4-Phenylbutyric acid | 4-PBA;Benzenebutyric acid | 苯丁酸 | HDAC

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4-Phenylbutyric acid/4-苯基丁酸 {[allProObj[0].p_purity_real_show]}

货号：A148817 同义名： 苯丁酸 / 4-PBA; Benzenebutyric acid

4-Phenylbutyric acid是一种 HDAC 抑制剂，可调控基因转录，具有抗肿瘤和神经保护作用。

4-Phenylbutyric acid/4-苯基丁酸化学结构
CAS号：1821-12-1

4-Phenylbutyric acid/4-苯基丁酸 3D分子结构
CAS号：1821-12-1

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4-Phenylbutyric acid/4-苯基丁酸纯度/质量文件产品仅供科研

货号：A148817 标准纯度： {[allProObj[0].p_purity_real_show]} 产品说明书

批次查询：批次纯度: COA SDS NMR HPLC CNMR LC-MS

全球学术期刊中引用的产品: • Science, 2025, 387(6729): eadp5637. Ambeed. [ A875019 ]; • Nat. Electron., 2025, 8, 66-74. Ambeed. [ A100095 ]; • Adv. Mater., 2025, 2416621. Ambeed. [ A255324 , A420052 ]; • Adv. Mater., 2025, 2410493. Ambeed. [ A838608 ]; • Adv. Mater., 2025, 2420319. Ambeed. [ A106129 ]; 更多 >

