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Benzenebutyric acid (4-Phenylbutyric acid)

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产品名称: Benzenebutyric acid (4-Phenylbutyric acid)
产品型号: GOY-Y3472
产品展商: 谷研
产品文档: 无相关文档
发布时间:2023-05-08

简单介绍

Benzenebutyric acid (4-Phenylbutyric acid)DMSO : ≥ 125 mg/mL (761.27 mM);H2O : 2 mg/mL (12.18 mM)


Benzenebutyric acid (4-Phenylbutyric acid)  的详细介绍

性能参数

产品名称

Benzenebutyric acid (4-Phenylbutyric acid)

规格

10mM*1mLinDMSO5g

货号

GOY-Y3472

 含量

>98.00%

CAS

1821-12-1

别名

N/A

 

 

化学名

N/A

分子式

C10H12O2

分子量

分子量 164.2

溶解度

DMSO : ≥ 125 mg/mL (761.27 mM);H2O : 2 mg/mL (12.18 mM)

储存条件

Store at RT

General tips

 

用途

仅供科研

价格

电询

详细内容

Benzenebutyric acid is an inhibitor of HDAC and endoplasmic reticulum (ER) stress, used in cancer and infection research.

Benzenebutyric acid is an inhibitor of HDAC, inhibits the growth of NSCLC Cell Lines at 2 mM. Benzenebutyric acid in combination with ciglitizone results in enhanced growth arrest of cancer cells[1]. Benzenebutyric acid (0-5 mM) inhibits ASFV infection in a dose-dependent manner. Benzenebutyric acid also inhibits the ASFV late protein synthesis and disrupts the virus-induced H3K9/K14 hypoacetylation status. Benzenebutyric acid and enrofloxacin act synergistically to abolish ASFV replication[2]. Addition of bafilomycin A1 results in accumulation of LC3II, whereas Benzenebutyric acid (4-PBA) substantially reduces this accumulation. LPS decreases the level of p62, whereas Benzenebutyric acid reverses this decrease upon LPS stimulation for 48 h. The percentage of cells with LPS-induced AVOs is increased at 48 h, whereas Benzenebutyric acid significantly reduces this percentage. Specifically, the percentage of cells with AVOs decreases from 61.6% to 53.1% upon Benzenebutyric acid treatment, supporting that Benzenebutyric acid inhibits LPS-induced autophagy. As a positive control for autophagy inhibition, bafilomycin A1 is used. The percentage of cells with LPS-induced AVOs is reduced by bafilomycin A1 treatment. The decreased OC area and fusion index observed after Benzenebutyric acid treatment are not observed with knockdown of ATG7. Inhibition of NF-κB using BAY 11-7082 and JSH23 reduce the LC3 II level upon LPS stimulation and completely abolish the inhibitory effect of Benzenebutyric acid on LPS-induced effects[3].

 

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