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Gefitinib

Cat. No. M1749
Gefitinib Structure
Synonym:

ZD-1839, Iressa

Size Price Availability Quantity
Free Sample (0.5-1 mg)  USD 0 In stock
10mM*1mL in DMSO USD 50  USD50 In stock
50mg USD 37  USD37 In stock
100mg USD 47  USD47 In stock
500mg USD 77  USD77 In stock
1g USD 117  USD117 In stock
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Quality Control
Biological Activity

Gefitinib (ZD1839) is an EGFR tyrosine kinase and Akt phosphorylation inhibitor. Gefitinib significantly down-regulates CD47 expression and increases DC phagocytosis in non-small cell lung cancer cells such as PC9, H1437 and H1573. Gefitinib combined with CD47 antibody can enhance the phagocytosis of macrophages.

Product Citations
Customer Product Validations & Biological Datas
Source Clinical Cancer Research (2018 Nov). Figure 1. Gefitinib (Abmole Bioscience)
Method Apoptosis and cell cycle analysis
Cell Lines EGFR mutant NSCLC cell lines
Concentrations 50 nM
Incubation Time 72 h
Results However, re-exposure to gefitinib over an additional 72 hrs period was inadequate to induce robust apoptosis in PC9 cells, and by the third cycle HCC827 cells also lost their ability to undergo apoptosis.
Source Clin Cancer Res (2017). Figure 2. Gefitinib (Abmole Bioscience)
Method apoptosis quantified
Cell Lines HCC4006 and H1975 cells
Concentrations 1μM
Incubation Time 72 h
Results We found directly inducing EMT by exogenous TWIST activation (Fig. 2) or chronic TGF- β treatment (Sup. Fig. 2) led to depressed levels of BIM resulting in suppression of EGFRi-induced apoptosis and resistance to EGFRi (WZ4002 and gefitinib).
Source Clin Cancer Res (2017). Figure 2. Gefitinib (Abmole Bioscience)
Method apoptosis quantified
Cell Lines HCC4006 and H1975 cells
Concentrations 1 μM
Incubation Time 72 h
Results We found directly inducing EMT by exogenous TWIST activation (Fig. 2) or chronic TGF- β treatment (Sup. Fig. 2) led to depressed levels of BIM resulting in suppression of EGFRi-induced apoptosis and resistance to EGFRi (WZ4002 and gefitinib).
Source Sci Rep (2017). Figure 7. Gefitinib (AbMole Bioscience, Houston, TX)
Method TKI gefitinib inhibits RIPK2-mediated dysglycemia in vivo.
Cell Lines C57Bl/6J (WT) and RIPK2−/− mice
Concentrations 100 mg/kg
Incubation Time 4 days
Results Pre-treatment with gefitinib attenuated lower blood glucose at 6 h post-FK565 injection. At the time of the glucose tolerance test (GTT, 24 h after FK565 injection) gefitinib pre-treatment did not alter fasting blood glucose.
Source Sci Rep (2017). Figure 6. Gefitinib (AbMole Bioscience, Houston, TX)
Method TKI gefitinib inhibits RIPK2-mediated inflammation in vivo.
Cell Lines RIPK2−/− mice
Concentrations 5–200 mg/kg
Incubation Time 4 days
Results Our results show that treatment with gefitinib at doses equal or greater than 50 mg/kg attenuated Nod1 mediated Cxcl1 protein levels in the circulation of mice in a dose-dependent manner.
Source Sci Rep (2017). Figure 5. Gefitinib (AbMole Bioscience, Houston, TX)
Method C57Bl/6J (WT) and RIPK2−/− mice
Cell Lines HEK293 cells
Concentrations 1 or 5 μM
Incubation Time
Results We assessed FK565- versus LPS-induced NF-κB activity using HEK293 cells stably over-expressing Nod1 or Tlr4. Consistent with cytokine secretion in adipocytes and macrophages, we find that treatment of HEK Nod1 cells with FK565 (10 μg/mL) increases NF-κB activation, which is attenuated in a dose-dependent manner by pre-incubation with gefitinib at 1 and 5 μM.
Source Sci Rep (2017). Figure 4. Gefitinib (AbMole Bioscience, Houston, TX)
Method
Cell Lines bacterial cell
Concentrations 0.2, 1 or 5 μM
Incubation Time 1 h
