货号:A169062 同义名: XL880;GSK1363089
Foretinib is an ATP-competitive inhibitor of HGFR and VEGFR, mostly for Met and KDR with IC50 of 0.4 nM and 0.9 nM in cell-free assays. Foretinib is less potent against Ron, Flt-1/3/4, Kit, PDGFRα/β and Tie-2, and with little activity to FGFR1 and EGFR.
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产品名称 | VEGFR1 ↓ ↑ | VEGFR2 ↓ ↑ | VEGFR3 ↓ ↑ | 其他靶点 | 纯度 | ||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Motesanib Diphosphate |
++++
VEGFR1, IC50: 2 nM |
++++
VEGFR2, IC50: 3 nM VEGFR2/Flk1, IC50: 3 nM |
+++
VEGFR3, IC50: 6 nM |
PDGFR,RET | 98% | ||||||||||||||
Tivozanib |
++
VEGFR1, IC50: 30 nM |
+++
VEGFR2, IC50: 6.5 nM |
++
VEGFR3, IC50: 15 nM |
99%+ | |||||||||||||||
Brivanib |
+
VEGFR1, IC50: 380 nM |
++
VEGFR2, IC50: 25 nM Flk1, IC50: 25 nM |
99%+ | ||||||||||||||||
Regorafenib |
+++
VEGFR1, IC50: 13 nM |
+++
VEGFR2, IC50: 4.2 nM |
+
VEGFR3, IC50: 46 nM |
RET | 98% | ||||||||||||||
Pazopanib |
+++
VEGFR1, IC50: 10 nM |
++
VEGFR2, IC50: 30 nM |
+
VEGFR3, IC50: 47 nM |
FGFR,PDGFR,c-Kit | 99% | ||||||||||||||
Sitravatinib |
+++
VEGFR1 (FLT1), IC50: 6 nM |
+++
VEGFR2 (KDR), IC50: 5 nM |
++++
VEGFR3 (FLT4), IC50: 2 nM |
99%+ | |||||||||||||||
Foretinib |
+++
VEGFR1/FLT1, IC50: 6.8 nM |
++++
KDR, IC50: 0.86 nM |
++++
VEGFR3/FLT4, IC50: 2.8 nM |
Tie-2 | 99%+ | ||||||||||||||
MGCD-265 analog |
++++
VEGFR1, IC50: 3 nM |
++++
VEGFR2, IC50: 3 nM |
++++
VEGFR3, IC50: 4 nM |
Tie-2 | 99%+ | ||||||||||||||
Lactate |
+++
VEGFR1/FLT1, IC50: 10 nM |
+++
VEGFR2/Flk1, IC50: 13 nM |
+++
VEGFR3/FLT4, IC50: 8 nM |
FLT3,c-Kit | 85% | ||||||||||||||
AEE788 |
+
FLT1, IC50: 59 nM |
+
KDR, IC50: 77 nM |
EGFR | 98+% | |||||||||||||||
Linifanib |
++++
VEGFR1/FLT1, IC50: 3 nM |
++++
VEGFR2/KDR, IC50: 4 nM |
+
VEGFR3/FLT4, IC50: 190 nM |
FLT3 | 99%+ | ||||||||||||||
Vatalanib 2HCl |
+
VEGFR1/FLT1, IC50: 77 nM |
++
VEGFR2/KDR, IC50: 37 nM VEGFR2/Flk1, IC50: 270 nM |
+
VEGFR3/FLT4, IC50: 660 nM |
c-Kit,c-Fms | 99%+ | ||||||||||||||
Axitinib |
++++
VEGFR1/FLT1, IC50: 0.1 nM |
++++
VEGFR2/KDR, IC50: 0.2 nM VEGFR2/Flk1, IC50: 0.18 nM |
98% | ||||||||||||||||
Dovitinib |
+++
VEGFR1/FLT1, IC50: 10 nM |
+++
VEGFR2/Flk1, IC50: 13 nM |
+++
VEGFR3/FLT4, IC50: 8 nM |
FLT3,c-Kit | 99%+ | ||||||||||||||
ZM 306416 |
+
VEGFR1, IC50: 0.33 μM |
Src | 99%+ | ||||||||||||||||
KRN-633 |
+
VEGFR1, IC50: 170 nM |
+
VEGFR2, IC50: 160 nM |
+
VEGFR3, IC50: 125 nM |
c-Kit,BTK | 98% | ||||||||||||||
OSI-930 |
+++
FLT1, IC50: 8 nM |
+++
KDR, IC50: 9 nM |
99%+ | ||||||||||||||||
Lenvatinib |
++
VEGFR1/FLT1, IC50: 22 nM |
++++
VEGFR2/KDR, IC50: 4.0 nM |
+++
VEGFR3/FLT4, IC50: 5.2 nM |
98% | |||||||||||||||
NVP-BAW2881 |
+
hVEGFR1, IC50: 820 nM |
+++
mVEGF2, IC50: 165 nM hVEGFR2, IC50: 9 nM |
+
hVEGFR3, IC50: 420 nM |
98% | |||||||||||||||
Cediranib |
+++
VEGFR1/FLT1, IC50: 5 nM |
++++
VEGFR2/KDR, IC50: 0.5 nM |
c-Kit | 99%+ | |||||||||||||||
Nintedanib |
++
VEGFR1, IC50: 34 nM |
+++
VEGFR2, IC50: 13 nM |
+++
VEGFR3, IC50: 13 nM |
FLT3 | 99+% | ||||||||||||||
BMS-794833 |
++
VEGFR2, IC50: 15 nM |
99%+ | |||||||||||||||||
SKLB1002 |
++
VEGFR2, IC50: 32 nM |
98% | |||||||||||||||||
Cabozantinib S-malate |
