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Sodium 4-phenylbutyrate
Sodium 4-phenylbutyrate (TriButyrate), a transcriptional regulator, reversibly inhibits class I and II histone deacetylases (HDACs )resulting in a global increase in gene expression, decreased cellular proliferation, increased cell differentiation, and the induction of apoptosis in susceptible tumor cell populations.
Catalog No. T1535Cas No. 1716-12-7
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Sodium 4-phenylbutyrate
Catalog No. T1535Cas No. 1716-12-7
Sodium 4-phenylbutyrate (TriButyrate), a transcriptional regulator, reversibly inhibits class I and II histone deacetylases (HDACs )resulting in a global increase in gene expression, decreased cellular proliferation, increased cell differentiation, and the induction of apoptosis in susceptible tumor cell populations.
All TargetMol products are for research purposes only and cannot be used for human consumption. We do not provide products or services to individuals. Please comply with the intended use and do not use TargetMol products for any other purpose. | Pack Size | Price | Availability | Quantity |
|---|---|---|---|
| 50 mg | $38 | In Stock | |
| 100 mg | $54 | In Stock | |
| 200 mg | $87 | In Stock | |
| 500 mg | $144 | In Stock | |
| 1 mL x 10 mM (in DMSO) | $50 | In Stock |
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CitedProduct Introduction
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| Description | Sodium 4-phenylbutyrate (TriButyrate), a transcriptional regulator, reversibly inhibits class I and II histone deacetylases (HDACs )resulting in a global increase in gene expression, decreased cellular proliferation, increased cell differentiation, and the induction of apoptosis in susceptible tumor cell populations. |
| In vitro | In G93A transgenic ALS mice, Phenylbutyrate improves clinical symptoms and increases survival. It induces the expression of NF-κB p50 in G93A mice, while reducing the expression of cytochrome c and caspases. Additionally, in transgenic mouse models of Huntington's disease (HD), Phenylbutyrate elevates brain protein acetylation levels and reduces histone methylation levels. |
| In vivo | In prostate cancer cells, Phenylbutyrate induces apoptosis by diminishing the expression levels of the cell apoptosis antagonist Bcl-X(L), the double-strand break repair protein DNA-dependent protein kinase, the prostate progression marker Caveolin-1, and the angiogenesis promoter Vascular Endothelial Growth Factor, thereby weakening their activity. |
| Alias | Sodium Phenylbutyrate, Buphenyl, TriButyrate |
| Molecular Weight | 186.18 |
| Formula | C10H11NaO2 |
| Cas No. | 1716-12-7 |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. | |||||||||||||||||||||||||||||||||||
| Solubility Information | H2O: 18.6 mg/mL (100 mM) DMSO: 50 mg/mL (268.56 mM)  | |||||||||||||||||||||||||||||||||||
Solution Preparation Table | ||||||||||||||||||||||||||||||||||||
H2O/DMSO
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Please enter your animal experiment information in the following box and click Calculate to obtain the mother liquor preparation method and in vivo formula preparation method:
For example, your dosage is 10 mg/kg Each animal weighs 20 g, and the dosage volume is 100 μL . A total of 10 animals were administered, and the formula you used is 5% 
DMSO+30% PEG300+5% Tween 80+60% ddH2O. So your working solution concentration is 2 mg/mL。Mother liquor preparation method: 2 mg of drug dissolved in 50 μL DMSO (mother liquor concentration of 40 mg/mL), if you need to configure a concentration that exceeds the solubility of the product, please contact us first.
(mother liquor concentration of 40 mg/mL), if you need to configure a concentration that exceeds the solubility of the product, please contact us first.Preparation method for in vivo formula: Take 50 μL DMSO main solution, add 300 μLPEG300 mix well and clarify, then add 50 more μL Tween 80, mix well and clarify, then add 600 more μLddH2O mix well and clarify
main solution, add 300 μLPEG300 mix well and clarify, then add 50 more μL Tween 80, mix well and clarify, then add 600 more μLddH2O mix well and clarifyFor Reference Only. Please develop an appropriate dissolution method based on your laboratory animals and route of administration.
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