Molecular Weight(MW): 110.09
Sodium butyrate, sodium salt of butyric acid, is a histone deacetylase inhibitor and competitively binds to the zinc sites of class I and II histone deacetylases (HDACs).
Cited by 9 Publications
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U87 cells were cultured with DMSO or 10 µM 5azadC for 72 h. For the latter, 1 µM Trichostatin A (TSA), 10 mM sodium butyrate (NaBu), 5 mM nicotinamide (NAM), or 0.5 µM apicidin were added in the last 24 h. IFNLR1 expression was determined by RT-qPCR.
PLoS Biol 2014 12(1), e1001758. Sodium butyrate purchased from Selleck.
Effects of combination of either MS-275, apicidin, SAHA or sodium butyrate (NaB) with bortezomib on proliferation of Wp-restricted BL cells. P3HR1-c16 cells were treated with combination of NaB (0, 0.6, 1.2, 2.4, 4.8 and 9.6 mM) for 48 h. Cell proliferation was determined by MTT assay and presented as percentages of cell proliferation of treated cells compared with those of untreated cells. Synergisms of proliferation inhibition of the cells following treatment with different drug combinations were analysed by isobologram analysis.
Br J Haematol 2014 167(5), 639-50. Sodium butyrate purchased from Selleck.
Purity & Quality Control
Choose Selective HDAC Inhibitors
|Description||Sodium butyrate, sodium salt of butyric acid, is a histone deacetylase inhibitor and competitively binds to the zinc sites of class I and II histone deacetylases (HDACs).|
Butyrate mediates growth inhibition of colonic cancer cells and thereby to elucidate the molecular link between a high-fiber diet and the arrest of colon carcinogenesis. Butyrate induces p21 mRNA expression in an immediate-early fashion, through transactivation of a promoter cis-element(s) located within 1.4 kb of the transcriptional start site, independent of p53 binding.  Sodium butyrate, at physiological concentrations, induces apoptosis in 2 adenoma cell lines, RG/C2 and AA/Cl, and in the carcinoma cell line PC/JW/FI.  Butyrate exerts potent effects on a variety of colonic mucosal functions such as inhibition of inflammation and carcinogenesis, reinforcing various components of the colonic defence barrier and decreasing oxidative stress.  Butyrate inhibits most HDAC except class III HDAC and class II HDAC6 and -10. Butyrate also is the most effective fatty acid in stimulating or repressing the expression of specific genes. 
|In vivo||Sodium butyrate significantly extends survival in a dose-dependent manner, improves body weight and motor performance, and delays the neuropathological sequelae in the R6/2 transgenic mouse model of Huntington's disease (HD). Sodium butyrate also increases histone and specificity protein-1 acetylation and protects against 3-nitropropionic acid neurotoxicity. |
-  Archer SY, et al. Proc Natl Acad Sci U S A, 1998, 95(12), 6791-6796.
-  Hague A, et al. Int J Cancer, 1993, 55(3), 498-505.
-  Hamer HM, et al. Aliment Pharmacol Ther, 2008, 27(2), 104-119.
|In vitro||Water||22 mg/mL (199.83 mM)|
|Ethanol||22 mg/mL (199.83 mM)|
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