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关于此项目
经验公式(希尔记法):
C31H33N5O4
化学文摘社编号:
分子量:
539.62
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
产品名称
尼达尼布, ≥98% (HPLC)
InChI
1S/C31H33N5O4/c1-34-15-17-36(18-16-34)20-27(37)35(2)24-12-10-23(11-13-24)32-29(21-7-5-4-6-8-21)28-25-14-9-22(31(39)40-3)19-26(25)33-30(28)38/h4-14,19,32H,15-18,20H2,1-3H3,(H,33,38)/b29-28-
InChI key
XZXHXSATPCNXJR-ZIADKAODSA-N
SMILES string
O=C(NC1=C2)/C(C1=CC=C2C(OC)=O)=C(C3=CC=CC=C3)\NC4=CC=C(C=C4)N(C(CN5CCN(CC5)C)=O)C
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 2 mg/mL, clear
storage temp.
2-8°C
Quality Level
Biochem/physiol Actions
口服活性,强效ATP竞争性VEGFR,FGFR,PDGFR,Flt3,Lck,Lyn,Src抑制剂,具有体内抗血管生成和抗纤维化功效。
尼达尼布(BIBF1120)是一种口服活性、强效ATP竞争性抑制剂,可抑制血管激酶VEGFR-1/2/3(IC50 = 34/21/13 nM)、FGFR-1/2/3/4(IC50 = 69/37/108/610 nM)、PDGFRα/β(IC50 = 59/65 nM)以及Flt-3、Lck、Lyn和Src(分别为IC50 = 26、16、195、156 nM),但不抑制33种其他激酶。尼达尼布在体内癌症和肺纤维化的培养物和动物模型中表现出抗血管生成和抗纤维化疗效。
signalword
Danger
Hazard Classifications
Acute Tox. 3 Oral - Eye Dam. 1 - Repr. 2 - Skin Irrit. 2 - STOT RE 1
存储类别
6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Nintedanib (BIBF-1120) inhibits hepatocellular carcinoma growth independent of angiokinase activity.
Wei-Tien Tai et al.
Journal of hepatology, 61(1), 89-97 (2014-03-25)
Nintedanib, a triple angiokinase inhibitor, is currently being evaluated against advanced HCC in phase I/II clinical trials. Here, we report the underlying molecular mechanism by which nintedanib (BIBF-1120) induces an anti-HCC effect. To further elucidate whether the effect of nintedanib
Xiaoping Cai et al.
Clinical and experimental pharmacology & physiology, 40(9), 662-670 (2013-07-04)
In the present study, we tested whether serum amyloid A (SAA) protein, an established biomarker of inflammation, also plays a role in stimulating neovascularization. To evaluate this possibility, human carotid artery endothelial (HCtAE) cells were cultured and cellular migration and
Frank Hilberg et al.
Cancer research, 68(12), 4774-4782 (2008-06-19)
Inhibition of tumor angiogenesis through blockade of the vascular endothelial growth factor (VEGF) signaling pathway is a novel treatment modality in oncology. Preclinical findings suggest that long-term clinical outcomes may improve with blockade of additional proangiogenic receptor tyrosine kinases: platelet-derived
Roman C Brands et al.
Oncology letters, 18(3), 2220-2231 (2019-08-28)
Multidrug resistance (MDR) remains one of the major causes of suboptimal outcome following therapy in head and neck squamous cell carcinoma (HNSCC). ATP-binding cassette (ABC) transporters are overexpressed in HNSCC, which contributes to the limited effect of chemotherapeutic treatment. In
Gerald J Roth et al.
Journal of medicinal chemistry, 52(14), 4466-4480 (2009-06-16)
Inhibition of tumor angiogenesis through blockade of the vascular endothelial growth factor (VEGF) signaling pathway is a new treatment modality in oncology. Preclinical findings suggest that blockade of additional pro-angiogenic kinases, such as fibroblast and platelet-derived growth factor receptors (FGFR
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