货号:A425350
同义名:
吉瑞替尼
/ ASP2215
Gilteritinib (ASP2215) 是一种强效和 ATP 竞争性的 FLT3/AXL 抑制剂,IC50 值分别为 0.29 nM 和 0.73 nM。
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产品名称 | FLT3 ↓ ↑ | 其他靶点 | 纯度 | ||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
R406 | ✔ | Syk | 99%+ | ||||||||||||||||
Go6976 | ✔ | 99%+ | |||||||||||||||||
Quizartinib |
+++
FLT3 (ITD), IC50: 1.1 nM FLT3 (WT), IC50: 4.2 nM |
99%+ | |||||||||||||||||
Gilteritinib |
++++
FLT3, IC50: 0.29 nM |
99%+ | |||||||||||||||||
Amuvatinib |
+
FLT3 (D835Y), IC50: 81 nM |
99%+ | |||||||||||||||||
Pacritinib |
++
FLT3 (D835Y), IC50: 6 nM FLT3, IC50: 22 nM |
97% | |||||||||||||||||
Dovitinib |
++++
FLT3, IC50: 1 nM |
c-Kit | 99%+ | ||||||||||||||||
Denfivontinib |
++++
FLT3 (D835Y), IC50: 0.4 nM FLT3, IC50: 0.4 nM |
RET | 99%+ | ||||||||||||||||
TAK-659 HCl |
++
FLT3, IC50: 4.6 nM |
Syk | 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 | Gilteritinib (ASP2215) effectively inhibits FLT3, leukocyte tyrosine kinase (LTK), anaplastic lymphoma kinase (ALK), and AXL kinases in 78 tested tyrosine kinases, achieving over 50% inhibition at 1 nM. Its IC50 for FLT3 is exceptionally low at 0.29 nM, making it roughly 800 times more potent against FLT3 than c-KIT[1]. Gilteritinib inhibits the activity of 8 of the 78 tested kinases by >50% at concentrations of 1 nM (Flt3, LTK, ALK, and Ax1) or 5 nM (TrkA, ROS, RET, and Mer). Its IC50s are 0.29 nM and 0.73 nM, respectively. Gilteritinib inhibits Flt3 with an IC50 approximately 800-fold higher than the concentration required to inhibit c-kit (230 NM). The antiproliferative activity of Gilteritinib is evaluated by MV4-11 and MOLM-13 cells endogenously expressing Flt3-ITD. After 5 days of treatment, the IC50 of gitlitinib for MV4-11 and MOLM-13 cells is 0.92 nM (95%CI: 0.23-3.6 nM) and 2.9 nM (95%CI: 1.4-5.8 nM), respectively. Growth inhibition of MV4-11 cells is accompanied by inhibition of Flt3 phosphorylation. The phosphorylation levels of Flt3 were 57%, 8%, and 1% after 2 h of Gilteritinib at 0.1 nM, 1 nM, and 10 nM compared to vehicle controls, respectively. In addition, doses as low as 0.1 nM or 1 nM inhibit phosphorylated ERK, STAT5, and AKT, all of which are downstream targets for Flt3 activation. To investigate the effect of Gilteritinib on Ax1 inhibition, MV4-11 cells expressing exogenous Ax1 are treated with Gilteritinib. Gilteritinib treatment reduces phosphorylated Axl levels by 38%, 29%, and 22%, respectively, at 4 h at concentrations of 1 nM, 10 nM, and 100 nM[2]. |
体内研究 | In mice with MV4-11 xenografts, oral Gilteritinib (ASP2215) administration at 10 mg/kg for 4 days results in tumor concentrations more than 20 times higher than in plasma. A 28-day treatment with Gilteritinib shows a dose-dependent reduction in MV4-11 tumor growth, achieving complete tumor regression at doses above 6 mg/kg. Additionally, Gilteritinib reduces the tumor load in the bone marrow and extends the survival of mice that received intravenous transplants of MV4-11 cells[1]. |
体外研究 | Gilteritinib (ASP2215) effectively inhibits FLT3, leukocyte tyrosine kinase (LTK), anaplastic lymphoma kinase (ALK), and AXL kinases in 78 tested tyrosine kinases, achieving over 50% inhibition at 1 nM. Its IC50 for FLT3 is exceptionally low at 0.29 nM, making it roughly 800 times more potent against FLT3 than c-KIT[1]. Gilteritinib inhibits the activity of 8 of the 78 tested kinases by >50% at concentrations of 1 nM (Flt3, LTK, ALK, and Ax1) or 5 nM (TrkA, ROS, RET, and Mer). Its IC50s are 0.29 nM and 0.73 nM, respectively. Gilteritinib inhibits Flt3 with an IC50 approximately 800-fold higher than the concentration required to inhibit c-kit (230 NM). The antiproliferative activity of Gilteritinib is evaluated by MV4-11 and MOLM-13 cells endogenously expressing Flt3-ITD. After 5 days of treatment, the IC50 of gitlitinib for MV4-11 and MOLM-13 cells is 0.92 nM (95%CI: 0.23-3.6 nM) and 2.9 nM (95%CI: 1.4-5.8 nM), respectively. Growth inhibition of MV4-11 cells is accompanied by inhibition of Flt3 phosphorylation. The phosphorylation levels of Flt3 were 57%, 8%, and 1% after 2 h of Gilteritinib at 0.1 nM, 1 nM, and 10 nM compared to vehicle controls, respectively. In addition, doses as low as 0.1 nM or 1 nM inhibit phosphorylated ERK, STAT5, and AKT, all of which are downstream targets for Flt3 activation. To investigate the effect of Gilteritinib on Ax1 inhibition, MV4-11 cells expressing exogenous Ax1 are treated with Gilteritinib. Gilteritinib treatment reduces phosphorylated Axl levels by 38%, 29%, and 22%, respectively, at 4 h at concentrations of 1 nM, 10 nM, and 100 nM[2]. |
作用机制 | Gilteritinib binds to FLT3 at the ATP-binding site.[2] |
Dose | Nude Mice: 3 mg/kg[3] (p.o.), 30 mg/kg[3] (p.o.) | ||||||||||||
Administration | p.o. | ||||||||||||
Pharmacokinetics |
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计算器 | ||||
存储液制备 | ![]() |
1mg | 5mg | 10mg |
1 mM 5 mM 10 mM |
1.81mL 0.36mL 0.18mL |
9.05mL 1.81mL 0.90mL |
18.09mL 3.62mL 1.81mL |
CAS号 | 1254053-43-4 |
分子式 | C29H44N8O3 |
分子量 | 552.712 |
别名 | 吉瑞替尼 ;ASP2215 |
运输 | 蓝冰 |
存储条件 |
粉末 Keep in dark place,Sealed in dry,2-8°C 液体 -20°C:3-6个月-80°C:12个月 |
溶解度 |
DMSO: 2 mg/mL(3.62 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 无水乙醇: 100 mg/mL(180.93 mM),配合低频超声,并调节pH至2,注意:无水乙醇开封后,易挥发,也会吸收空气中的水分,导致溶解能力下降,请避免使用开封较久的乙醇 |
动物实验配方 |