[CAS NO. 1716-12-7] Sodium4-phenylbutyrate

Name: Sodium4-phenylbutyrate
Brand: Arctom Scientific
SKU: AS099293

Ships within

Stock

Price

Qty

Total

$0.00

Please click "REQUEST A QUOTE" button if you need other sizes or custom synthesis

request a quote

If there is no stock, or you need other sizes or custom synthesis, please:

PRODUCTS SPECIFICATIONS [1716-12-7]

Store

Catalog

AS099293

Brand

Arctom Scientific

CAS

1716-12-7

DESCRIPTION [1716-12-7]

Overview

MDL	MFCD00800247
Molecular Weight	186.18
Molecular Formula	C10H11NaO2
SMILES	O=C(O[Na])CCCC1=CC=CC=C1

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

67 Publications Citing Use of MCE

Summary

Sodium 4-phenylbutyrate (4-PBA sodium) is an inhibitor of HDAC and endoplasmic reticulum (ER) stress, used in cancer and infection research ^[1] .

IC50 & Target

HDAC

In Vitro

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] .

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. 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] .

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
NCT00590538	Children´s Hospital of Philadelphia\|Cystic Fibrosis Foundation	Cystic Fibrosis	February 2003	Phase 1\|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

Appearance

Solid

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

4°C, sealed storage, away from moisture

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

Solvent & Solubility

In Vitro:

H ₂ O : 100 mg/mL ( 537.11 mM ; Need ultrasonic)

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.

In Vivo:

1.

Add each solvent one by one: PBS

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

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

References

Synonyms

Benzenebutanoic acid, sodium salt (1:1)

Butyric acid, 4-phenyl-, sodium salt

Benzenebutanoic acid, sodium salt

Sodium phenylbutyrate

Sodium 4-phenylbutyrate

Sodium γ-phenylbutyrate

TriButyrate

Buphenyl

NSC 657802

Pheburane

Ammonaps