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417716-92-8 分子结构
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4-{3-chloro-4-[(cyclopropylcarbamoyl)amino]phenoxy}-7-methoxyquinoline-6-carboxamide

ChemBase编号:72847
分子式:C21H19ClN4O4
平均质量:426.85296
单一同位素质量:426.10948279
SMILES和InChIs

SMILES:
c1(c(cc2c(c1)c(ccn2)Oc1cc(c(cc1)NC(=O)NC1CC1)Cl)OC)C(=O)N
Canonical SMILES:
COc1cc2nccc(c2cc1C(=O)N)Oc1ccc(c(c1)Cl)NC(=O)NC1CC1
InChI:
InChI=1S/C21H19ClN4O4/c1-29-19-10-17-13(9-14(19)20(23)27)18(6-7-24-17)30-12-4-5-16(15(22)8-12)26-21(28)25-11-2-3-11/h4-11H,2-3H2,1H3,(H2,23,27)(H2,25,26,28)
InChIKey:
WOSKHXYHFSIKNG-UHFFFAOYSA-N

引用这个纪录

CBID:72847 http://www.chembase.cn/molecule-72847.html

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名称和登记号

名称和登记号

名称 登记号
IUPAC标准名
4-{3-chloro-4-[(cyclopropylcarbamoyl)amino]phenoxy}-7-methoxyquinoline-6-carboxamide
IUPAC传统名
lenvatinib
别名
E7080
CAS号
417716-92-8
PubChem SID
162037768
PubChem CID
9823820

数据来源

数据来源

所有数据来源 商品来源 非商品来源
数据来源 数据ID 价格
Selleck Chemicals
S1164 external link 加入购物车 请登录
数据来源 数据ID
PubChem 9823820 external link

理论计算性质

理论计算性质

JChem
Acid pKa 12.369414  质子受体
质子供体 LogD (pH = 5.5) 2.2813666 
LogD (pH = 7.4) 2.5174384  Log P 2.5216067 
摩尔折射率 112.2141 cm3 极化性 43.4982 Å3
极化表面积 115.57 Å2 可自由旋转的化学键
里宾斯基五规则 true 

分子性质

分子性质

安全信息 药理学性质 产品相关信息 生物活性(PubChem)
保存条件
-20°C expand 查看数据来源
作用靶点
VEGFR-PDGFR expand 查看数据来源
成盐信息
Free Base expand 查看数据来源

详细说明

详细说明

Selleck Chemicals Selleck Chemicals
Selleck Chemicals -  S1164 external link
Biological Activity
Description E7080 (Lenvatinib) is a multi-target inhibitor of VEGFR2 and VEGFR3 with IC50 of 4 nM and 5.2 nM, respectively.
Targets VEGFR2 VEGFR3 VEGFR1 FGFR1 PDGFRα PDGFRβ
IC50 4 nM 5.2 nM 22 nM [1] 46 nM [1] 51 nM [1] 39 nM [1]
In Vitro E7080, as a potent inhibitor of in vitro angiogenesis, shows a significantly inhibitory effect on VEGF/KDR and SCF/Kit signaling. According to the in vitro receptor tyrosine and serine/threonine kinase assays, E7080 inhibits Flt-1, KDR, Flt-4 with IC50 of 22, 4.0 and 5.2 nM, respectively. In addition to these kinases, E7080 also inhibits FGFR1 and PDGFR tyrosine kinases with IC50 value of 46, 51 and 100 nM for FGFR1, PDGFRα and PDGFRβ, respectively. [1] E7080 potently inhibits phosphorylation of VEGFR2 (IC50, 0.83 nM) and VEGFR3 (IC50, 0.36 nM) in HUVECs which is stimulated by VEGF and VEGF-C, respectively. [2] A recent study shows that E7080 treatment (both at 1 μM and 10 μM) results in a significant inhibition of cell migration and invasion by inhibiting FGFR and PDGFR signaling. [3]
In Vivo When orally administrated in a H146 xenograft model, E7080 inhibits the growth of H146 tumor at 30 and 100 mg/kg in a dose-dependent manner and leads to tumor regression at 100 mg/kg. Furthermore, E7080 at 100 mg/kg decreases microvessel density more than anti-VEGF antibody and imatinib treatment. [1] E7080 significantly inhibits local tumor growth in a MDA-MB-231 mammary fat pad (m.f.p.) model with RTVs (calculated tumor volume on day 8/tumor volume on day 1) of 0.81, and reduces both angiogenesis and lymphangiogenesis of established metastatic nodules of MDA-MB-231 tumor in the lymph nodes. [2]
Clinical Trials E7080 is currently in Phase I clinical trials in patients with Refractory Solid Tumors Lymphomas.
Features
Protocol
Cell Assay [2]
Cell Lines HUVECs
Concentrations 0-10 μM
Incubation Time 72 hours
Methods HUVECs (1,000 cells in each well in serum-free medium containing 2% fetal bovine serum) and L6 rat skeletal muscle myoblasts (5,000 cells in each well in serum-free DMEM) are dispensed in a 96-well plate and incubated overnight. E7080 and either VEGF (20 ng/mL) or FGF-2 (20 ng/mL) containing 2% fetal bovine serum and PDGFβ (40 ng/mL) are added to each well. Cells are incubated for 3 days and then the ratios of surviving cells are measured by WST-1 reagent. For proliferation assay, samples are duplicated and three separate experiments are done.
Animal Study [1]
Animal Models H146 tumor cells are implanted subcutaneously (s.c.) into the flank region of female BALB/c nude mice.
Formulation E7080 is dissolved in suspended in 0.5% methylcellulose.
Doses ≤100 mg/kg
Administration Administered via p.o.
References
[1] Matsui J, et al. Int J Cancer. 2008, 122(3), 664-671.
[2] Matsui J, et al. Clin Cancer Res. 2008, 14(17),5459-5465.
[3] Glen H, et al. BMC Cancer. 2011, 11, 309.

参考文献

参考文献

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专利

专利

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