Gefitinib

カタログ番号 T1181 CAS 184475-35-2

別名: ZD1839

Gefitinib (ZD1839) is an EGFR first-generation inhibitor with oral activity that inhibits the EGFR 19 Del and L858R mutations. Gefitinib has antitumor activity and is used for the treatment of EGFR-mutated non-small-cell lung cancers. Gefitinib administration RESULTS in the development of the EGFR C797S resistance mutation.

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Gefitinib, CAS 184475-35-2

パッケージサイズ	在庫状況	単価(税別)
サンプルについてお問い合わせ
100 mg	在庫あり	￥ 11,500
500 mg	在庫あり	￥ 13,000
1 g	在庫あり	￥ 17,000
5 g	在庫あり	￥ 34,000
1 mL * 10 mM (in DMSO)	在庫あり	￥ 11,500

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純度: 100%

COA DATASHEET SDS HNMR HPLC

純度: 100%

COA DATASHEET SDS HNMR LCMS

純度: 100%

DATASHEET SDS

純度: 100%

COA DATASHEET SDS LCMS HNMR

純度: 100%

COA DATASHEET SDS HNMR LCMS

純度: 100%

COA DATASHEET SDS HNMR LCMS

純度: 99.92%

COA DATASHEET SDS HNMR HPLC

COA DATASHEET SDS HNMR

COA DATASHEET SDS

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生物学的特性に関する説明

化学的特性

保存条件 & 溶解度情報

説明	Gefitinib (ZD1839) is an EGFR first-generation inhibitor with oral activity that inhibits the EGFR 19 Del and L858R mutations. Gefitinib has antitumor activity and is used for the treatment of EGFR-mutated non-small-cell lung cancers. Gefitinib administration RESULTS in the development of the EGFR C797S resistance mutation.
ターゲット＆IC50	Tyr1173:26 nM (NR6W cells), Tyr1173:37 nM (NR6wtEGFR cells), Tyr992:37 nM (NR6wtEGFR cells) , Tyr992:57 nM (NR6W cells)
In vitro	METHODS: Twenty-three tumor cells were treated with Gefitinib for 72 h, and cell viability was measured by MTT. RESULTS: Only the PC9 cell line had an IC50 <1 μmol/L (highly sensitive), 14 cell lines had an IC50 >10 μmol/L (resistant), and the remaining 8 cell lines had an IC50 of 1-10 μmol/L (moderately sensitive). [1] METHODS: Tumor cells HT29, KB, Du145 and A549 were treated with Gefitinib (0.032-50 μM) for 2 h. EGF (0.1 μg/mL) was added five minutes prior to cell lysis, and the expression levels of target proteins were detected using Western Blot. RESULTS: Gefitinib produced a dose-dependent inhibition of EGFR autophosphorylation in all tumor cell lines. [2]
In vivo	METHODS: To detect anti-tumor activity in vivo, Gefitinib (3.125-200 mg/kg in 0.5% polysorbate 80) was administered orally to nude mice harboring tumors A431, Du145, or A549 once a day for seven to fifteen days. RESULTS: Gefitinib inhibited the growth of A431, Du145 or A549 tumors in a dose-dependent manner. [2] METHODS: To assay antitumor activity in vivo, Gefitinib (40 mg/kg once daily) or Gefitinib (200 mg/kg every five days) was administered by gavage for two weeks to athymic nude mice harboring the human lung cancer tumor H3255. RESULTS: Weekly treatment showed better inhibition than daily treatment. Compared with the daily dosing regimen, the weekly dosing regimen showed stronger inhibition of p-EGFR, p-ERK, and p-AKT. [3]
細胞研究	The human NSCLC H1299, H1975, A549, H460, GLC82, H460, and CALU-3 cell lines were provided by the American Type Culture Collection and maintained in RPMI-1640 supplemented with 10% FBS in a humidified atmosphere with 5% CO2. CALU-3 GEF-R is a cell line obtained in vitro as previously described. Briefly, over a period of 12 months, human CALU-3 lung adenocarcinoma cells were continuously exposed to increasing concentrations of gefitinib. The starting dose was the dose causing the inhibition of 50% of cancer cell growth (IC50; gefitinib, 1 μmol/L). The drug dose was progressively increased to 15 μmol/L in approximately 2 months, to 20 μmol/L after other 2 months, to 25 μmol/L after additional 2 months, and, finally, to 30 μmol/L for a total of 12 months. The established resistant cancer cell lines were then maintained in continuous culture with the maximally achieved dose of each TKI that allowed cellular proliferation (30 μmol/L for each drug) [2].
動物実験	Four- to 6-week old female balb/c athymic (nu+/nu+) mice were purchased from Charles River Laboratories. Mice were acclimatized for 1 week before being injected with cancer cells and injected subcutaneously with 107 H1299 and CALU-3 GEF-R cells that had been resuspended in 200 μL of Matrigel. When established tumors of approximately 75 mm3 in diameter were detected, mice were left untreated or treated with oral administrations of metformin (200 mg/mL metformin diluted in drinking water and present throughout the experiment), gefitinib (150 mg/kg daily orally by gavage), or both for the indicated time periods. Each treatment group consisted of 10 mice. Tumor volume was measured using the formula π/6 × larger diameter × (smaller diameter)2. Tumor tissues were collected from the xenografts and analyzed by Western blotting for the expression and activation of EGFR, AMPK, mitogen-activated protein kinase (MAPK), and S6 [2].
植物由来	天然物製品 > セリ科 > ツボクサ属

