1. Cell Cycle/DNA Damage
    Epigenetics
    Autophagy
  2. HDAC
    Autophagy
  3. Sodium phenylbutyrate

Sodium phenylbutyrate (Synonyms: Sodium 4-phenylbutyrate; TriButyrate)

Cat. No.: HY-15654 Purity: 99.75%
Handling Instructions

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

For research use only. We do not sell to patients.

Sodium phenylbutyrate Chemical Structure

Sodium phenylbutyrate Chemical Structure

CAS No. : 1716-12-7

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Based on 4 publication(s) in Google Scholar

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Description

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

IC50 & Target

HDAC

 

In Vitro

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].

In Vivo

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].

Clinical Trial
Molecular Weight

186.18

Formula

C₁₀H₁₁NaO₂

CAS No.

1716-12-7

SMILES

[O-]C(CCCC1=CC=CC=C1)=O.[Na+]

Shipping

Room temperature in continental US; may vary elsewhere

Storage
Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month
Solvent & Solubility
In Vitro: 

H2O : 23.5 mg/mL (126.22 mM; Need ultrasonic and warming)

Preparing
Stock Solutions
Concentration Solvent Mass 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
*Please refer to the solubility information to select the appropriate solvent.
References
Cell Assay
[1]

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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Administration
[3]

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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

References
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Sodium phenylbutyrate
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HY-15654
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