金精三羧酸

生物活性靶点体外研究金精三羧酸试剂级价格

金精三羧酸

CAS号:4431-00-9
英文名:AURINTRICARBOXYLIC ACID
中文名:金精三羧酸
CBNumber:CB7463004
分子式:C22H14O9
分子量:422.34
MOL File:4431-00-9.mol

金精三羧酸化学性质

熔点 :300 °C(lit.)
沸点 :458.99°C (rough estimate)
密度 :1.3860 (rough estimate)
折射率 :1.6230 (estimate)
储存条件 :+15C to +30C
溶解度 :1 M NH₄OH: 10 mg/mL
形态 :powder
酸度系数(pKa) :2.20±0.20(Predicted)
颜色 :dark red to brown
水溶解性 :Insoluble in water.
BRN :2228904
CAS 数据库 :4431-00-9(CAS DataBase Reference)
EPA化学物质信息 :Benzoic acid, 5-[(3-carboxy-4-hydroxyphenyl)(3-carboxy-4-oxo-2,5-cyclohexadien-1-ylidene)methyl]-2-hydroxy- (4431-00-9)

安全信息

危险品标志 :Xi
危险类别码 :36/37/38
安全说明 :26-36
WGK Germany :3
RTECS号 :GU4790000
TSCA :Yes

金精三羧酸性质、用途与生产工艺

生物活性 Aurintricarboxylic acid 是高效的，αβ- 亚甲基 -ATP 敏感选择性 P2X1Rs 和 P2X3Rs 变构拮抗剂，对 rP2X1R 和 rP2X3R 作用的 IC50 值分别为 8.6 nM 和 72.9 nM。Aurintricarboxylic acid 是一种有效的抗流感剂，通过直接抑制神经氨酸酶 (neuraminidase) 作用。Aurintricarboxylic acid 也是拓扑异构酶 II 和凋亡抑制剂。Aurintricarboxylic acid 是选择性的 TWEAK-Fn14 信号通路抑制剂。Aurintricarboxylic acid 也是一种胱硫醚-γ-裂解酶 (CSE) 抑制剂，其 IC50 值为 0.6 μM。Aurintricarboxylic acid 是能够调节 miRNA 功能的 miRNA 调节剂。

靶点

Topoisomerase II

rP2X1R

8.6 nM (IC ₅₀ )

rP2X3R

72.9 nM (IC ₅₀ )

Apoptosis

miRNA

0.47 μM (IC ₅₀ )

体外研究

Aurintricarboxylic acid strongly inhibits rP2X1Rs and rP2X3Rs with IC ₅₀ values of 8.6 nM and 72.9 nM, respectively, and more weakly inhibits P2X2/3Rs, P2X2Rs, P2X4Rs or P2X7Rs.
Aurintricarboxylic acid inhibition of ATP-induced currents is concentration dependent.
Aurintricarboxylic acid is a non-competitive antagonist of P2X3R.
Aurintricarboxylic acid can inhibit the severe acute respiratory syndrome-associated coronavirus (SARS-CoV) and vaccinia virus.
Aurintricarboxylic acid protects MDCK cells from infection with influenza A strains PR8, NY or N.
Aurintricarboxylic acid inhibits replication of influenza A and B viruses.
Aurintricarboxylic acid inhibits neuraminidase activities of influenza A and B viruses.
Aurintricarboxylic acid inhibits TWEAK-Fn14-mediated NF-κB activation.
Aurintricarboxylic acid (10 μM;0.5-2 hours) suppresses TWEAK-Fn14-mediated NF-κB, Akt, and Src phosphorylation in GBM cells.
Aurintricarboxylic acid blocks TWEAK-stimulated Rac1 activation and TRAF2 recruitment to Fn14 cytoplasmic domain in glioma cells.
Aurintricarboxylic acid represses TWEAK-stimulated glioma cell migration and invasion without causing cell cytotoxicity.
Aurintricarboxylic acid (Compound 8) cannot regulate loading of endogenous let-7 onto AGO2 inside cultured cells, whereas can inhibit RISC loading of exogenous siRNA.

Western Blot Analysis

Cell Line:	T98G, A172, GBM44 glioma cells
Concentration:	10 μM
Incubation Time:	0.5 hour, 1 hour, 2 hours
Result:	Abrogated TWEAK activation of downstream signals including phosphorylation of the NF-κB family member p65, Akt, and Src in all three GBM cell lines.