1. Cell Cycle/DNA Damage
  2. HDAC

Benzenebutyric acid (Synonyms: 4-Phenylbutyric acid)

Cat. No.: HY-A0281 Purity: 99.97%
Handling Instructions

Benzenebutyric acid 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.

Benzenebutyric acid Chemical Structure

Benzenebutyric acid Chemical Structure

CAS No. : 1821-12-1

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10 mM * 1 mL in DMSO USD 55 In-stock
Estimated Time of Arrival: December 31
5 g USD 50 In-stock
Estimated Time of Arrival: December 31
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  • Biological Activity

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  • References


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

IC50 & Target[1]



In Vitro

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

Clinical Trial
Solvent & Solubility
In Vitro: 

DMSO : ≥ 250 mg/mL (1522.53 mM)

H2O : 2 mg/mL (12.18 mM; Need ultrasonic)

*"≥" means soluble, but saturation unknown.

Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 6.0901 mL 30.4507 mL 60.9013 mL
5 mM 1.2180 mL 6.0901 mL 12.1803 mL
10 mM 0.6090 mL 3.0451 mL 6.0901 mL
*Please refer to the solubility information to select the appropriate solvent.
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].

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

Animal Administration

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.

Molecular Weight








Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month

Room temperature in continental US; may vary elsewhere

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Product Name:
Benzenebutyric acid
Cat. No.:

Benzenebutyric acid

Cat. No.: HY-A0281