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抑制剂/激活剂

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凋亡与自噬

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Gilteritinib ASP2215

Gilteritinib (ASP2215) 是一种有效的 ATP 竞争性的 FLT3/AXL 抑制剂，IC50 分别为 0.29 nM/0.73 nM。

货号：
TK0558
规格：

1mg

2mg

5mg

10mg
价格：
￥0.00

产品参数

CAS No.	1254053-43-4
生物活性	Gilteritinib (ASP2215) is a potent and ATP-competitive FLT3/AXL inhibitor with IC50s of 0.29 nM/0.73 nM, respectively.
分子式	C29H44N8O3
分子量	552.71
运输条件	Room temperature in continental US; may vary elsewhere.
储存条件	4°C, stored under nitrogen
溶解性数据	DMSO : 2 mg/mL (3.62 mM; Need ultrasonic)
体内研究	In MV4-11 xenografted-mice, the concentration of Gilteritinib (ASP2215) in tumors is more than 20-fold higher than that in plasma with oral administration of Gilteritinib at 10 mg/kg for 4 days. Treatment of Gilteritinib for 28 days results in dose-dependent inhibition of MV4-11 tumor growth and induces complete tumor regression at more than 6 mg/kg. Further, Gilteritinib decreases tumor burden in bone marrow and prolonged the survival of mice intravenously transplanted with MV4-11 cells.
体外研究	Of the 78 tyrosine kinases tested, Gilteritinib (ASP2215) inhibits FLT3, leukocyte tyrosine kinase (LTK), anaplastic lymphoma kinase (ALK), and AXL kinases by over 50% at 1 nM with an IC50 value of 0.29 nM for FLT3, approximately 800-fold more potent than for c-KIT. Gilteritinib inhibits the activity of eight of the 78 tested kinases by over 50% at concentrations of either 1 nM (FLT3, LTK, ALK, and AXL) or 5 nM (TRKA, ROS, RET, and MER). The IC50s are 0.29 nM for FLT3 and 0.73 nM for AXL. Gilteritinib inhibits FLT3 at an IC50 that is approximately 800-fold more potent than the concentration required to inhibit c-KIT (230 nM). The antiproliferative activity of Gilteritinib is evaluated against MV4-11 and MOLM-13 cells, which endogenously express FLT3-ITD. After 5 days of treatment, Gilteritinib inhibits the growth of MV4-11 and MOLM-13 cells with mean IC50s of 0.92 nM (95% CI: 0.23-3.6 nM) and 2.9 nM (95% CI: 1.4-5.8 nM), respectively. Growth suppression of MV4-11 cells is accompanied by inhibition of FLT3 phosphorylation. Relative to vehicle control cells, phosphorylated FLT3 levels are 57%, 8%, and 1% after 2 h of treatment with 0.1 nM, 1 nM, and 10 nM Gilteritinib, respectively. In addition, doses as low as 0.1 nM or 1 nM result in the suppression of phosphorylated ERK, STAT5, and AKT, all of which are downstream targets of FLT3 activation. To investigate the effects of Gilteritinib on AXL inhibition, MV4-11 cells that expressed exogenous AXL are treated with Gilteritinib. At concentrations of 1 nM, 10 nM, and 100 nM for 4 h, Gilteritinib treatment decreases phosphorylated AXL levels by 38%, 29%, and 22%, respectively.
文献	•Science. 2017 Dec 1;358(6367):eaan4368. •Blood Cancer J. 2022 Jan 11;12(1):5. •Haematologica. 2018 Nov;103(11):1862-1872. •Cancers. 2020 Aug 19;12(9):2341. •Cancers. 2020 Jun 14;12(6):1574. •Mol Cancer Res. 2021 Oct 11. •Front Pharmacol. 2021 Mar 8;12:644342. •Cancer Cell Int. 2020 Jun 17;20:250. •Sci Rep. 2021 Mar 11;11(1):5715. •J Oncol. 21 Sep 2021. •Department of Pharmacology & Toxicology. 2020 Jul.
纯度及产品资料	98%

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