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Gefitinib/吉非替尼 {[allProObj[0].p_purity_real_show]}

货号：A109874 同义名： 吉非替尼 (ZD1839) / ZD1839

Gefitinib（ZD1839）是一种强效、选择性和口服活性的EGFR酪氨酸激酶抑制剂。

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Type HazMat fee for 500 gram (Estimated)
Excepted Quantity USD 0.00
Limited Quantity USD 15-60
Inaccessible (Haz class 6.1), Domestic USD 80+
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Gefitinib/吉非替尼 化学结构 CAS号：184475-35-2
Gefitinib/吉非替尼 化学结构
CAS号：184475-35-2
Gefitinib/吉非替尼 3D分子结构
CAS号：184475-35-2
Gefitinib/吉非替尼 化学结构 CAS号：184475-35-2
Gefitinib/吉非替尼 3D分子结构 CAS号：184475-35-2
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Gefitinib/吉非替尼 纯度/质量文件 产品仅供科研

货号：A109874 标准纯度： {[allProObj[0].p_purity_real_show]}
批次查询： 批次纯度:

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产品名称 EGFR/ErbB1 ↓ ErbB3 ↓ ErbB4 ↓ HER2/ErbB2 ↓ mutant EGFR ↓ 其他靶点 纯度
WZ-3146 ++++

EGFR (E746_A750), IC50: 2 nM

EGFR (E746_A750/T790M), IC50: 14 nM

 		99%+
Daphnetin +

EGFR, IC50: 7.67 μM

 		PKC,PKA 95%
Lifirafenib ++

EGFR, IC50: 29 nM

 		+

EGFR(T790M/L858R), IC50: 495 nM

 		98%
PD168393 ++++

EGFR, IC50: 0.70 nM

 		99%+
Nazartinib ++

mutant EGFR, Ki: 0.031 μM

 		++

mutant EGFR, Ki: 0.031 μM

 		98%
Norcantharidin ✔ 98%
CL-387785 ++++

EGFR, IC50: 370 pM

 		98%
WHI-P154 +++

EGFR, IC50: 4 nM

 		Src,VEGFR 98%
Tyrphostin A9 +

EGFR, IC50: 460 μM

 		PDGFR 98%
AG 555 +

EGFR, IC50: 0.7 μM

 		98%
AG 494 +

EGFR, IC50: 1.2 μM

 		99%+
AG-556 +

EGFR, IC50: 5 μM

 		98%
RG13022 +

EGFR, IC50: 4 μM

 		99%+
Tyrphostin RG 14620 ✔ 99%+
Vandetanib +

EGFR, IC50: 500 nM

 		99%
CNX-2006 ++

mutant EGFR, IC50: <20 nM

 		++

mutant EGFR, IC50: <20 nM

 		99%
AZD3759 ++++

EGFR (WT), IC50: 0.3 nM

EGFR (L858R), IC50: 0.2 nM

 		98%
Erlotinib ++++

EGFR, IC50: 2 nM

 		95%
Saracatinib +++

EGFR (L861Q), IC50: 4 nM

EGFR, IC50: 5 nM

 		99%+
AG1557 ✔ 99%
Rociletinib ++

EGFR (wt), Ki: 303.3 nM

EGFR (L858R/T790M), Ki: 21.5 nM

 		98%
AG490 +

EGFR, IC50: 0.1 μM

 		98%
Cetuximab ++++

EGFR, Kd: 0.39 nM

 		95%
Osimertinib ++

WT EGFR, IC50: 12.92 nM

L858R/T790M EGFR, IC50: 11.44 nM

 		98%
Osimertinib mesylate ✔ 98% (Content MsOH 15.2-18.2%)
Chrysophanol ✔ mTOR 98%
PD153035 ++++

