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A8486

Sigma-Aldrich

N-（对甲酰基肉桂酰）邻氨基苯甲酸

≥98% (HPLC)

别名:

2-[[1-氧代-3-（4-戊基苯基）-2-丁-1-基]氨基]-苯甲酸, ACA, N-（4-戊基肉桂酰胺）邻氨基苯甲酸

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About This Item

经验公式（希尔记法）:
C21H23NO3
CAS号:
99196-74-4
分子量:
337.41
MDL號碼:
MFCD00211365
分類程式碼代碼:
12352106
PubChem物質ID:
329770958
NACRES:
NA.77

化驗

≥98% (HPLC)

形狀

powder

顏色

white to off-white

溶解度

DMSO: ≥20 mg/mL

儲存溫度

room temp

SMILES 字串

CCCCCc1ccc(\C=C\C(=O)Nc2ccccc2C(O)=O)cc1

InChI

1S/C21H23NO3/c1-2-3-4-7-16-10-12-17(13-11-16)14-15-20(23)22-19-9-6-5-8-18(19)21(24)25/h5-6,8-15H,2-4,7H2,1H3,(H,22,23)(H,24,25)/b15-14+

InChI 密鑰

GAMRBCZMOOMBSQ-CCEZHUSRSA-N

一般說明

氨基苯甲酸 (ACA) 是一种广谱磷脂酶 A2 抑制剂，可阻断瞬时受体电位 (TRP) 通道。抑制心室肌细胞中钙激活的氯化物电流。ACA 调节多种离子通道。

應用

N -（ p -戊基肉桂酰）邻氨基苯甲酸已被用作瞬时受体电位阳离子通道亚家族 M 成员 2 (TRPM2) 抑制剂，研究其在调节活性氧 (ROS) 产生中的作用。
N-（p-氨酰肉桂酰）邻氨基苯甲酸是一种广谱 PLA2 抑制剂和 TRP 通道阻滞剂。N-（p-戊酰肉桂酰）邻氨基苯甲酸已被用于研究多巴胺能 SNc 神经元中 TRPM2 通道的功能表达。

生化／生理作用

广谱磷脂酶 A2 (PLA2) 抑制剂和 TRP 通道阻断剂。

特點和優勢

该化合物在受体分类和信号转导手册的磷脂酶A2 页面上有重点介绍。想要浏览手册的其他页面， 请单击此处。

象形圖

Environment
GHS09

訊號詞

Warning

危險聲明

H410

防範說明

P273 - P391 - P501

危險分類

Aquatic Acute 1 - Aquatic Chronic 1

儲存類別代碼

11 - Combustible Solids

水污染物質分類（WGK）

WGK 3

閃點（°F）

Not applicable

閃點（°C）

Not applicable

分析证书(COA)

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N-(p-amylcinnamoyl) anthranilic acid (ACA): a phospholipase A2 inhibitor and TRP channel blocker
Harteneck C, et al.
Cardiovascular Drug Reviews, 25(1), 61-75 (2007)
Bo Pang et al.
Pflugers Archiv : European journal of physiology, 463(2), 309-318 (2011-10-25)
Sustained increase in [Ca(2+)](c) (Δ[Ca(2+)](c)) is a critical early signal from T-cell receptor (TCR/CD3). In general, Ca(2+)-release activated Ca(2+) channels (CRAC) are responsible for the Ca(2+) influx and Δ[Ca(2+)](c) after TCR/CD3 stimulation. However, T cells also express Ca(2+)-permeable nonselective cation
Arif Demirdaş et al.
Cellular and molecular neurobiology, 37(1), 133-144 (2016-03-05)
Calcium ions (Ca
A dual role of transient receptor potential melastatin 2 channel in cytotoxicity induced by silica nanoparticles
Yu P, et al.
Scientific Reports, 5, 18171-18171 (2015)
Mathias Gelderblom et al.
Stroke, 45(11), 3395-3402 (2014-09-23)
Brain injury during stroke results in oxidative stress and the release of factors that include extracellular Ca(2+), hydrogen peroxide, adenosine diphosphate ribose, and nicotinic acid adenine dinucleotide phosphate. These alterations of the extracellular milieu change the activity of transient receptor
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