1. Cell Cycle/DNA Damage
    Epigenetics
    Autophagy
  2. HDAC
    Autophagy
  3. Sodium Butyrate

Sodium Butyrate (Synonyms: Butanoic acid sodium salt)

Cat. No.: HY-B0350A Purity: >98.00%
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Sodium Butyrate (Butanoic acid sodium salt) is a histone deacetylase (HDAC) inhibitor, with anti-tumor effects in several cancers.

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

Sodium Butyrate Chemical Structure

Sodium Butyrate Chemical Structure

CAS No. : 156-54-7

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Customer Review

Based on 4 publication(s) in Google Scholar

Top Publications Citing Use of Products

    Sodium Butyrate purchased from MCE. Usage Cited in: Neurobiol Dis. 2017 Dec 14;111:12-25.

    Cdc42-Rac1 activation mediates the effect of SB on microglial process elongation. Representative images showing the activation effect of Cdc42 and Rac1 by Sodium butyrate (SB) (5 mM) at different time points (5, 10 min) in primary cultured microglia.
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    Description

    Sodium Butyrate (Butanoic acid sodium salt) is a histone deacetylase (HDAC) inhibitor, with anti-tumor effects in several cancers.

    IC50 & Target[2]

    HDAC

     

    In Vitro

    Sodium Butyrate induces morphological changes, inhibits cell proliferation and impairs cell viability in NPC cells. Sodium Butyrate (1, 5, 10 mM) is cytotoxic to NPC cells, inducing a dose- and time-dependent decrease in cell viability, in both 5-8F and 6-10B cells. Sodium Butyrate induces nasopharyngeal carcinoma cell apoptosis by activating the mitochondrial apoptotic axis. Moreover, SOCE inhibition and disruption of the CRAC channel can attenuate the apoptosis induced by Sodium Butyrate[1]. Sodium butyrate significantly decreases cell viability, accompanied by reduced levels of p-mTOR and PCNA protein. Sodium butyrate, in a dose-dependent manner, induces cell cycle arrest in G0/G1 phase and reduces the numbers of cells in S phase. In addition, relative expression of p21, p27, and pro-apoptosis bak genes, and protein levels of p21Waf1/Cip1, p27Kip1, cyclinD3, CDK4, and Cleave-caspase3 are increased by higher concentrations of sodium butyrate (1, 5, 10 mM), and the levels of cyclinD1 and CDK6 are reduced by 5 and 10 mM butyrate[3].

    In Vivo

    Sodium Butyrate (300 mg/kg, s.c.) administration immediately after HI provided almost complete neuroprotection in comparison with non-treated animals. Sodium butyrate administration results in an increased number of microglial cells to 150% of vehicle-treated animals in the ipsilateral side. Sodium butyrate promotes the polarization of microglia from M1- to M2-like phenotype after neonatal hypoxia-ischemia[2]. Sodium butyrate (300 mg/kg, s.c.) in combination with AK-7 (20 mg/kg, i.p.) significantly alleviates this reduction of the time spent exploring new objects, ameliorates the reduction of the number of Ki67-positive cells and DCX-immunoreactive neuroblasts in the dentate gyrus of the mice. In addition, sodium butyrate reverses SIRT2-related age phenotypes[4].

    Clinical Trial
    Molecular Weight

    110.09

    Formula

    C₄H₇NaO₂

    CAS No.

    156-54-7

    SMILES

    CCCC([O-])=O.[Na+]

    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: 

    H2O : ≥ 100 mg/mL (908.35 mM)

    *"≥" means soluble, but saturation unknown.

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 9.0835 mL 45.4174 mL 90.8348 mL
    5 mM 1.8167 mL 9.0835 mL 18.1670 mL
    10 mM 0.9083 mL 4.5417 mL 9.0835 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Sodium butyrate (SB) is prepared in PBS[5].

    References
    Cell Assay
    [1]

    Cells are seeded at a density of 2,000 cells/well in 96-well plates with 200 µL culture medium containing Sodium Butyrate at different concentrations. Then, the cells are consecutively cultured for 72 h. Every 24 h, 20 µL 5 mg/mL MTT solution is added into the corresponding well, and the cells are cultured for another 4 h. Then, the solution is replaced with 150 µL dimethylsulfoxide, followed by gentle agitation of the plates for 15 min at room temperature. Finally, the absorbance at 492 nm is measured to represent the cell viability.

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

    Animal Administration
    [2]

    Seven-day-old rat pups are subjected to unilateral carotid artery ligation followed by 60 min of hypoxia (7.6% O2). Sodium Butyrate (300 mg/kg) is administered in a 5-day regime with the first injection given immediately after hypoxic exposure. The damage of the ipsilateral hemisphere is evaluated by hematoxylin-eosin staining 6 days after the insult. Samples are collected at 24 and 48 h and 6 days.

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

    References

    Purity: >98.00%

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