Sodium 4-phenylbutyrate (4-PBA sodium) is an inhibitor ofHDACand endoplasmic reticulum(ER)stress, used incancerandinfectionresearch^[1].

Sodium 4-phenylbutyrate (Sodium phenylbutyrate) is an inhibitor of HDAC, inhibits the growth of NSCLC Cell Lines at 2 mM. Sodium 4-phenylbutyrate in combination with ciglitizone results in enhanced growth arrest of cancer cells^[1]. Sodium 4-phenylbutyrate (Sodium phenylbutyrate; 0-5 mM) inhibits ASFV infection in a dose-dependent manner. Sodium 4-phenylbutyrate also inhibits the ASFV late protein synthesis and disrupts the virus-induced H3K9/K14 hypoacetylation status. Sodium 4-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 4-phenylbutyrate (Sodium phenylbutyrate) attenuates LPS-induced bone loss. Treatment with Sodium 4-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 4-phenylbutyrate alone. OC.S/BS as assessed by TRAP staining is also significantly reduced when Sodium 4-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 4-phenylbutyrate and LPS. These results indicate that the effect of Sodium 4-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 4-phenylbutyrate administered to LPS-injected mice. However, co-treatment with Sodium 4-phenylbutyrate do not significantly affect the levels of serum ALP and osteocalcin, 2 markers of bone formation in vivo, compared with LPS alone. Sodium 4-phenylbutyrate also reduces the LPS-induced rise in serum MCP-1, indicating that Sodium 4-phenylbutyrate decreases systemic inflammation induced by LPS^[3].

186.18

Solid

C₁₀H₁₁NaO₂

1716-12-7

苯丁酸钠

Room temperature in continental US; may vary elsewhere.

4°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

H₂O : 100 mg/mL(537.11 mM;Need ultrasonic)

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℃, 6 months; -20℃, 1 month (sealed storage, away from moisture)。-80℃ 储存时，请在 6 个月内使用，-20℃ 储存时，请在 1 个月内使用。

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照In Vitro方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： PBS

  Solubility: 100 mg/mL (537.11 mM); Clear solution; Need ultrasonic