EGFR, Ki: 5.2 pM

 		99%+
Olmutinib ✔ BTK 99%+
WZ4002 ++++

EGFR (L858R/T790M), IC50: 8 nM

EGFR (L858R), IC50: 2 nM

 		99%+
Icotinib +++

EGFR, IC50: 5 nM

 		99%
Desmethyl Erlotinib HCl ++++

EGFR, IC50: 2 nM

 		98%
Cyasterone ✔ 99%+
PP 3 +

EGFR tyrosine kinase, IC50: 2.7 μM

 		98%
WZ8040 ✔ 99%+
(-)-Epigallocatechin Gallate ✔ 99%
AG 18 +

EGFR, IC50: 35 μM

 		99%+
O-Desmethyl gefitinib ++

EGFR, IC50: 36 nM

 		99%
Falnidamol ✔ 99%+
AZ-5104 ++++

EGFR (L861Q) , IC50: <1 nM

EGFR (L858R), IC50: 6 nM

 		+++

ErbB4, IC50: 7 nM

 		BRK 99%+
Butein ✔ 95%
Genistein ✔ 98%
SU5214 +

EGFR, IC50: 36.7 μM

 		99%+
Naquotinib ✔ 99%+
Gefitinib ++

EGFR, IC50: 15.5 nM

 		+

EGFR (858R/T790M), IC50: 823.3 nM

 		98%
Theliatinib +++

WT EGFR, IC50: 3 nM

 		++

EGFR T790M/L858R, IC50: 22 nM

 		99%
Lazertinib ++++

WT EGFR, IC50: 76 nM

L858R/T790M EGFR, IC50: 2 nM

 		++++

Del19/T790M, IC50: 1.7 nM

 		99%+
Gefitinib-based PROTAC 3 ++

EGFR, DC50: 22.3 nM

 		99%+
MTX-211 ✔ PI3K 98%
(E)-AG 99 ✔ 99%+
Licochalcone D ✔ Caspase,PARP 99%
Zipalertinib +++

EGFR (L861Q), IC50: 4.1 nM

EGFR WT, IC50: 8 nM

 		+++

HER4, IC50: 4 nM

 		++++

EGFR(d746-750), IC50: 1.4 nM

EGFR L858R, IC50: 2 nM

 		97%
JND3229 +++

EGFR WT, IC50: 6.8 nM

 		++

EGFR L858R/T790M, IC50: 30.5 nM

 		99%+
Firmonertinib mesylate ✔ 99%+
Tyrphostin AG30 ✔ 99%+
EGFR-IN-12 ++

EGFR, IC50: 21 nM

 		99%+
Mobocertinib ✔ 98%
(Rac)-JBJ-04-125-02 ✔ 95%
(S)-Sunvozertinib ✔ 99%
BLU-945 ✔ 95%
Poziotinib +++