別名	ZD1839
分子量	446.9
分子式	C22H24ClFN4O3
CAS No.	184475-35-2

保存条件

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

溶解度情報

DMSO: 18.33 mg/mL (41.02 mM)

Ethanol: 4.5 mg/mL (10 mM)

参考文献

1. Noro R, et al. Gefitinib (IRESSA) sensitive lung cancer cell lines show phosphorylation of Akt without ligand stimulation. BMC Cancer. 2006 Dec 6;6:277. 2. Wakeling AE, et al. ZD1839 (Iressa): an orally active inhibitor of epidermal growth factor signaling with potential for cancer therapy. Cancer Res. 2002 Oct 15;62(20):5749-54. 3. Zhang Q, et al. Effect of weekly or daily dosing regimen of Gefitinib in mouse models of lung cancer. Oncotarget. 2017 Aug 2;8(42):72447-72456. 4. Tan J, et al. Tyrosine kinase inhibitors show different anti-brain metastases efficacy in NSCLC: A direct comparative analysis of icotinib, gefitinib, and erlotinib in a nude mouse model. Oncotarget. 2017 Oct 19;8(58):98771-98781. 6. Dhar D, et al. Liver Cancer Initiation Requires p53 Inhibition by CD44-Enhanced Growth Factor Signaling. Cancer Cell. 2018 Jun 11;33(6):1061-1077.e6. 8. Teng J F, Qin D L, Mei Q, et al. Polyphyllin VI, a saponin from Trillium tschonoskii Maxim. induces apoptotic and autophagic cell death via the ROS triggered mTOR signaling pathway in non-small cell lung cancer[J]. Pharmacological Research. 2019: 104396. 9. . circSETD3 Contributes to Acquired Resistance to Gefitinib in Non-Small-Cell Lung Cancer by Targeting the miR-520h/ABCG2 Pathway. Molecular Therapy-Nucleic Acids. 2020 10. Quan C, Chen Y, Wang X, et al. Loss of histone lysine methyltransferase EZH2 confers resistance to tyrosine kinase inhibitors in non-small cell lung cancer. cancer letters. 2020