组蛋白去乙酰化酶亚型比较

产品名称	HD1 ↓ ↑	HD2 ↓ ↑	HDAC ↓ ↑	HDAC1 ↓ ↑	HDAC10 ↓ ↑	HDAC11 ↓ ↑	HDAC2 ↓ ↑	HDAC3 ↓ ↑	HDAC4 ↓ ↑	HDAC5 ↓ ↑	HDAC6 ↓ ↑	HDAC7 ↓ ↑	HDAC8 ↓ ↑	HDAC9 ↓ ↑	其他靶点	纯度
Givinostat HCl monohydrate	++++ HD1-A, IC50: 16 nM HD1-B, IC50: 7.5 nM	+++ HD2, IC50: 10 nM														99%+
MC1568	++ HD1-B (Maize), IC50: 3.4 μM HD1-A (Maize), IC50: 100 nM															96%
Trichostatin A			++++ HDAC, IC50: ~1.8 nM													99%+
Scriptaid			✔													99%+
Valproic acid sodium			✔												Autophagy	97%
AR-42			+++ HDAC, IC50: 30 nM													99%+
Dacinostat			+++ HDAC, IC50: 32 nM													98+%
CUDC-101			++++ HDAC, IC50: 4.4 nM	++++ HDAC1, IC50: 4.5 nM	+++ HDAC10, IC50: 26.1 nM		+++ HDAC2, IC50: 12.6 nM	++++ HDAC3, IC50: 9.1 nM	+++ HDAC4, IC50: 13.2 nM	+++ HDAC5, IC50: 11.4 nM	++++ HDAC6, IC50: 5.1 nM	+ HDAC7, IC50: 373 nM	++ HDAC8, IC50: 79.8 nM	++ HDAC9, IC50: 67.2 nM	EGFR,HER2	99%+
M344			++ HDAC, IC50: 100 nM													99%+
Splitomicin			+ Sir2p, IC50: 60 μM													99%
Panobinostat			++++ HDAC (MOLT-4 cells), IC50: 5 nM HDAC (Reh cells), IC50: 20 nM													98%
Sodium 4-Phenylbutyrate			✔													98%
Vorinostat			+++ HDAC, IC50: ~10 nM													98%
Curcumin			✔												NF-κB,Nrf2	98%
Belinostat			+++ HDAC, IC50: 27 nM													98%
RG-2833				++ HDAC1, Ki: 32 nM				++ HDAC3, Ki: 5 nM								98%
Valproic acid				+ HDAC1, IC50: 0.4 mM												98%
BG45				+ HDAC1, IC50: 2 μM			+ HDAC2, IC50: 2.2 μM	+ HDAC3, IC50: 289 nM								99%+
Entinostat				+ HDAC1, IC50: 0.51 μM				+ HDAC3, IC50: 1.7 μM								98%
Resminostat				+++ HDAC1, IC50: 42.5 nM				++ HDAC3, IC50: 50.1 nM			++ HDAC6, IC50: 71.8 nM					98+%
Romidepsin				+++ HDAC1, IC50: 36 nM			+++ HDAC2, IC50: 47 nM									99%+
Parthenolide				✔											p53,NF-κB	97% HPLC
Tacedinaline				+ HDAC1, IC50: 0.9 μM			+ HDAC2, IC50: 0.9 μM	+ HDAC3, IC50: 1.2 μM								98%
Mocetinostat				++ HDAC1, IC50: 0.15 μM		+ HDAC11, IC50: 0.59 μM	+ HDAC2, IC50: 0.29 μM	+ HDAC3, IC50: 1.66 μM								98%
WT-161				++++ HDAC1, IC50: 8.35 nM			+++ HDAC2, IC50: 15.4 nM				++++ HDAC6, IC50: 0.4 nM					99%+
Fimepinostat				++++ HDAC1, IC50: 1.7 nM	++++ HDAC10, IC50: 2.8 nM	++++ HDAC11, IC50: 5.4 nM	++++ HDAC2, IC50: 5.0 nM	++++ HDAC3, IC50: 1.8 nM			+++ HDAC6, IC50: 27 nM					99%+
Tucidinostat				++ HDAC1, IC50: 95 nM	++ HDAC10, IC50: 78 nM		++ HDAC2, IC50: 160 nM	++ HDAC3, IC50: 67 nM								99%+
Santacruzamate A							++++ HDAC2, IC50: 119 pM									99%+
(E,E)-RGFP966								++ HDAC3, IC50: 80 nM								99%+
LMK-235									+++ HDAC4, IC50: 11.9 nM	++++ HDAC5, IC50: 4.2 nM						99%+
Tasquinimod									✔							99%+
CAY10603											++++ HDAC6, IC50: 2 pM					98%
Tubastatin A											+++ HDAC6, IC50: 15 nM					98%
Tubacin											++++ HDAC6, IC50: 4 nM					99%+
ACY-738											++++ HDAC6, IC50: 1.7 nM					99%+
Nexturastat A											++++ HDAC6, IC50: 5 nM					99%+
BRD73954											+++ HDAC6, IC50: 36 nM		++ HDAC8, IC50: 120 nM			99%
Tubastatin A HCl											+++ HDAC6, IC50: 15 nM		+ HDAC8, IC50: 854 nM			98%
PCI-34051													+++ HDAC8, IC50: 10 nM			99%+
Ricolinostat				++ HDAC1, IC50: 58 nM			++ HDAC2, IC50: 48 nM	++ HDAC3, IC50: 51 nM			++++ HDAC6, IC50: 4.7 nM		++ HDAC8, IC50: 100 nM			99%+
Droxinostat								+ HDAC3, IC50: 16.9 μM			+ HDAC6, IC50: 2.47 μM		+ HDAC8, IC50: 1.46 μM			99%+
Abexinostat				++++ HDAC1, Ki: 7 nM	+++ HDAC10, IC50: 24 nM		+++ HDAC2, Ki: 19 nM	++++ HDAC3/SMRT, Ki: 8.2 nM			+++ HDAC6, Ki: 17 nM		+ HDAC8, IC50: 280 nM			98%+
Citarinostat				+++ HDAC1, IC50: 35 nM			+++ HDAC2, IC50: 45 nM	+++ HDAC3, IC50: 46 nM			++++ HDAC6, IC50: 2.6 nM		++ HDAC8, IC50: 137 nM			99%+
HPOB				+ HDAC1, IC50: 2.9 μM	+ HDAC10, IC50: 3.0 μM		+ HDAC2, IC50: 4.4 μM	+ HDAC3, IC50: 1.7 μM			++ HDAC6, IC50: 56 nM		+ HDAC8, IC50: 2.8 μM			97%
Quisinostat 2HCl				++++ HDAC1, IC50: 0.11 nM	++++ HDAC10, IC50: 0.46 nM	++++ HDAC11, IC50: 0.37 nM	++++ HDAC2, IC50: 0.33 nM	++++ HDAC3, IC50: 4.86 nM	++++ HDAC4, IC50: 0.64 nM	++++ HDAC5, IC50: 3.69 nM			++++ HDAC8, IC50: 4.26 nM			97%
Domatinostat				+ HDAC1, IC50: 1.20 μM	+ HDAC10, IC50: 21 μM	+ HDAC11, IC50: 9.7 μM	+ HDAC2, IC50: 1.12 μM	+ HDAC3, IC50: 0.57 μM		+ HDAC5, IC50: 11.3 μM				+ HDAC9, IC50: 50 μM		99%+
TMP269									++ HDAC4, IC50: 157 nM	++ HDAC5, IC50: 97 nM		+++ HDAC7, IC50: 43 nM		+++ HDAC9, IC50: 23 nM		99%+
Pracinostat				++ HDAC1, IC50: 49 nM	+++ HDAC10, IC50: 40 nM	++ HDAC11, IC50: 93 nM	++ HDAC2, IC50: 96 nM	+++ HDAC3, IC50: 43 nM	++ HDAC4, IC50: 56 nM	+++ HDAC5, IC50: 47 nM	+ HDAC6, IC50: 1.008 μM	++ HDAC7, IC50: 137 nM	++ HDAC8, IC50: 140 nM	++ HDAC9, IC50: 70 nM		99%+
TMP195									++ HDAC4, Ki: 59 nM	++ HDAC5, Ki: 60 nM		+++ HDAC7, Ki: 26 nM		+++ HDAC9, Ki: 15 nM		99%+
1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多，抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用，但抑制强度暂时没有相关数据。

