SML0273
VAS2870
≥97% (HPLC)
别名:
1，3-苯并恶唑-2-基-3-苄基-3H- [1，2，3]三唑并[4，5-d]嘧啶-7-基硫醚, 7-（1，3-苯并恶唑-2-基硫烷基）-3-苄基-3H- [1，2，3]三唑并[4，5-d]嘧啶, 7-（2-苯并恶唑基硫）-3-（苯基甲基）-3H-1,2,3-三唑并[4,5-d]嘧啶, VAS 2870, VAS-2870
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所有图片(1)
About This Item
经验公式（希尔记法）:
C18H12N6OS
CAS号:
分子量:
360.39
MDL编号:
UNSPSC代码:
12352200
PubChem化学物质编号:
NACRES:
NA.77
质量水平
检测方案
≥97% (HPLC)
形式
powder
颜色
white to beige
溶解性
DMSO: ≥5 mg/mL
储存温度
room temp
SMILES字符串
C(c1ccccc1)n2nnc3c(Sc4nc5ccccc5o4)ncnc23
InChI
1S/C18H12N6OS/c1-2-6-12(7-3-1)10-24-16-15(22-23-24)17(20-11-19-16)26-18-21-13-8-4-5-9-14(13)25-18/h1-9,11H,10H2
InChI key
HZSOKHVVANONPV-UHFFFAOYSA-N
应用
使用 VAS2870 作为烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶（NOX）的抑制剂：
- 研究 NOX 衍生的活性氧簇在斑马鱼表皮生长过程中细胞骨架组织、上皮细胞钙粘蛋白的正确定位和细胞运动中的重要性
- 研究 Nox2 和 Nox4 在高脂饮食（HFD）喂养小鼠的脂多糖（LPS）诱导肠道损伤中的作用
- 降低单核细胞活性氧水平并研究其对抑制训练型先天免疫诱导的影响
生化/生理作用
VAS2870 是一种细胞渗透性特异性 NADPH 氧化酶（NOX）抑制剂，可有效抑制血管平滑肌细胞（VSMC）中生长因子介导的 ROS 释放。
除了能抑制 NOX4 之外，VAS2870 还可抑制多种类型细胞中活性氧簇（ROS）的产生。它可有效地抑制肝癌细胞的生长，增加转化生长因子β（TGF β）诱导的细胞凋亡。因此，通过 VAS2870 抑制 NOX 酶可能成为一种潜在的肝癌治疗方案。
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
Yahya Sohrabi et al.
Frontiers in immunology, 9, 3155-3155 (2019-02-07)
Introduction: Cells of the innate immune system particularly monocytes and macrophages have been recognized as pivotal players both during the initial insult as well as the chronic phase of atherosclerosis. It has recently been shown that oxidized low-density lipoprotein (oxLDL)
Qi-An Sun et al.
Free radical biology & medicine, 52(9), 1897-1902 (2012-03-13)
Specific inhibitors of the production of reactive oxygen species (ROS) by the NADPH oxidases (Nox's) are potentially important therapeutic agents in the wide range of human diseases that are characterized by excessive ROS production. It has been proposed that VAS2870
Patricia Sancho et al.
Biochemical pharmacology, 81(7), 917-924 (2011-02-01)
Liver tumor cells show several molecular alterations which favor pro-survival signaling. Among those, we have proposed the NADPH oxidase NOX1 as a prosurvival signal for liver tumor cells. On the one side, we have described that FaO rat hepatoma cells
Austin T Robinson et al.
American journal of physiology. Heart and circulatory physiology, 312(5), H896-H906 (2017-02-27)
High blood pressure has been shown to elicit impaired dilation in the vasculature. The purpose of this investigation was to elucidate the mechanisms through which high pressure may elicit vascular dysfunction and determine the mechanisms through which regular aerobic exercise
I-Jung Tsai et al.
International journal of molecular sciences, 20(18) (2019-09-13)
Patients with a relapse of idiopathic nephrotic syndrome have significantly increased levels of serum complement component 5a (C5a), and proteinuria has been noted in mice treated with C5a via changes in permeability of kidney endothelial cells (KECs) in established animal
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