Gefitinib 吉非替尼

目录号 M1749 所有产品仅供科研使用，严禁用于人或动物的治疗等任何其他用途，不为任何个人提供产品和服务

Gefitinib (ZD1839)是一种EGFR酪氨酸激酶和Akt磷酸化抑制剂，吉非替尼可以显著下调非小细胞肺癌细胞(如PC9、H1437和H1573)中CD47的表达，并增加DC的吞噬功能。吉非替尼联合应用CD47抗体可增强巨噬细胞的吞噬功能。

别名：ZD-1839, Iressa

规格	价格	库存状态
Free Sample (0.5-1 mg)	¥ 0	中国库存现货
10mM*1mL in DMSO	¥ 450	中国库存现货
50mg	¥ 300	中国库存现货
100mg	¥ 440	中国库存现货
500mg	¥ 627	中国库存现货
1g	¥ 987	中国库存现货

其他规格数量报价？

质量标准及产品资料

纯度： 99.97%
COA
MSDS
H-NMR
HPLC

产品信息

生物活性

使用AbMole产品发表的文献

Cancer Cell Int. 2023 Jul 2;23(1):129.

Exosome-derived circKIF20B suppresses gefitinib resistance and cell proliferation in non-small cell lung cancer
Clin Transl Oncol. 2023 May;25(5):1425-1435.

ADAM12 promotes gemcitabine resistance by activating EGFR signaling pathway and induces EMT in bladder cancer
Endocrinology. 2020 May 30;bqaa086.

RIPK2 Dictates Insulin Responses to Tyrosine Kinase Inhibitors in Obese Male Mice
Clin Cancer Res. 2018 Nov 15;24(22):5658-5672.

Increased Synthesis of MCL-1 Protein Underlies Initial Survival of EGFR-Mutant Lung Cancer to EGFR Inhibitors and Provides a Novel Drug Target.
Clin Cancer Res. 2018 Jan 1;24(1):197-208.

Epithelial-to-mesenchymal transition antagonizes response to targeted therapies in lung cancer by suppressing BIM
Sci Rep. 2017 May 8;7(1):1578.

Tyrosine kinase inhibitors of Ripk2 attenuate bacterial cell wallmediated lipolysis, inflammation and dysglycemia

产品使用成果展示

	数据来源	Clinical Cancer Research (2018 Nov). Figure 1. Gefitinib (Abmole Bioscience)
	方法	Apoptosis and cell cycle analysis
	细胞系/动物模型	EGFR mutant NSCLC cell lines
	浓度	50 nM
	处理时间	72 h
	实验结果	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.

	数据来源	Clin Cancer Res (2017). Figure 2. Gefitinib (Abmole Bioscience)
	方法	apoptosis quantified
	细胞系/动物模型	HCC4006 and H1975 cells
	浓度	1μM
	处理时间	72 h
	实验结果	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).

	数据来源	Clin Cancer Res (2017). Figure 2. Gefitinib (Abmole Bioscience)
	方法	apoptosis quantified
	细胞系/动物模型	HCC4006 and H1975 cells
	浓度	1 μM
	处理时间	72 h
	实验结果	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).

	数据来源	Sci Rep (2017). Figure 7. Gefitinib (AbMole Bioscience, Houston, TX)
	方法	TKI gefitinib inhibits RIPK2-mediated dysglycemia in vivo.
	细胞系/动物模型	C57Bl/6J (WT) and RIPK2−/− mice
	浓度	100 mg/kg
	处理时间	4 days
	实验结果	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.

	数据来源	Sci Rep (2017). Figure 6. Gefitinib (AbMole Bioscience, Houston, TX)
	方法	TKI gefitinib inhibits RIPK2-mediated inflammation in vivo.
	细胞系/动物模型	RIPK2−/− mice
	浓度	5–200 mg/kg
	处理时间	4 days
	实验结果	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.

	数据来源	Sci Rep (2017). Figure 5. Gefitinib (AbMole Bioscience, Houston, TX)
	方法	C57Bl/6J (WT) and RIPK2−/− mice
	细胞系/动物模型	HEK293 cells
	浓度	1 or 5 μM
	处理时间
	实验结果	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.

	数据来源	Sci Rep (2017). Figure 4. Gefitinib (AbMole Bioscience, Houston, TX)
	方法
	细胞系/动物模型	bacterial cell
	浓度	0.2, 1 or 5 μM
	处理时间	1 h
	实验结果	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.

	数据来源	Sci Rep (2017). Figure 3. Gefitinib (AbMole Bioscience, Houston, TX)
	方法	Westen Blot
	细胞系/动物模型	bacterial cell
	浓度	5 μM
	处理时间	1 h
	实验结果	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).

	数据来源	Sci Rep (2017). Figure 2. Gefitinib (AbMole Bioscience, Houston, TX)
	方法	TKIs inhibit cytokine response
	细胞系/动物模型	bacterial cell
	浓度	1 or 5 μM
	处理时间	1 h
	实验结果	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.

	数据来源	Sci Rep (2017). Figure 1. Gefitinib (AbMole Bioscience, Houston, TX)
	方法	bacterial cell wall-induced lipolysis
	细胞系/动物模型	Murine 3T3-L1 preadipocytes
	浓度	5 μM
	处理时间	48 h
	实验结果	Only 1 or 5 μM gefitinib and 1 or 5 μM SB203580 dose dependently attenuated the increased rate of glycerol release induced by FK565.

实验参考

体外实验*
细胞系	MDA-361, SKBR-3, MDA-453 and BT-474 cells
方法	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.).
浓度	0.1–10 µ M
处理时间	4 days

*上述方法来自公开文献，仅供相同目的实验参考。如实验目的、材料、方法不同，请参考其他文献。

体内实验*
动物模型	BT-474 cells Xenograft in Athymic Mice
配制	0.05% Tween 80
剂量	200 mg/kg/day for 28 days
给药处理	oral gavage

*上述方法来自公开文献，仅供相同目的实验参考。如实验目的、材料、方法不同，请参考其他文献。

化学性质

分子量	446.90
分子式	C22H24ClFN4O3
CAS号	184475-35-2
溶解性（25°C）	DMSO 68 mg/mL
储存条件	粉末型式 -20°C 3年；4°C 2年溶于溶剂 -80°C 6个月；-20°C 1个月
运输方式	冰袋运输，根据产品的不同，可能会有相应调整。

储备液配制

*下述溶液配置方法仅为基于分子量计算出的理论值。不同产品在配置溶液前，需考虑其在不同溶剂中的溶解度限制。

Concentration / Solvent Volume / Mass	1 mg	5 mg	10 mg
1 mM	2.2376 mL	11.1882 mL	22.3764 mL
5 mM	0.4475 mL	2.2376 mL	4.4753 mL
10 mM	0.2238 mL	1.1188 mL	2.2376 mL

不同实验动物依据体表面积的等效剂量转换表（参考来源于公开文献）

	小鼠	大鼠	兔	豚鼠	仓鼠	狗
重量 (kg)	0.02	0.15	1.8	0.4	0.08	10
体表面积 (m²)	0.007	0.025	0.15	0.05	0.02	0.5
K_m 系数	3	6	12	8	5	20

动物 A (mg/kg) = 动物 B (mg/kg) ×	动物 B的K_m系数
	动物 A的K_m系数

例如，依据体表面积折算法，将化合物用于小鼠的剂量20 mg/kg 换算成大鼠的剂量，需要将20 mg/kg 乘以小鼠的K_m系数（3），再除以大鼠的K_m系数（6），得到化合物用于大鼠的等效剂量为10 mg/kg。

参考文献

[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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