[CAS NO. 1821-12-1] 4-Phenylbutyricacid

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PRODUCTS SPECIFICATIONS [1821-12-1]

Catalog

HY-A0281

Brand

MCE

CAS

1821-12-1

DESCRIPTION [1821-12-1]

Overview

MDL	MFCD00004403
Molecular Weight	164.20
Molecular Formula	C10H12O2
SMILES	O=C(O)CCCC1=CC=CC=C1

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

67 Publications Citing Use of MCE

Summary

4-Phenylbutyric acid (4-PBA) is an inhibitor of HDAC and endoplasmic reticulum (ER) stress, used in cancer and infection research.

IC50 & Target

HDAC

In Vitro

4-Phenylbutyric acid (4-PBA) 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] . 4-Phenylbutyric 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 4-Phenylbutyric acid 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 4-Phenylbutyric 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 4-Phenylbutyric 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] .

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

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. 4-Phenylbutyric acid (4-PBA) attenuates LPS-induced bone loss. Treatment with 4-Phenylbutyric 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] .

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

Clinical Trial

NCT Number	Sponsor	Condition	Start Date	Phase
NCT00067756	University of Florida\|Alpha-1 Foundation\|Brantly, Mark L., M.D.	Alpha 1-Antitrypsin Deficiency	November 2001	Phase 2
NCT00016744	Children´s Hospital of Philadelphia\|Cystic Fibrosis Foundation\|National Center for Research Resources (NCRR)	Cystic Fibrosis	September 2001	Phase 1\|Phase 2
NCT00590538	Children´s Hospital of Philadelphia\|Cystic Fibrosis Foundation	Cystic Fibrosis	February 2003	Phase 1\|Phase 2

Appearance

Solid

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:

DMSO : ≥ 100 mg/mL ( 609.01 mM )

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

* "≥" means soluble, but saturation unknown.

Preparing
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.

In Vivo:

1.

Add each solvent one by one: 20% HP-β-CD in saline

Solubility: 33.33 mg/mL (202.98 mM); Suspended solution; Need ultrasonic
2.

Add each solvent one by one: 10% DMSO >> 40% PEG300 >> 5% Tween-80 >> 45% saline

Solubility: ≥ 2.08 mg/mL (12.67 mM); Clear solution
3.

Add each solvent one by one: 10% DMSO >> 90% (20% SBE-β-CD in saline)

Solubility: ≥ 2.08 mg/mL (12.67 mM); Clear solution
4.

Add each solvent one by one: 10% DMSO >> 90% corn oil

Solubility: ≥ 2.08 mg/mL (12.67 mM); Clear solution

* All of the co-solvents are available by MCE.

References

Synonyms

Benzenebutanoic acid

Butyric acid, 4-phenyl-

Butyric acid, γ-phenyl-

4-Phenylbutyric acid

Benzenebutyric acid

γ-Phenylbutyric acid

4-Phenylbutanoic acid

ω-Phenylbutanoic acid

γ-Phenylbutanoic acid

4-Phenyl-n-butyric acid

NSC 295