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Crizotinib

CAS No. : 877399-52-5

MCE 国际站：Crizotinib

产品活性：Crizotinib (PF-02341066) 是一种具有口服活性的，ATP 竞争性的 ALK 和 c-Met 抑制剂，IC₅₀ 分别为 20 和 8 nM。在细胞的实验中，Crizotinib 抑制 NPM-ALK 的酪氨酸磷酸化和 c-Met 的酪氨酸磷酸化，IC₅₀ 分别为 24 和 11 nM。Crizotinib 也是 ROS1 抑制剂。Crizotinib 具有有效的肿瘤生长抑制作用。

研究领域：Protein Tyrosine Kinase/RTK  |  Autophagy

作用靶点：Anaplastic lymphoma kinase (ALK)  |  c-Met/HGFR  |  ROS Kinase  |  Autophagy

In Vitro: Crizotinib (PF-02341066) displays similar potency against c-Met phosphorylation in mIMCD3 mouse or MDCK canine epithelial cells with IC₅₀ of 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 IC₅₀ of 19 nM, 2 nM and 15 nM, respectively, compared with NIH3T3 cells expressing wild-type receptor with IC₅₀ of 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 IC₅₀ of 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 IC₅₀ of 13 nM and 16 nM, respectively, which express the endogenous c-Met variants R988C and T1010I, respectively.
Crizotinib (PF-02341066) also potently inhibits NPM-ALK phosphorylation in Karpas299 or SU-DHL-1 ALCL cells with an IC₅₀ of 24 nM. PF-2341066 potently prevents cell proliferation, which is associated with G(1)-S-phase cell cycle arrest and induction of apoptosis in ALK-positive ALCL cells with IC₅₀ of 30 nM, but not ALK-negative lymphoma cells.

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.
Treatment of c-MET-amplified GTL-16 xenografts with 50 mg/kg PF-2341066 elicits tumor regression that is associated with a slow reduction in 18F-FDG uptake and decreases expression of the glucose transporter 1, GLUT-1.

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