HER1, IC50: 3.2 nM

 		++

HER4, IC50: 23.5 nM

 		+++

HER2, IC50: 5.3 nM

 		98%
TAK-285 ++

EGFR/HER1, IC50: 23 nM

 		+

HER4, IC50: 260 nM

 		++

HER2, IC50: 17 nM

 		99%+
ARRY-380 analog ✔ 99%
Canertinib ++++

EGFR, IC50: 1.5 nM

 		+++

ErbB2, IC50: 9.0 nM

 		99%+
Dacomitinib +++

EGFR, IC50: 6.0 nM

 		+

ErbB4, IC50: 73.7 nM

 		+

ErbB2, IC50: 45.7 nM

 		98%
EGFR/ErbB-2/ErbB-4 inhibitor-2 +

ErbB4, IC50: 1.91 μM

 		+

ErbB2, IC50: 0.08 μM

 		99%+
(E/Z)-CP-724714 ++

HER2/ErbB2, IC50: 10 nM

 		95%
Lapatinib ++

EGFR, IC50: 10.8 nM

 		+

ErbB4, IC50: 367 nM

 		+++

ErbB2, IC50: 9.2 nM

 		98%
AEE788 ++++

EGFR, IC50: 2 nM

 		+

HER4/ErbB4, IC50: 160 nM

 		+++

HER2/ErbB2, IC50: 6 nM

 		c-Fms/CSF1R 98+%
AV-412 free base ++++

EGFR, IC50: 0.75 nM

 		++

ErbB2, IC50: 19 nM

 		++++

EGFRL858R/T790M, IC50: 0.51 nM

EGFRT790M, IC50: 0.79 nM

 		98+%
Neratinib +

EGFR, IC50: 92 nM

 		+

HER2, IC50: 59 nM

 		Src 98%
BMS-599626 ++

HER1, IC50: 20 nM

 		+

HER4, IC50: 190 nM

 		++

HER2, IC50: 30 nM

 		98%
Tucatinib +++

ErbB2, IC50: 8 nM

 		98%
Allitinib ++++

EGFR, IC50: 0.5 nM

 		++++

ErbB4, IC50: 0.8 nM

 		+++

ErbB2, IC50: 3.0 nM

 		99%
Pelitinib +

EGFR, IC50: 38.5 nM

 		+

ErbB2, IC50: 1.255 μM

 		Src,Raf 99%+
Sapitinib +++

EGFR, IC50: 4 nM

 		+++

ErbB3, IC50: 4 nM

 		+++

ErbB2, IC50: 3 nM

 		99%+
CUDC-101 +++

EGFR, IC50: 2.4 nM

 		++

HER2, IC50: 15.7 nM

 		HDAC 99%+
Varlitinib +++

ErbB1, IC50: 7 nM

 		++++

ErbB2, IC50: 2 nM

 		99%+
Afatinib dimaleate ++++

EGFR (wt), IC50: 0.5 nM

EGFR (L858R/T790M), IC50: 0.4 nM

 		++

HER2, IC50: 14 nM

 		98%
Canertinib 2HCl +++

EGFR, IC50: 7.4 nM

 		+++

ErbB2, IC50: 9 nM

 		99%
Allitinib tosylate ++++

EGFR (T790M/L858R), IC50: 12 nM

EGFR, IC50: 0.5 nM

 		++++

ErbB4, IC50: 0.8 nM

 		+++

ErbB2, IC50: 3.0 nM

 		99%
Tyrphostin AG 528 +

EGFR, IC50: 4.9 μM

 		+

HER2, IC50: 2.1 μM

 		97%
Afatinib ++++

EGFR (wt), IC50: 0.5 nM

EGFR (L858R), IC50: 10 nM

 		++++

ErbB4, IC50: 1 nM

 		++

HER2, IC50: 14 nM

 		99%
Pyrotinib dimaleate ++

EGFR, IC50: 0.013 μM

 		++

HER2, IC50: 0.038 μM

 		98%
Epertinib HCl ++++

EGFR, IC50: 1.48 nM

 		+++

HER4, IC50: 2.49 nM

 		+++

HER2, IC50: 7.15 nM

 		99%
Tuxobertinib ++++

EGFR, Kd: 0.2 nM

 		++++

HER2, Kd: 0.76 nM

 		99%
ALK-IN-1 ++

EGFR(C797S/del19), IC50: 138.6 nM

EGFR(del19), IC50: 36.8 nM

 		ALK 99%
Brigatinib +

EGFR(C797S/T790M/del19), IC50: 67.2 nM

EGFR(del19), IC50: 39.9 nM

 		ALK,FLT3 98%
Avitinib ++++

EGFR L858R/T790M, IC50: 0.18 nM

 		BTK 99%+
EAI045 ✔ 97%
Almonertinib ✔ 99%
BI-4020 ++++

EGFRdel19 T790M C797S, IC50: 0.2 nM

 		99%+
EGFR-IN-7 ++++

EGFRL858R/T790M, IC50: 0.19 nM

EGFRd746-750/T790M/C797S, IC50: 0.26 nM

 		99%
1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多，抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用，但抑制强度暂时没有相关数据。

Gefitinib/吉非替尼 生物活性

靶点

  • EGFR/ErbB1

    Tyr1173 (NR6W cells), IC50:57 nM

    Tyr992 (NR6wtEGFR cells), IC50:37 nM

  • EGFR/ErbB1

    EGFR, IC50:15.5 nM

  • mutant EGFR

    EGFR (858R/T790M), IC50:823.3 nM
描述 EGFR (epidermal growth factor receptor) family consists of four members that belong to the ErbB lineage of proteins (ErbB1 - 4) with an external domain that binds activating ligands, such as EGF, and is overexpressed in a significant percentage of carcinomas and contributes to the malignant phenotype. Upon activation, EGFR phosphorylates both the receptor itself and a variety of “effector” protein. Gefitinib is an effective EGFR inhibitor with IC50 values of 37 nM, 37 nM, 26 nM and 57 nM for Tyr1173, Tyr992, Tyr1173 and Tyr992 EGFR sites (measured by EGFR tyrosine phosphorylations in cells), respectively in NR6 wt EGFR and NR6W cells. Gefitinib can sufficiently suppress all tyrosine phosphorylation sites, with less sensitivity to Tyr1173 and Tyr992 sites, on EGFR in both the high and low-EGFR-expressing cell lines, as well as EGFR-mediated proliferation. However, EGFR-mediated anchorage-independent growth was not sufficient to inhibit these features in cells expressing EGFRvIII, with approximately four times as resistant to gefitinib as EGFR. Long-term exposure of EGFRvIII-expressing cells to low concentrations of gefitinib (0.01 - 0.1 μM) resulted in increased phosphotyrosine load of the receptor, increased signaling to ERK and stimulation of proliferation and anchorage-independent growth while higher concentrations of gefitinib (1 - 2 μM) completely showed the opposite effect, presumably by inducing EGFRvIII dimerization[1]. Gefitinib (40 mg/kg body weight/day) showed significant inhibition of tumor load when treated with weekly or weekly intermittent dosing regimens in lung adenocarcinoma model whereas a daily dosing regimen did not decrease the tumor load significantly[2].
作用机制 Gefitinib is an ATP-competitive inhibitor of EGFR[3].

