Sodium butyrate

Catalog No.S1999

Sodium butyrate Chemical Structure

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).

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2 Customer Reviews

  • 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.

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Biological Activity

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).
Histone deacetylase [6]
In vitro

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. [1] 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. [2] 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. [3] 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. [4]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human K562 cells NHrGfnpRem:uaX\ldoF1cW:wIHHzd4F6 NIW1UlYyKG2P NYfO[odOSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDLOVYzKGOnbHzzJIF1KDFibV2gbY4heHKnc3XuZ4Uhd2ZiZ4Xhco9{cW6n NFTBSoYzOzl|N{m3PS=>
human H1299 cells NIjRW3RHfW6ldHnvckBie3OjeR?= NGPpSIE4KGSjeYO= Mk[3TY5pcWKrdHnvckBw\iCqdX3hckBWW1BzL2XBSlEhcW5iaIXtZY4hUDF{OUmgZ4VtdHNiYYPz[ZN{\WRiYYOgdoVlfWO2aX;uJIlvKGOxbH;ufUBnd3KvYYTpc44h[W[2ZYKgO{Bl[Xm|LDDFR|UxRTNizszN NE[yTZczPTJ{OU[0Ny=>
human JEG3 cells M2LaUmZ2dmO2aX;uJIF{e2G7 MUnJcohq[mm2aX;uJI9nKGG{b33heIF{\SCrbjDoeY1idiCMRVezJINmdGy|IHL5JJNkcW62aXzsZZRqd25ic4DlZ5Rzd22ndIL5MEBKSzVyPUCuNFAyPSEQvF2= M3fNXVIxOTR6NU[0

... Click to View More Cell Line Experimental Data

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. [5]


Solubility (25°C)

In vitro Water 22 mg/mL (199.83 mM)
Ethanol 22 mg/mL (199.83 mM)
DMSO Insoluble

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 110.09


CAS No. 156-54-7
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03010865 Not yet recruiting Schizophrenic Disorder|Cognitive Impairment Shanghai Mental Health Center|Stanley Medical Research Institute June 2017 Phase 2|Phase 3
NCT02654405 Withdrawn Schizophrenic Disorders|Cognitive Function Nathan Kline Institute for Psychiatric Research|Stanley Medical Research Institute April 2016 Phase 2|Phase 3

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HDAC Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID