Crizotinib

Pricing Availability   Qty
说明: Potent c-MET/ALK inhibitor
别名: PF 02341066,PF 2341066
化学名: 3-[(1R)-1-(2,6-Dichloro-3-fluorophenyl)ethoxy]-5-[1-(4-piperidinyl)-1H-pyrazol-4-yl]-2-pyridinamine
纯度: ≥99% (HPLC)
说明书
引用文献 (9)
评论

生物活性 for Crizotinib

Crizotinib is a potent inhibitor of c-MET and anaplastic lymphoma kinase (ALK) (cell IC50 values are 8.0 and 20 nM respectively). Selective for c-MET and ALK against >120 different kinases. Displays antitumor efficacy in multiple tumor models; inhibits c-MET-dependent proliferation, migration and invasion of human tumor cells in vitro. Orally bioavailable.

许可信息

Sold for research purposes under agreement from Pfizer Inc.

技术数据 for Crizotinib

分子量 450.34
公式 C21H22Cl2FN5O
储存 Store at +4°C
纯度 ≥99% (HPLC)
CAS Number 877399-52-5
PubChem ID 11626560
InChI Key KTEIFNKAUNYNJU-GFCCVEGCSA-N
Smiles ClC1=[C@@]([C@H](OC2=C(N)N=CC(C3=CN(C4CCNCC4)N=C3)=C2)C)C(Cl)=CC=C1F

上方提供的技术数据仅供参考。批次相关数据请参见分析证书。

Tocris products are intended for laboratory research use only, unless stated otherwise.

溶解性数据 for Crizotinib

溶剂 最高浓度 mg/mL 最高浓度 mM
溶解性
DMSO 4.5 10
2eq.HCl 45.03 100

制备储备液 for Crizotinib

以下数据基于产品分子量 450.34。 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.

选择批次从而根据批次分子量重新计算:
浓度/溶剂体积/质量 1 mg 5 mg 10 mg
1 mM 2.22 mL 11.1 mL 22.21 mL
5 mM 0.44 mL 2.22 mL 4.44 mL
10 mM 0.22 mL 1.11 mL 2.22 mL
50 mM 0.04 mL 0.22 mL 0.44 mL

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产品说明书 for Crizotinib

分析证书/产品说明书
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查看全部 ALK Inhibitors

关键词: Crizotinib, Crizotinib supplier, c-MET, alk, anaplastic, lymphoma, kinases, antitumor, selective, potent, PF2341066, PF02341066, PF, 02341066, 2341066, MET, Receptors, ALK, 4368, Tocris Bioscience

9 篇 Crizotinib 的引用文献

引用文献是使用了 Tocris 产品的出版物。 Crizotinib 的部分引用包括:

Zhu et al (2016) Crosstalk between bone marrow-derived myofibroblasts and gastric cancer cells regulates cancer stemness and promotes tumorigenesis. Oncogene 35 5388 PMID: 27109105

Qi et al (2011) Multiple mutations and bypass mechanisms can contribute to development of acquired resistance to MET inhibitors. Cancer Res 71 1081 PMID: 21266357

Alan M et al (2020) Synergistic activity of agents targeting growth factor receptors, CDKs and downstream signaling molecules in a panel of pancreatic cancer cell lines and the identification of antagonistic combinations: Implications for future clinical trials in pancreatic Oncol Rep 44 2581-2594 PMID: 33125153

Gimenez-Xavier et al (2017) Genomic and Molecular Screenings Identify Different Mechanisms for Acquired Resistance to MET Inhibitors in Lung Cancer Cells. Mol Cancer Ther 16 1366 PMID: 28396363


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