Gefitinib/吉非替尼 细胞实验

Cell Line
Concentration Treated Time Description References
HL-60 cells 10 μM 10 minutes Identify Syk as a target for AML differentiation Cancer Cell. 2009 Oct 6;16(4):281-94.
human primary hepatocytes 20 µM 24 h To investigate the effects of Gefitinib on apoptosis and autophagy, results showed that Gefitinib significantly induced apoptosis and autophagy. Autophagy. 2021 Oct;17(10):3221-3237.
HL-7702 cells 20 µM 24 h To investigate the effects of Gefitinib on apoptosis and autophagy, results showed that Gefitinib significantly induced apoptosis and autophagy. Autophagy. 2021 Oct;17(10):3221-3237.
PC-9 cells 0.01 μM 96 h To evaluate the anti-cancer effect of gefitinib in combination with Ad/ABE-TP53-EGFR, the results showed that the Ad/ABE-oncoSNP system unexpectedly elicited a significant cancer cell killing effect in PC-9 cells. Mol Ther. 2024 Oct 2;32(10):3618-3628.
H1975 cells 15 μM 96 h To evaluate the anti-cancer effect of gefitinib in combination with Ad/ABE-TP53-EGFR, the results showed that the combination treatment significantly enhanced the sensitivity to gefitinib and inhibited tumor cell proliferation. Mol Ther. 2024 Oct 2;32(10):3618-3628.

Gefitinib/吉非替尼 动物实验

Species
Animal Model
Administration Dosage Frequency Description References
NSG mice HCC827 and ERC4 cell lines xenografts Oral gavage 20 mg/kg 17 weeks Investigate the effect of EDN1 on tumor growth and drug penetration, results showed EDN1 overexpression led to reduced tumor growth and drug penetration, while EDN1 receptor antagonist bosentan improved drug penetration and tumor response Cancer Res. 2020 Oct 1;80(19):4224-4232
C57BL/6J mice Silicosis mouse model Oral 200 mg/kg Once daily for two weeks Gefitinib and fostamatinib potently inhibited the level of p-EGFR and p-SYK respectively, and effectively alleviated silica-induced diffuse alveolitis revealed by histological examination. Meanwhile, qPCR analysis showed that the levels of pro-inflammatory cytokines (such as Interleukin-1 β (Il-1β), Interleukin-6 (Il-6), and Tumor necrosis factor α (Tnf-α)) were markedly decreased in lung tissues following drug treatment. Moreover, Van Gieson and sirius red staining data showed that collagen deposition of lung tissue was effectively suppressed by gefitinib or fostamatinib treatment in silicosis mice. Signal Transduct Target Ther. 2022 May 13;7(1):157
Mice Atg7+/− mice By gavage 200 mg/kg Once daily for 4 weeks To evaluate the hepatotoxicity of Gefitinib, results showed that Gefitinib significantly induced liver injury, and autophagy inhibition alleviated liver damage. Autophagy. 2021 Oct;17(10):3221-3237.
Nude mice H1975 tumor xenograft model Oral 100 mg/kg Once daily for 5 days To evaluate the anti-tumor effect of gefitinib in combination with Ad/ABE-TP53-EGFR, the results showed that the combination treatment significantly inhibited tumor growth and reversed gefitinib resistance. Mol Ther. 2024 Oct 2;32(10):3618-3628.

