Sodium Phenylbutyrate
(Synonyms: 苯丁酸钠; 4-PBA sodium; 4-Phenylbutyric acid sodium; Benzenebutyric acid sodium) 目录号 : GC15002
A chemical chaperone
Cas No.:1716-12-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Cell experiment: | Briefly, viable cells, as judged by trypan blue dye exclusion, are seeded at a density of 4 × 104 cells/mL in 60-mm dishes in RPMI 1640 with 10% fetal bovine serum and 0.35% agarose on a base layer of 0.7% agarose. DMSO, TSA, or PB is added to both bottom and top agarose layers. Assays are performed in triplicate on at least three separate occasions, and colonies are counted at 10-14 days[1]. |
Animal experiment: | Mice[3]Female 10-week-old C57BL/6J mice are housed in the pathogen-free animal facility of IRC. Animals are randomized into the following 4 groups: vehicle control (n=5), vehicle+Benzenebutyric acid (n=6), LPS (n=6), and LPS+Benzenebutyric acid (n=6). Mice are treated with LPS in 200 μL phosphate-buffered saline (PBS) once a week (5 mg/kg, i.p.) for 3 weeks. Benzenebutyric acid solution is prepared by titrating equimolecular amounts of Benzenebutyric acid and sodium hydroxide to reach pH 7.4; mice are injected daily intraperitoneally in 200 μL PBS (or with PBS as a vehicle) at a dose of 240 mg/kg for 3 weeks. Mice are sacrificed by CO2 asphyxiation. To determine the bone mineral density (BMD) and microarchitecture of the long bone, the right femur is scanned. Scans are performed with an effective detector pixel size of 6.9 μm and a threshold of 77-255 mg/cc. Trabecular bone is analyzed in a region 1.6 mm in length and located 0.1 mm below the distal femur growth plate[3]. |
References: [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. | |
Sodium phenylbutyrate is an inhibitor of HDAC and endoplasmic reticulum (ER) stress, used in cancer and infection research.
Sodium phenylbutyrate is an inhibitor of HDAC, inhibits the growth of NSCLC Cell Lines at 2 mM. Sodium phenylbutyrate in combination with ciglitizone results in enhanced growth arrest of cancer cells[1]. Sodium phenylbutyrate (0-5 mM) inhibits ASFV infection in a dose-dependent manner. Sodium phenylbutyrate also inhibits the ASFV late protein synthesis and disrupts the virus-induced H3K9/K14 hypoacetylation status. Sodium phenylbutyrate 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].
LPS induces significant bone loss and decreases bone mineral density (BMD), bone volume (BV/TV), and trabecular thickness (Tb. Th) compared with PBS alone, whereas trabecular space (Tb. Sp.) is increased. Sodium phenylbutyrate attenuates LPS-induced bone loss. Treatment with Sodium phenylbutyrate increases BMD, BV/TV, and Tb. Th. compared with LPS alone, in addition to decreasing the enlargement of Tb. Sp., but no change is observed when mice are treated with Sodium phenylbutyrate alone. OC.S/BS as assessed by TRAP staining is also significantly reduced when Sodium phenylbutyrate is administered to LPS-treated mice. However, OC.N/BS tends to decrease, although not with statistical significance, when mice are treated with Sodium phenylbutyrate and LPS. These results indicate that the effect of Sodium phenylbutyrate on OC from LPS-treated mice is to reduce its size rather than number. Consistent with these findings, a marker of bone resorption in vivo, serum CTX-1 which is elevated by LPS treatment is decreased when Sodium phenylbutyrate administered to LPS-injected mice. However, co-treatment with Sodium phenylbutyrate do not significantly affect the levels of serum ALP and osteocalcin, 2 markers of bone formation in vivo, compared with LPS alone. Sodium phenylbutyrate also reduces the LPS-induced rise in serum MCP-1, indicating that Sodium phenylbutyrate decreases systemic inflammation induced by LPS[3].
References:
[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.
| Cas No. | 1716-12-7 | SDF | |
| 别名 | 苯丁酸钠; 4-PBA sodium; 4-Phenylbutyric acid sodium; Benzenebutyric acid sodium | ||
| 化学名 | sodium;4-phenylbutanoate | ||
| Canonical SMILES | C1=CC=C(C=C1)CCCC(=O)[O-].[Na+] | ||
| 分子式 | C10H11O2.Na | 分子量 | 186.18 |
| 溶解度 | ≥ 27.65 mg/mL in Water, ≥ 6.3 mg/mL in DMSO, ≥ 50.9 mg/mL in EtOH with ultrasonic | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 5.3711 mL | 26.8557 mL | 53.7115 mL |
| 5 mM | 1.0742 mL | 5.3711 mL | 10.7423 mL |
| 10 mM | 0.5371 mL | 2.6856 mL | 5.3711 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。