CAS NO: | 877399-52-5 |
包装 | 价格(元) |
10 mM * 1 mL in DMSO | 电议 |
10mg | 电议 |
50mg | 电议 |
100mg | 电议 |
200mg | 电议 |
500mg | 电议 |
1 g | 电议 |
5 g | 电议 |
生物活性 | Crizotinib (PF-02341066) is an orally bioavailable, ATP-competitiveALKandc-Metinhibitor withIC50s of 20 and 8 nM, respectively. Crizotinib inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC50s of 24 and 11 nM in cell-based assays, respectively. Crizotinib is also aROS1inhibitor. Crizotinib has effective tumor growth inhibition[1][2][3]. | ||||||||||||||||
IC50& Target | IC50: 20 nM (ALK), 8 nM (c-Met)[3] | ||||||||||||||||
体外研究 (In Vitro) | Crizotinib (PF-02341066) displays similar potency against c-Met phosphorylation in mIMCD3 mouse or MDCK canine epithelial cells with IC50of 5 nM and 20 nM, respectivly. PF-2341066 shows improved or similar activity against NIH3T3 cells engineered to express c-Met ATP-binding site mutants V1092I or H1094R or the P-loop mutant M1250T with IC50of 19 nM, 2 nM and 15 nM, respectively, compared with NIH3T3 cells expressing wild-type receptor with IC50of 13 nM. In contrast, a marked shift in potency of PF-2341066 is observed against cells engineered to express c-Met activation loop mutants Y1230C and Y1235D with IC50of 127 nM and 92 nM, respectively, compared with wild-type receptor. PF-2341066 also potently prevents the phosphorylation of c-Met in NCI-H69 and HOP92 cells, with IC50of 13 nM and 16 nM, respectively, which express the endogenous c-Met variants R988C and T1010I, respectively[1]. | ||||||||||||||||
体内研究 (In Vivo) | Crizotinib (PF-02341066) reveals the ability to cause marked regression of large established tumors (>600 mm3) in both the 50 mg/kg/day and 75 mg/kg/day treatment cohorts, with a 60% decrease in mean tumor volume over the 43-day administration schedule in the GTL-16 model. In an another study, PF-2341066 displays the ability to completely inhibits GTL-16 tumor growth for >3 months, with only 1 of 12 mice exhibiting a significant increase in tumor growth over the 3-month treatment schedule at 50 mg/kg/day. A significant dose-dependent reduction of CD31-positive endothelial cells is observed at 12.5 mg/kg/day, 25 mg/kg/day, and 50 mg/kg/day in GTL-16 tumors, indicating that inhibition of MVD shows a dose-dependent correlation to antitumor efficacy. PF-2341066 displays a significant dose-dependent reduction of human VEGFA and IL-8 plasma levels in both the GTL-16 and U87MG models. Marked inhibition of phosphorylated c-Met, Akt, Erk, PLCλ1, and STAT5 levels is observed in GTL-16 tumors following p.o. administration of PF-2341066[1]. | ||||||||||||||||
Clinical Trial | |||||||||||||||||
分子量 | 450.34 | ||||||||||||||||
性状 | Solid | ||||||||||||||||
Formula | C21H22Cl2FN5O | ||||||||||||||||
CAS 号 | 877399-52-5 | ||||||||||||||||
中文名称 | 克唑替尼;可唑替尼;克卓替尼;克唑替尼;克里唑替尼 | ||||||||||||||||
运输条件 | Room temperature in continental US; may vary elsewhere. | ||||||||||||||||
储存方式 |
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溶解性数据 | In Vitro: DMSO : 33.33 mg/mL(74.01 mM;Need ultrasonic) H2O :< 0.1 mg/mL (ultrasonic)(insoluble) 配制储备液
* 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效。 In Vivo: 请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照In Vitro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,建议您现用现配,当天使用;
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