Gefitinib/吉非替尼 动物研究

Dose Mice (p.o.): min = 5 mg/kg[4], max = 300 mg/kg[5]
Administration p.o.
Pharmacokinetics
Animal Rats[6]
Dose 5 mg/kg
Administration i.v.
p.o.
Cmax 230 ng/ml (p.o.)
T1/2 5.3 h (i.v.)
4.1 h (p.o.)
Vdss 9.8 L/kg (i.v.)
AUC0-8 1130 ng·h/ml (p.o.)
F 49.8% (p.o.)
AUC0-inf 3540 ng·h/ml (i.v.)
1780 ng·h/ml (p.o.)
Tmax 4 h (p.o.)
CL 23.6 ml/min/kg (i.v.)

Gefitinib/吉非替尼 临床研究

NCT号 适应症或疾病 临床期 招募状态 预计完成时间 地点
NCT00206414 BREAST CANCER Phase 2 Terminated(Difficulty accruing... 展开 >> subjects the study accrual was closed) 收起 << - United States, Texas ... 展开 >> Baylor Breast Center Houston, Texas, United States, 77030 收起 <<
NCT00820417 Colorectal Cancer ... 展开 >> Head and Neck Cancer Non Small Cell Lung Cancer (NSCLC) 收起 << Phase 1 Completed - Belgium ... 展开 >> UZ Gasthuisberg Leuven, Belgium, 3000 Spain Hospital Universitari Vall d'Hebron Barcelona, Spain, 08035 收起 <<
NCT00025207 Advanced Malignant Mesotheliom... 展开 >>a Epithelial Mesothelioma Recurrent Malignant Mesothelioma Sarcomatous Mesothelioma 收起 << Phase 2 Completed - United States, Illinois ... 展开 >> Cancer and Leukemia Group B Chicago, Illinois, United States, 60606 收起 <<

Gefitinib/吉非替尼 参考文献

[1]Pedersen MW, Pedersen N, et al. Differential response to gefitinib of cells expressing normal EGFR and the mutant EGFRvIII. Br J Cancer. 2005 Oct 17;93(8):915-23.

[2]Zhang Q, Li R, 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.

[3]Gokhale AG, Rajagopal P, et al. Cockroach in right main bronchus--an unusual foreign body. Indian J Chest Dis Allied Sci. 1992 Apr-Jun;34(2):103-5.

[4]Kishino D, Kiura K, et al. Effect of gefitinib on N-nitrosamine-4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone induced lung tumorigenesis in A/J mice. Lung Cancer. 2009 Sep;65(3):284-9.

[5]Mikumo H, Yanagihara T, et al. Neutrophil elastase inhibitor sivelestat ameliorates gefitinib-naphthalene-induced acute pneumonitis in mice. Biochem Biophys Res Commun. 2017 Apr 22;486(1):205-209.

[6]Pharmacokinetics of gefitinib

Gefitinib/吉非替尼 实验方案

计算器
存储液制备 1mg 5mg 10mg

1 mM

5 mM

10 mM

2.24mL

0.45mL

0.22mL

11.19mL

2.24mL

1.12mL

22.38mL

4.48mL

2.24mL

Gefitinib/吉非替尼 技术信息

CAS号184475-35-2
分子式C22H24ClFN4O3
分子量 446.9
SMILES Code C1=C3C(=CC(=C1OC)OCCCN2CCOCC2)C(=NC=N3)NC4=CC=C(C(=C4)Cl)F
MDL No. MFCD04307832
别名 吉非替尼 (ZD1839) ;ZD1839
运输蓝冰
InChI Key XGALLCVXEZPNRQ-UHFFFAOYSA-N
Pubchem ID 123631
存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Keep in dark place, sealed in dry, room temperature
溶解方案

DMSO: 105 mg/mL(234.95 mM)，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO

请根据您的动物给药指南选择适当的溶解方案。
以下溶解方案都请先按照体外实验的方式配制澄清的储备液，再依次添加助溶剂：
——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议现用现配，当天使用； 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶
方案 一
方案 二
方案 三
方案 四
配制的工作液建议现用现配，短期内尽快用完。 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶。
方案 一
方案 二

Tags: Gefitinib | ZD1839 | 吉非替尼 (ZD1839) | EGFR | AmBeed-信号通路专用抑制剂 | Gefitinib/吉非替尼 纯度/质量文件 | Gefitinib/吉非替尼 亚型比较 | Gefitinib/吉非替尼 生物活性 | Gefitinib/吉非替尼 动物研究 | Gefitinib/吉非替尼 临床数据 | Gefitinib/吉非替尼 参考文献 | Gefitinib/吉非替尼 实验方案 | Gefitinib/吉非替尼 技术信息

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