++++
VEGFR2/KDR, IC50: 0.035 nM |
99+% | |||||||||||||||||
Ki8751 |
++++
VEGFR2, IC50: 0.9 nM |
c-Kit | 98+% | ||||||||||||||||
SU 5402 |
++
VEGFR2, IC50: 20 nM |
98% | |||||||||||||||||
Rivoceranib Mesylate |
++++
VEGFR2, IC50: 1 nM |
RET | 98+% | ||||||||||||||||
Ponatinib |
++++
VEGFR2, IC50: 1.5 nM |
98% | |||||||||||||||||
LY2874455 |
+++
VEGFR2, IC50: 7 nM |
99%+ | |||||||||||||||||
ZM323881 HCl |
++++
VEGFR2, IC50: <2 nM |
98% | |||||||||||||||||
AZD2932 |
+++
VEGFR-2, IC50: 8 nM |
c-Kit | 98% | ||||||||||||||||
Cabozantinib |
++++
VEGFR2/KDR, IC50: 0.035 nM |
98% | |||||||||||||||||
Sorafenib |
++
VEGFR2, IC50: 90 nM VEGFR2/Flk1, IC50: 90 nM |
99% | |||||||||||||||||
CYC-116 |
++
VEGFR2, Ki: 44 nM |
FLT3 | 99%+ | ||||||||||||||||
Golvatinib |
++
VEGFR2, IC50: 16 nM |
99%+ | |||||||||||||||||
Sunitinib |
+
VEGFR2 , IC50: 80 nM |
FLT3 | 98% | ||||||||||||||||
RAF265 |
++
VEGFR2, EC50: 30 nM |
99%+ | |||||||||||||||||
PD173074 | 99%+ | ||||||||||||||||||
BFH772 |
++++
VEGFR2, IC50: 3 nM |
98% | |||||||||||||||||
Semaxinib |
+
VEGFR2/Flk1, IC50: 1.23 μM |
98% | |||||||||||||||||
Vandetanib |
++
VEGFR2, IC50: 40 nM |
+
VEGFR3, IC50: 110 nM |
EGFR | 98% | |||||||||||||||
SAR131675 |
++
VEGFR3, IC50: 23 nM |
99%+ | |||||||||||||||||
ENMD-2076 |
+
VEGFR2/KDR, IC50: 58.2 nM |
++
VEGFR3/FLT4, IC50: 15.9 nM |
FLT3,RET | 98% | |||||||||||||||
Telatinib |
+++
VEGFR2, IC50: 6 nM |
++++
VEGFR3, IC50: 4 nM |
c-Kit | 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。 |
靶点 |
|
描述 | The overexpression and activation of the Met receptor and its ligand HGF (hepatocyte growth factor) are associated with a wide variety of human malignancies. Meanwhile, it is found that VEGFRs can cooperate with Met to induce tumor invasion and vascularization. Foretinib is a multiple RTKs inhibitor with IC50 values of 0.4, 0.9/2.8 and 3nM for Met, VEGFR2/3 and Ron, less potent to Tie-2, Flt-3, PDGFRα, KIT, VEGFR1, PDGFRβ with IC50 values of 1.1nM, 3.6nM, 3.6nM, 6.7nM, 6.8nM and 9.6nM, with almost no inhibition of FGFR1 or EGFR (measured by in vitro kinase assay). Potent inhibition of p-Met by Foretinib with IC50 values of 23 and 21nM in PC-3 and B16F10 cells, as well as the suppression of p-ERK and p-VEGFR2 induced by VEGF with IC50 of 16nM in HUVECs can be observed, suggesting the cellular RTKs inhibition. Foretinib can block HGF-induced migration with IC50 value of 44nM, as well as inhibit the anchorage-independent tumor cell colony growth of B16F10 cells with IC50 of 40nM. A further study on Inhibition of endothelial tubule formation and migration by Foretinib showed that Foretinib at concentration of 5nM or higher can both inhibit VEGF-induced tubule formation and block VEGF- or HGF-stimulated migration of HMVEC-L cells. Once daily oral administration of Foretinib at dose of 30 and 100mg/kg reduced lung surface tumor burden by 50% and 58%, respectively, in mice intravenously implanted B16F10 cells. Similarly, Foretinib at dose of 30 and 100mg/kg resulted in tumor growth inhibition of 64% and 87%, respectively, in mice bearing B16F10 solid tumors[1]. |
作用机制 | Foretinib is an ATP-competitive inhibitor of HGFR and VEGFR.[1] |
