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    Sodium Phenylbutyrate (4-PBA sodium)
    Sodium Phenylbutyrate (4-PBA sodium)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V0284
    CAS #: 1716-12-7Purity ≥98%

    Description: Sodium phenylbutyrate (4-Phenylbutyric acid sodium; 4-PBA sodium), an orphan drug marketed by Ucyclyd Pharma, is a novel and potent histone deacetylase (HDAC) inhibitor used as an as adjunctive therapy for chronic treatment of urea cycle disorders involving deficiencies of argininosuccinic acid synthetase (AS), ornithine transcarbamylase (OTC), or carbamylphosphate synthetase (CPS). As the metabolites of Sodium phenylbutyrate offer an alternative pathway to the urea cycle to allow excretion of excess nitrogen. It also has potent anti-cancer activity.

    References: Neuromolecular Med. 2004;5(3):235-41; J Neurochem. 2005;93(5):1087-98; J Biol Chem. 2005;280(1):556-63.

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    Molecular Weight (MW)186.18
    CAS No.1716-12-7
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 30 mg/mL (161.1 mM)
    Water: <1 mg/mL
    Ethanol: 8 mg/mL (43.0 mM)
    Solubility (In vivo)

    Chemical Name: sodium 4-phenylbutanoate


    InChi Code: InChI=1S/C10H12O2.Na/c11-10(12)8-4-7-9-5-2-1-3-6-9;/h1-3,5-6H,4,7-8H2,(H,11,12);/q;+1/p-1

    SMILES Code: O=C([O-])CCCC1=CC=CC=C1.[Na+]


    4-PBA sodium; Sodium 4-phenylbutyrate; Sodium phenylbutyrate; 4-phenylbutyrate (4-PBA); 4-phenylbutyric acid; Buphenyl

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    In Vitro

    In vitro activity: Phenylbutyrate is a well-known HDAC inhibitor, which increases gene transcription of a number of genes, and also exerts neuroprotective effects. Phenylbutyrate significantly attenuates MPTP-induced depletion of striatal dopamine and loss of tyrosine hydroxylase-positive neurons in the substantia nigra. Phenylbutyrate attenuates the expression of the apoptosis antagonist Bcl-X(L), the double-strand break repair protein DNA-dependent protein kinase, the prostate progression marker caveolin-1, and the pro-angiogenic vascular endothelial growth factor in prostate cancer cells. Phenylbutyrate is found to act in synergy with ionizing radiation to induce apoptosis in prostate cancer cells.

    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.

    In VivoPhenylbutyrate significantly extends survival and improved both the clinical and neuropathological phenotypes in G93A transgenic ALS mice. Phenylbutyrate administration ameliorates histone hypoacetylation observed in G93A mice and induced expression of nuclear factor-kappaB (NF-kappaB) p50, the phosphorylated inhibitory subunit of NF-kappaB (pIkappaB) and beta cell lymphoma 2 (bcl-2), but reduced cytochrome c and caspase expression. Phenylbutyrate acts to phosphorylate IkappaB, translocating NF-kappaB p50 to the nucleus, or to directly acetylate NF-kappaB p50. Phenylbutyrate increases brain histone acetylation and decreased histone methylation levels as assessed by both immunocytochemistry and Western blots in a transgenic mousemodel of Huntington's disease (HD). Phenylbutyrate increases mRNA for components of the ubiquitin-proteosomal pathway and down-regulated caspases implicated in apoptotic cell death, and active caspase 3 immunoreactivity in the striatum.
    Animal modelMice: 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
    Formulation & Dosage5 mg/kg, i.p.

    Neuromolecular Med. 2004;5(3):235-41; J Neurochem. 2005 Jun;93(5):1087-98; J Biol Chem. 2005 Jan 7;280(1):556-63.

    These protocols are for reference only. InvivoChem does not independently validate these methods.

    Sodium Phenylbutyrate
    Effects of administration of phenylbutyrate starting at 75 days of age on survival in the N171-82Q transgenic mouse model of HD. J Biol Chem. 2005 Jan 7;280(1):556-63.
    Sodium Phenylbutyrate
    Western blots showing the effects of phenylbutyrate treatment (100 mg/kg intraperitoneal) on histone acetylation in the brain of N171-82Q at 0, 1, 2, 3, and 4 h after administration. J Biol Chem. 2005 Jan 7;280(1):556-63.
    Sodium Phenylbutyrate
    Western blots showing the effects of phenylbutyrate treatment on histone methylation in the brain of N171-82Q mice and age-matched wild-type (Wt) mice at 0, 1, 2, and 3 h after administration, or 3 h after vehicle (PBS). J Biol Chem. 2005 Jan 7;280(1):556-63.


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