4-Phenylbutyric acid/4-苯基丁酸生物活性

描述

4-Phenylbutyric acid (4-PBA), known as an inhibitor of histone deacetylases (HDAC), effectively inhibits the growth of non-small cell lung cancer (NSCLC) cell lines at a concentration of 2 mM. When combined with ciglitizone, 4-Phenylbutyric acid further enhances the growth arrest of cancer cells^[1]. Additionally, 4-Phenylbutyric acid, at concentrations ranging from 0 to 5 mM, dose-dependently inhibits African swine fever virus (ASFV) infection. 4-Phenylbutyric acid also disrupts ASFV-induced hypoacetylation of histone H3 at lysines 9 and 14 and inhibits late protein synthesis by the virus. The synergistic effect of 4-Phenylbutyric acid with enrofloxacin significantly eliminates ASFV replication^[2]. The introduction of bafilomycin A1 leads to an increase in the accumulation of LC3II, a marker for autophagy, whereas 4-Phenylbutyric acid (4-PBA) substantially reduces this buildup. Lipopolysaccharide (LPS) lowers p62 levels, a process that is reversed by Benzenebutyric acid after 48 hours of LPS stimulation. Furthermore, while LPS increases the percentage of cells with acidotic vesicular organelles (AVOs) at 48 hours, 4-Phenylbutyric acid significantly lowers this percentage. Specifically, treatment with Benzenebutyric acid reduces the percentage of cells with AVOs from 61.6% to 53.1%, indicating that 4-Phenylbutyric acid inhibits LPS-induced autophagy^[3].

体内研究

In the context of bone health, LPS exposure results in substantial bone loss, decreases in bone mineral density (BMD), bone volume fraction (BV/TV), and trabecular thickness (Tb. Th), while increasing trabecular spacing (Tb. Sp.). Conversely, 4-Phenylbutyric acid treatment effectively attenuates these negative effects induced by LPS. It increases BMD, BV/TV, and Tb. Th, and reduces the enlargement of Tb. Sp. observed with LPS treatment alone. However, no significant changes are noted when mice are treated solely with Benzenebutyric acid. Additionally, the osteoclast surface per bone surface (OC.S/BS), assessed by tartrate-resistant acid phosphatase (TRAP) staining, is significantly reduced in LPS-treated mice when administered Benzenebutyric acid^[3].

体外研究

Additionally, 4-Phenylbutyric acid, at concentrations ranging from 0 to 5 mM, dose-dependently inhibits African swine fever virus (ASFV) infection. 4-Phenylbutyric acid also disrupts ASFV-induced hypoacetylation of histone H3 at lysines 9 and 14 and inhibits late protein synthesis by the virus. The synergistic effect of 4-Phenylbutyric acid with enrofloxacin significantly eliminates ASFV replication^[2].

The introduction of bafilomycin A1 leads to an increase in the accumulation of LC3II, a marker for autophagy, whereas 4-Phenylbutyric acid (4-PBA) substantially reduces this buildup. Lipopolysaccharide (LPS) lowers p62 levels, a process that is reversed by Benzenebutyric acid after 48 hours of LPS stimulation. Furthermore, while LPS increases the percentage of cells with acidotic vesicular organelles (AVOs) at 48 hours, 4-Phenylbutyric acid significantly lowers this percentage. Specifically, treatment with Benzenebutyric acid reduces the percentage of cells with AVOs from 61.6% to 53.1%, indicating that 4-Phenylbutyric acid inhibits LPS-induced autophagy^[3].

4-Phenylbutyric acid/4-苯基丁酸参考文献

[1]Chang TH, et al. Enhanced growth inhibition by combination differentiation therapy with ligands of peroxisome proliferator-activated receptor-gamma and inhibitors of histone deacetylase in adenocarcinoma of the lung. Clin Cancer Res. 2002 Apr;8(4):1206-12

[2]Frouco G, et, al. Sodium phenylbutyrate abrogates African swine fever virus replication by disrupting the virus-induced hypoacetylation status of histone H3K9/K14. Virus Res. 2017 Oct 15;242:24-29.

[3]Park HJ, et al. 4-Phenylbutyric acid protects against lipopolysaccharide-induced bone loss by modulating autophagy in osteoclasts. Biochem Pharmacol. 2018 May;151:9-17.

4-Phenylbutyric acid/4-苯基丁酸实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

6.09mL

1.22mL

0.61mL

30.45mL

6.09mL

3.05mL

60.90mL

12.18mL

6.09mL

4-Phenylbutyric acid/4-苯基丁酸技术信息

CAS号	1821-12-1
分子式	C₁₀H₁₂O₂
分子量	164.2
SMILES Code	O=C(O)CCCC1=CC=CC=C1
MDL No.	MFCD00004403

别名	苯丁酸 ;4-PBA; Benzenebutyric acid
运输	蓝冰
InChI Key	OBKXEAXTFZPCHS-UHFFFAOYSA-N
Pubchem ID	4775

存储条件

In solvent -20°C:3-6个月-80°C:12个月

Pure form Sealed in dry,2-8°C

溶解方案

细胞实验：

DMSO: 105 mg/mL(639.46 mM)，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO

H₂O: 2 mg/mL(12.18 mM)，配合低频超声助溶

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