Results Time course of FK565-stimulated Cxcl1 secretion in BMDMs (B) n = 4–12. Levels of Cxcl1 released from WT (left panel) or RIPK2−/−(right panel) BMDMs after stimulation with the Tlr4 ligand LPS (0.5 μg/mL) for 48 h and pre-incubated for 1 h with 0.2, 1 or 5 μM gefitinib or SB203580 (C) n = 4–12.
Source Sci Rep (2017). Figure 3. Gefitinib (AbMole Bioscience, Houston, TX)
Method Westen Blot
Cell Lines bacterial cell
Concentrations 5 μM
Incubation Time 1 h
Results Quantitative comparison was conducted between samples from 4 different blots derived from the same experiment and processed in parallel. (n = 8 total (n = 2/condition per blot).
Source Sci Rep (2017). Figure 2. Gefitinib (AbMole Bioscience, Houston, TX)
Method TKIs inhibit cytokine response
Cell Lines bacterial cell
Concentrations 1 or 5 μM
Incubation Time 1 h
Results Our results show that pre-incubation with 1–5 μM gefitinib or 1–5 μM SB203580, but not 1–5 μM imatinib significantly attenuated FK565-induced Cxcl1 and Il6 release in a dose-dependent manner in adipocytes.
Source Sci Rep (2017). Figure 1. Gefitinib (AbMole Bioscience, Houston, TX)
Method bacterial cell wall-induced lipolysis
Cell Lines Murine 3T3-L1 preadipocytes
Concentrations 5 μM
Incubation Time 48 h
Results Only 1 or 5 μM gefitinib and 1 or 5 μM SB203580 dose dependently attenuated the increased rate of glycerol release induced by FK565.
Protocol
Cell Experiment
Cell lines MDA-361, SKBR-3, MDA-453 and BT-474 cells
Preparation method Monolayer Growth and Anchorage-independent Growth Assays. For monolayer growth, cells were seeded at a density of 3–4 104 cells in 12-well plates. Twenty-four h later, ZD1839 was added to the cells. Fresh medium ZD1839 was replaced on day 3. On day 5, cells were harvested by trypsinization and counted with a Zeiss Coulter Counter (Beckman Coulter, Miami, FL). Colony-forming assays in soft agarose were performed as described previously (30). Tumor cell colonies measuring 50 m were counted after 7 days using an Omnicon 3800 colony counter and Tumor Colony Analysis V2.IIA software (Imaging Products International, Inc.).
Concentrations 0.1–10 µ M
Incubation time 4 days
Animal Experiment
Animal models BT-474 cells Xenograft in Athymic Mice
Formulation 0.05% Tween 80
Dosages 200 mg/kg/day for 28 days
Administration oral gavage
Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)
Species Mouse Rat Rabbit Guinea pig Hamster Dog
Weight (kg) 0.02 0.15 1.8 0.4 0.08 10
Body Surface Area (m2) 0.007 0.025 0.15 0.05 0.02 0.5
Km factor 3 6 12 8 5 20
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of Compound A used for a mouse (20 mg/kg) to a dose based on the BSA for a rat, multiply 20 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for Compound A of 10 mg/kg.

Chemical Information
Molecular Weight 446.90
Formula C22H24ClFN4O3
CAS Number 184475-35-2
Purity 99.97%
Solubility DMSO 68 mg/mL
Storage at -20°C
References

[1] Lankheet NA et al. Biomed Chromatogr. Method development and validation for the quantification of dasatinib, erlotinib, gefitinib, imatinib, lapatinib, nilotinib, sorafenib and sunitinib in human plasma by liquid chromatography coupled with tandem mass spectrometry.

[2] Lee SJ et al. Invest New Drugs. A pilot study for the early assessment of the effects of BMS-754807 plus gefitinib in an H292 tumor model by [(18)F]fluorothymidine-positron emission tomography.

[3] Kwon SH et al. Arch Dermatol. Gefitinib-Induced Paronychia: Response to Autologous Platelet-Rich Plasma.

[4] Erdem L et al. Curr Top Med Chem. Polymorphisms to predict outcome to the tyrosine kinase inhibitors gefitinib, erlotinib, sorafenib and sunitinib.

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Keywords: Gefitinib, ZD-1839, Iressa supplier, EGFR/HER2, inhibitors

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