细胞系 | 浓度 | 检测类型 | 检测时间 | 活动说明 | 数据源 |
A172 | 100/300/900 nM | Function Assay | 1 h | inhibits the phosphorylation of MerTK | 24658326 |
A172 | 100/300/900 nM | Function Assay | 1 h | inhibits the activity of Axl, Tyro3 | 24658326 |
A172 | 100/300/900 nM | Function Assay | 1 h | decreases Akt phosphorylation in a concentration dependent manner | 24658326 |
A172 | 100/300/900 nM | Growth Inhibition Assay | 48 h | reduces cell survival at 900 nM significantly | 24658326 |
NCT号 | 适应症或疾病 | 临床期 | 招募状态 | 预计完成时间 | 地点 |
NCT01068587 | Lung Cancer | Phase 1 Phase 2 | Completed | - | Canada, British Columbia ... 展开 >> BCCA - Vancouver Cancer Centre Vancouver, British Columbia, Canada, V5Z 4E6 Canada, Ontario Juravinski Cancer Centre at Hamilton Health Sciences Hamilton, Ontario, Canada, L8V 5C2 Ottawa Health Research Institute - General Division Ottawa, Ontario, Canada, K1H 8L6 Univ. Health Network-Princess Margaret Hospital Toronto, Ontario, Canada, M5G 2M9 收起 << |
NCT00725712 | Neoplasms, Gastrointestinal Tr... 展开 >>act 收起 << | Phase 2 | Completed | - | United States, Alabama ... 展开 >> GSK Investigational Site Birmingham, Alabama, United States, 35294 United States, Arizona GSK Investigational Site Scottsdale, Arizona, United States, 85258 United States, California GSK Investigational Site Los Angeles, California, United States, 90024 GSK Investigational Site Stanford, California, United States, 94305 United States, District of Columbia GSK Investigational Site Washington, D.C., District of Columbia, United States, 20007 United States, Georgia GSK Investigational Site Atlanta, Georgia, United States, 30309 United States, Illinois GSK Investigational Site Chicago, Illinois, United States, 60637 United States, Massachusetts GSK Investigational Site Boston, Massachusetts, United States, 02114 United States, Michigan GSK Investigational Site Detroit, Michigan, United States, 48201 United States, Montana GSK Investigational Site Billings, Montana, United States, 59101 United States, New Mexico GSK Investigational Site Albuquerque, New Mexico, United States, 87131 United States, New York GSK Investigational Site New York, New York, United States, 10016 GSK Investigational Site New York, New York, United States, 10021 United States, North Carolina GSK Investigational Site Durham, North Carolina, United States, 27710 United States, Oregon GSK Investigational Site Portland, Oregon, United States, 97239 United States, Texas GSK Investigational Site Austin, Texas, United States, 78705 United States, Wisconsin GSK Investigational Site Madison, Wisconsin, United States, 53792 收起 << |
NCT00725712 | - | Completed | - | - | |
计算器 | ||||
存储液制备 | 1mg | 5mg | 10mg | |
1 mM 5 mM 10 mM |
1.58mL 0.32mL 0.16mL |
7.90mL 1.58mL 0.79mL |
15.81mL 3.16mL 1.58mL |
CAS号 | 849217-64-7 |
分子式 | C34H34F2N4O6 |
分子量 | 632.654 |
别名 | XL880;GSK1363089;EXEL-2880;GSK089 |
运输 | 蓝冰 |
存储条件 |
液体 -20°C:3-6个月-80°C:12个月 粉末 Sealed in dry,Store in freezer, under -20°C |
溶解度 |
DMSO: 80 mg/mL(126.45 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 |
动物实验配方 |
30% propylene glycol+5% Tween 80+65% water 30 mg/mL suspension |