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Sodium butyrate

Catalog No.
B1835
Histone deacetylase inhibitor
Grouped product items
SizePriceStock Qty
10mM (in 1mL H2O)
$47.00
In stock
1g
$42.00
In stock

Tel: +1-832-696-8203

Email: [email protected]

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Background

Sodium butyrate is a kind of histone deacetylases (HDACs) inhibitors studied clinically, which works on histones and transcription factors to modulate transcription [1].

Interaction of HDACs and histone acetyltransferases determines histone acetylation, which affects the final transcription process. The transcription dysregulation results in functional and degenerative changes [2].

In the adenoma RG/C2 cell line, sodium butyrate reduced the number of attached cells to 50% of that of the control group, and the number of floating cells is increased induced by cell apoptosis. Compare with RG/C2, AA/CI showed more sensitivity to sodium butyrate [3].

In the experiments of the R6/2 cell line transgenic Huntingtin disease (HD) mouse model, seven different intraperitoneal dosings of sodium butyrate were administrated daily. The survival time, weight and athletic ability were improved together, and the neuropathologic sequelae were delayed, too. Besides, sodium butyrate increased the acetylation level of histone and specificity protein-1 and prevent the neurotoxicity inducing by 3-nitropropionic acid [1].

Reference:

[1]. Ferrante R J, Kubilus J K, Lee J, et al. Histone deacetylase inhibition by sodium butyrate chemotherapy ameliorates the neurodegenerative phenotype in Huntington's disease mice [J]. Journal of Neuroscience, 2003, 23(28): 9418-9427.

[2]. Cha J H. Transcriptional dysregulation in Huntington's disease [J]. Trends in Neurosciences, 2000, 23(9): 387-392.

[3]. Hague A, Manning A M, Hanlon K A, et al. Sodium butyrate induces apoptosis in human colonic tumour cell lines in a p53-independent pathway: implications for the possible role of dietary fibre in the prevention of large-bowel cancer [J]. International Journal of Cancer, 1993, 55(3): 498-505.

Product Citation

Chemical Properties

Physical AppearanceA solid
StorageStore at -20°C
M.Wt110.09
Cas No.156-54-7
FormulaC4H7NaO2
Solubilityinsoluble in DMSO; ≥4 mg/mL in H2O; ≥5.87 mg/mL in EtOH
Chemical Namesodium;butanoate
SDFDownload SDF
Canonical SMILESCCCC(=O)[O-].[Na+]
Shipping ConditionShip with blue ice, or upon other requests.
General tipsFor obtaining a higher solubility, please warm the tube at 37°C and shake it in the ultrasonic bath for a while. We do not recommend long-term storage for the solution, please use it up soon.

Protocol

Cell experiment [1]:

Cell lines

2 adenoma-derived cell lines (AA/Cl and RG/C2)

Preparation method

The solubility of this compound in DMSO is limited. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below - 20 °C for several months.

Reacting condition

1 ~ 4 mM; 4 days

Applications

In RG/C2 cells, Sodium Butyrate at the concentrations of 2 mM and above reduced the attached-cell yield to approximately 50% of the control, and significantly increased the proportion of floating cells. It was demonstrated that the increase in the percentage of floating cells was attributed to the induction of apoptosis and not simply due to increased necrosis. Compared with RG/C2 cells, AA/Cl cells were more sensitive to Sodium Butyrate.

Animal experiment [2]:

Animal models

An R6/2 transgenic mouse model of Huntington's disease (HD)

Dosage form

100, 200, 400, 600, 1200, 5000 and 10,000 mg/kg; i.p.; q.d.

Applications

In an R6/2 transgenic mouse model of HD, Sodium Butyrate significantly extended survival in a dose-dependent manner, improved body weight and motor performance, as well as delayed the neuropathological sequelae. Moreover, Sodium Butyrate increased the level of histone and specificity protein-1 acetylation, and protected against 3-nitropropionic acid-induced neurotoxicity.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

References:

[1]. Hague A1, Manning AM, Hanlon KA, Huschtscha LI, Hart D, Paraskeva C. Sodium butyrate induces apoptosis in human colonic tumour cell lines in a p53-independent pathway: implications for the possible role of dietary fibre in the prevention of large-bowel cancer. Int J Cancer. 1993 Sep 30;55(3):498-505.

[2]. Ferrante RJ1, Kubilus JK, Lee J, Ryu H, Beesen A, Zucker B, Smith K, Kowall NW, Ratan RR, Luthi-Carter R, Hersch SM. Histone deacetylase inhibition by sodium butyrate chemotherapy ameliorates the neurodegenerative phenotype in Huntington's disease mice. J Neurosci. 2003 Oct 15;23(28):9418-27.

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