end of the treatment. |
-  Pedersen MW, et al. Br J Cancer. 2005, 93(8), 915-923.
-  Moasser MM, et al. Cancer Res. 2001, 61(19), 7184-7188.
-  Williams KJ, et al. Br J Cancer, 2002, 86, 1157–1161.
|In vitro||DMSO||89 mg/mL (199.14 mM)|
|Ethanol||4 mg/mL (8.95 mM)|
|In vivo||Add solvents individually and in order:
5% DMSO+corn oil
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03050164||Completed||Bioequivalence Study||Hunan Kelun Pharmaceutical Co., Ltd.||September 8, 2016||Phase 1|
|NCT02856893||Not yet recruiting||NSCLC||European Organisation for Research and Treatment of Cancer - EORTC|AstraZeneca||March 2017||Phase 2|
|NCT02976116||Recruiting||NSCLC||Hutchison Medipharma Limited||December 2016||Phase 2|
|NCT02951637||Not yet recruiting||Lung Adenocarcinoma||Shanghai Chest Hospital|Ruijin Hospital|Changhai Hospital||December 2016||Phase 2|
|NCT02930954||Not yet recruiting||Non-small-cell Lung Cancer||Caicun Zhou|Tongji University||November 2016||Phase 2|
|NCT02929693||Enrolling by invitation||Cancer||Shanghai University of Traditional Chinese Medicine|Shanghai Chest Hospital|Shanghai Pulmonary Hospital, Shanghai, China||October 2016||Phase 3|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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Frequently Asked Questions
I try to dissolve Gefitinib (ZD1839) in 0.5% methylcellulose+0.2% Tween 80 for in vivo experiments. However, when I prepare the mixture, it forms precipitates. Exists another way to dissolve completely the compound?
S1025 can be dissovled in both 5% DMSO+corn oil and 5% DMSO+30% PEG 300+5% Tween 80+ddH2O at 2.5 mg/ml clearly. It dissolves in DMSO not readily, please sonicate and warm it in water bath at about 45 degree, and dissolve it clearly first. Then add other solvent.