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1716-12-7

1716-12-7 structure
1716-12-7 structure
  • Name: Sodium phenylbutyrate
  • Chemical Name: sodium phenylbutyrate
  • CAS Number: 1716-12-7
  • Molecular Formula: C10H11NaO2
  • Molecular Weight: 186.183
  • Catalog: Biochemical Inhibitor Epigenetics HDAC inhibitor
  • Create Date: 2018-05-31 08:00:00
  • Modify Date: 2024-01-02 16:38:22
  • Sodium phenylbutyrate is an inhibitor of HDAC and endoplasmic reticulum (ER) stress, used in cancer and infection research.
Name sodium phenylbutyrate
Synonyms Benzenebutanoic acid, sodium salt
4-phenylbutyrate
Ammonaps
4-Phenylbutyrate, sodium
Benzenebutanoic acid, sodium salt (1:1)
Sodium phenylbutyrate
4-Phenylbutyric Acid Sodium Salt
Phenylbutyric acid sodium salt
4-PBA,4-Phenylbutyric acid,4-phenylbutyrate
Sodium 4-phenylbutanoate
4-phenylbutanoic acid, sodium salt
MFCD00800247
BUPHENYL
triButyrate
Sodium 4-Phenylbutyrate
Description Sodium phenylbutyrate is an inhibitor of HDAC and endoplasmic reticulum (ER) stress, used in cancer and infection research.
Related Catalog
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 (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].
Cell Assay 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 Admin 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.

[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.
Density 1.095g/cm3
Boiling Point 290.7ºC at 760mmHg
Melting Point 207 °C (dec.)(lit.)
Molecular Formula C10H11NaO2
Molecular Weight 186.183
Flash Point 187.9ºC
Exact Mass 186.065674
PSA 40.13000
LogP 0.75920
Vapour Pressure 0.00288mmHg at 25°C
Storage condition Desiccate at -20°C
Symbol GHS07
GHS07
Signal Word Warning
Hazard Statements H319
Precautionary Statements P305 + P351 + P338
Hazard Codes Xi
Risk Phrases R36/37/38:Irritating to eyes, respiratory system and skin .
Safety Phrases S26-S36
RIDADR NONH for all modes of transport
WGK Germany 3
RTECS XJ1921000
HS Code 2916399090
Precursor  1

DownStream  1

HS Code 2916399090
Summary 2916399090 other aromatic monocarboxylic acids, their anhydrides, halides, peroxides, peroxyacids and their derivatives VAT:17.0% Tax rebate rate:9.0% Supervision conditions:none MFN tariff:6.5% General tariff:30.0%

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title: CAS No. 1716-12-7 | Chemsrc address: https://www.chemsrc.com/en/baike/889106.html

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