Home Epigenetics HDAC inhibitor - Autophagy activator - Apoptosis related activator Sodium butyrate

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Sodium butyrate HDAC inhibitor

Cat.No.S1999

Sodium butyrate (NaB, Butanoic acid sodium salt), 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). This compound inhibits cell cycle progression, promotes differentiation, and induces apoptosis and autophagy in several types of cancer cells.
Sodium butyrate HDAC inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 110.09

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Cell Culture, Treatment & Working Concentration

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human K562 cells Proliferation assay 1 mM Antiproliferative activity against human K562 cells at 1 mM in presence of guanosine
human H1299 cells Function assay 7 days Inhibition of human USP1/UAF1 in human H1299 cells assessed as reduction in colony formation after 7 days, EC50=3 μM
human JEG3 cells Function assay Inhibition of aromatase in human JEG3 cells by scintillation spectrometry, IC50=0.0015 μM
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Chemical Information, Storage & Stability

Molecular Weight 110.09 Formula

C4H7NaO2

 Storage (From the date of receipt)
CAS No. 156-54-7 Download SDF Storage of Stock Solutions

Synonyms NaB, Butanoic acid sodium salt Smiles CCCC(=O)[O-].[Na+]

Solubility

In vitro
Batch:

Water : 22 mg/mL

Ethanol : 8 mg/mL

DMSO : Insoluble
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

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Mass Concentration Volume Molecular Weight

In vivo
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Mechanism of Action

Targets/IC50/Ki
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. This compound 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] It 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] This chemical inhibits most HDAC except class III HDAC and class II HDAC6 and -10. It also is the most effective fatty acid in stimulating or repressing the expression of specific genes. [4]
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). This compound also increases histone and specificity protein-1 acetylation and protects against 3-nitropropionic acid neurotoxicity. [5]
References
  • [4] https://pubmed.ncbi.nlm.nih.gov/12840228/
  • [5] https://pubmed.ncbi.nlm.nih.gov/14561870/
  • [6] https://pubmed.ncbi.nlm.nih.gov/649576/

Applications

Methods Biomarkers Images PMID
Western blot Cyclin D3 / CDK4 / CDK6 / CDK2 p15INK4b / p21Cip1 Phospho-H3 Ser10 / Acetyl-H3Lys9 / Acetyl-H3Lys14 / Dimethyl-H3 S1999-WB1 24280698
Immunofluorescence Acetyl-H3Lys9 S1999-IF1 24280698

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT00800930 Completed
Shigellosis
International Centre for Diarrhoeal Disease Research Bangladesh|Swedish International Development Cooperation Agency (SIDA)|Karolinska Institutet
 January 2005 Phase 2

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