引用文献

1. Oeller M, Jaksch-Bogensperger H, Templin M, et al.Transcription Factors STAT3 and MYC Are Key Players of Human Platelet Lysate-Induced Cell Proliferation.International Journal of Molecular Sciences.2022, 23(24): 15782. 2. He S, Shi J, Zhou H H, et al.Lnc-ABCA12-8 confers acquired resistance to gefitinib in non-small cell lung cancer by regulating the alternative splicing of fibronectin 1 in the IIICS region.Cancer Gene Therapy.2022, 29(11): 1686-1696. 3. Wen C, Li Y, Huang Y, et al.CircSETD3 mediates acquired resistance to gefitinib in non-small lung cancer cells by FXR1/ECT2 pathway.The International Journal of Biochemistry & Cell Biology.2022: 106344. 4. Hu L, Liu Y, Fu C, et al.The Tumorigenic Effect of the High Expression of Ladinin-1 in Lung Adenocarcinoma and Its Potential as a Therapeutic Target.Molecules.2023, 28(3): 1103. 5. Chen J, Lei C, Nie D, et al.Inorganic arsenic exposure promotes malignant progression by HDAC6‐mediated down‐regulation of HTRA1.Journal of Applied Toxicology.2023 6. Jiao D, Chen Y, Liu X, et al.Targeting MET endocytosis or degradation to overcome HGF-induced gefitinib resistance in EGFR-sensitive mutant lung adenocarcinoma.Biochemical and Biophysical Research Communications.2023 7. Yang S, Yang S, Zhang H, et al. Targeting Na+/K+‐ATPase by berbamine and ouabain synergizes with sorafenib to inhibit hepatocellular carcinoma. British Journal of Pharmacology. 2021 8. Zhao X, Zhang N, Huang Y, et al. Lansoprazole Alone or in Combination With Gefitinib Shows Antitumor Activity Against Non-small Cell Lung Cancer A549 Cells in vitro and in vivo. Frontiers in Cell and Developmental Biology. 2021, 9: 947 9. Wang L, Liu X X, Yang Y M, et al. RHBDF2 gene functions are correlated to facilitated renal clear cell carcinoma progression. Cancer Cell International. 2021, 21(1): 1-18. 10. Shi J, Huang Y, Wen C, et al. Genome-wide identification and characterization of long non-coding RNAs involved in acquired resistance to gefitinib in non-small-cell lung cancer. Computational Biology and Chemistry. 2020, 87: 107288.

11. Zhao Deng,Chenbin Cui,Yanan Wang,Jiangjin Ni, et al. FSGHF3 and peptides, prepared from fish skin gelatin, exert a protective effect on DSS-induced colitis via the Nrf2 pathway. Food & Function. 2020 12. Cao D, Chen D, Xia J N, et al. Artesunate promoted anti-tumor immunity and overcame EGFR-TKI resistance in non-small-cell lung cancer by enhancing oncogenic TAZ degradation. Biomedicine & Pharmacotherapy. 2022, 155: 113705. 13. Liu Y, Luo Y, Yan S, et al. CRL2KLHDC3 mediates p14ARF N-terminal ubiquitylation degradation to promote non-small cell lung carcinoma progression. Oncogene. 2022: 1-14 14. Kang J, Guo Z, Zhang H, et al. Dual Inhibition of EGFR and IGF-1R Signaling Leads to Enhanced Antitumor Efficacy against Esophageal Squamous Cancer. International Journal of Molecular Sciences. 2022, 23(18): 10382 15. Teng J F, Qin D L, Mei Q, et al. Polyphyllin VI, a saponin from Trillium tschonoskii Maxim. induces apoptotic and autophagic cell death via the ROS triggered mTOR signaling pathway in non-small cell lung cancer. Pharmacological Research. 2019: 104396. 16. Shang J, Ning S, Chen Y, et al. MDL-800, an allosteric activator of SIRT6, suppresses proliferation and enhances EGFR-TKIs therapy in non-small cell lung cancer. Acta Pharmacologica Sinica. 2021, 42(1): 120-131 17. Zheng P, Huang Z, Tong D C, et al. Frankincense myrrh attenuates hepatocellular carcinoma by regulating tumor blood vessel development through multiple epidermal growth factor receptor-mediated signaling pathways. World Journal of Gastrointestinal Oncology. 2022, 14(2): 450 18. Yu J, Zhang L, Peng J, et al. Dictamnine, a novel c-Met inhibitor, suppresses the proliferation of lung cancer cells by downregulating the PI3K/AKT/mTOR and MAPK signaling pathways. Biochemical pharmacology. 2022, 195: 114864. 19. Yutang Huang,Yi Dai,Chunjie Wen,Shuai He,Jingjing Shi,Dezhang Zhao,Lanxiang Wu,Honghao Zhou circSETD3 Contributes to Acquired Resistance to Gefitinib in Non-Small-Cell Lung Cancer by Targeting the miR-520h/ABCG2 Pathway. Molecular Therapy-Nucleic Acids. 2020 20. Liang J, Bi G, Sui Q, et al.Transcription factor ZNF263 enhances EGFR-targeted therapeutic response and reduces residual disease in lung adenocarcinoma.Cell Reports.2024, 43(2). 21. Shao J, Ye Z, Shen Z, et al.Chidamide improves gefitinib treatment outcomes in NSCLC by attenuating recruitment and immunosuppressive function of myeloid-derived suppressor cells.Biomedicine & Pharmacotherapy.2024, 173: 116306.

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投与量変換

You can also refer to dose conversion for different animals. 詳細

In vivo投与量計算 (透明溶液)

ステップ1: 以下の情報を入力してください

投与量

mg/kg

動物の平均体重

動物あたりの投与量

動物数

溶媒の組成を入力してください

% DMSO+

% +

% Tween 80+

% ddH₂O

%DMSO+

計算するリセット

計算結果:

作業濃度: mg/ml;

DMSO溶液の作成方法: mg あらかじめ溶解した薬剤 μL DMSO (マスター溶液の濃度 mg/mL)，濃度がそのバッチの薬剤のDMSO溶解度を超える場合は、まずご連絡ください。

生体内薬剤の調合法：取る μL DMSO マスター溶液、次に追加 μL PEG300，確実に混ぜてから加える μL Tween 80，確実に混ぜてから加える μL ddH₂O, 確実に混ぜる

お問合せ内容:

必ず順番通りに溶媒を加えてください。ボルテックスミキサーや超音波、湯煎することで溶解しやすくなります

計算器

モル濃度計算機

希釈計算機

再構成計算

分子量計算機

質量

濃度

体積

分子量

モル度計算機では以下の計算が可能です

既知の体積と濃度の溶液を調製するために必要な化合物の質量
質量が既知の化合物を目的の濃度まで溶解させるのに必要な溶液の量
特定の体積の中に既知の質量の化合物を入れて得られる溶液の濃度

参考例

モル濃度計算機を使用したモル濃度計算の例
化合物の分子量が197.13g/molである場合、10mlの水に10mMのストック溶液を作るのに必要な化合物の質量はどれくらいですか？
［分子量（MW）］の欄に［197.13］と入力してください
[濃度]ボックスに10と入力し、正しい単位（millimolar）を選択します
[容量]ボックスに10と入力し、正しい単位（milliliter）を選択します
計算を押します
答えの19.713mgが質量欄に表示されます

濃度 (開始)

体積 (開始)

濃度 (終了)

体積 (終了)

溶液を作るのに必要な希釈率の計算

溶液の調製に必要な希釈率の算出
希釈計算機は、既知の濃度の原液をどのように希釈するかを計算することができる便利なツールです。V1を計算するためにC1、C2＆V2を入力します。

参考例

Tocrisの希釈計算器を用いた希釈計算の一例
50μMの溶液を20ml作るためには、10mMの原液を何ml必要ですか？
C1V1=C2V2という式を用いて、C1=10mM、C2=50μM、V2=20ml、V1を未知数とします。
濃度（開始）ボックスに10を入力し正しい単位(millimolar)を選択してください
濃度（終了）ボックスに50を入力し正しい単位(millimolar)を選択してください
体積（終了）ボックスに20を入力し正しい単位(millimolar)を選択してください
計算を押します
100 microliter (0.1 ml) という答えが体積（開始）ボックスに表示されます。

分子式

分子量 g/mol

化合物の化学式を入力して、そのモル質量や元素組成を計算します

Tヒント：化学式は大文字と小文字を区別します。: C10H16N2O2 c10h16n2o2

化合物のモル質量（分子量）を計算する手順:
化学物質のモル質量を計算するには、その化学式を入力し、「計算」をクリックしてください。.
分子質量、分子量、モル質量、モル重量の定義:
分子質量（分子量）とは、物質の1分子の質量であり、統一された原子質量単位（u）で表されます。(1uは炭素12の1原子の質量の1/12に等しい）
モル質量（molar weight）とは、ある物質の1モルの質量のことで、単位はg/molです。

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Keywords

Gefitinib 184475-35-2 Angiogenesis Autophagy JAK/STAT signaling Tyrosine Kinase/Adaptors EGFR Tyrosine Kinases EGFR tyrosine kinase lung cancer breast cancer phosphorylation ZD1839 Inhibitor Apoptosis inhibit TAMs NSCLCs antitumour Epidermal growth factor receptor HER1 tumor metastasis ZD-1839 ZD 1839 ErbB-1 inhibitor

本ウェブサイトに掲載されている製品は全て研究用試薬です。研究目的以外の用途にはご使用できません。

Gefitinib

保存条件

溶解度情報

参考文献

引用文献

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関連製品

投与量変換

In vivo投与量計算 (透明溶液)

計算器

モル度計算機では以下の計算が可能です

溶液を作るのに必要な希釈率の計算

バイアルを再構成するのに必要な溶媒の量を計算する.

化合物の化学式を入力して、そのモル質量や元素組成を計算します

技術サポート

Keywords