当前位置:首页 > Sodium butyrate 156-54-7 GlpBio
Peptides, Inhibitors, Agonists
www.glpbio.com
Product Data Sheet
Product Name:Cat. No.:
Sodium butyrateGC15857
Chemical Properties
Cas No.ChemicalNameCanonicalSMILESFormulaSolubilityGeneraltipsShippingCondition
156-54-7
sodium;butanoateCCCC(=O)[O-].[Na+]C4H7NaO2
≥4mg/mL in H2O
M.WtStorage
110.09Store at -20°C
For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in theultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.Evaluation sample solution : ship with blue ice All other available size: ship with RT , orblue ice upon request.
Structure
Caution: Producthasnot been fully validated for medical applications. For research use only.
Tel: (626) 353-8530 Fax: (626) 353-8530 E-mail: tech@glpbio.com
Address: 10292 Central Ave. #205, Montclair, CA, USA
1www.glpbio.com
Peptides, Inhibitors, Agonists
www.glpbio.com
Product Data Sheet
实验参考方法
Cell experiment [1]:Cell lines2 adenoma-derived cell lines (AA/Cl and RG/C2)
The solubility of this compound in DMSO is limited. General tips for obtaining ahigher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake
Preparation method
it in the ultrasonic bath for a while. Stock solution can be stored below - 20 °C forseveral months.
Reacting condition1 ~ 4 mM; 4 days
In RG/C2 cells, Sodium Butyrate at the concentrations of 2 mM and abovereduced the attached-cell yield to approximately 50% of the control, and
signi?cantly increased the proportion of ?oating cells. It was demonstrated that
Applications
the increase in the percentage of ?oating cells was attributed to the induction ofapoptosis 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 modelsAn R6/2 transgenic mouse model of Huntington's disease (HD)Dosage form100, 200, 400, 600, 1200, 5000 and 10,000 mg/kg; i.p.; q.d.
In an R6/2 transgenic mouse model of HD, Sodium Butyrate signi?cantly
extended survival in a dose-dependent manner, improved body weight and motor
Applicationsperformance, as well as delayed the neuropathological sequelae. Moreover,
Sodium Butyrate increased the level of histone and speci?city protein-1
acetylation, and protected against 3-nitropropionic acid-induced neurotoxicity.Please test the solubility of all compounds indoor, and the actual solubility may
Other notesslightly di?er 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 inducesapoptosis in human colonic tumour cell lines in a p53-independent pathway: implications for thepossible role of dietary ?bre in the prevention of large-bowel cancer. Int J Cancer. 1993 Sep30;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 amelioratesthe neurodegenerative phenotype in Huntington's disease mice. J Neurosci. 2003 Oct15;23(28):9418-27.
Background
Sodium butyrate is a short chain fatty acid that has e?ects at the molecular, cellular, and tissue level.It has long been known as an inhibitor of histone deacetylases (HDACs).[1],[2] In cells, this alters the
Caution: Producthasnot been fully validated for medical applications. For research use only.
Tel: (626) 353-8530 Fax: (626) 353-8530 E-mail: tech@glpbio.com
Address: 10292 Central Ave. #205, Montclair, CA, USA
2www.glpbio.com
Peptides, Inhibitors, Agonists
www.glpbio.com
Product Data Sheet
expression of a select group of genes containing butyrate response elements and may also involveSp1/Sp3 binding sites.[3] Sodium butyrate also induces growth arrest, di?erentiation and apoptosis incancer cells, primarily through its e?ects on HDAC activity.[4] In addition, it suppresses in?ammation,in part by reducing the expression of pro-in?ammatory cytokines, including interferon-γ, interleukin(IL)-6, and IL-1β.[5]
Reference:
[1]. Bo?a, L.C., Vidali, G., Mann, R.S., et al. Suppression of histone deacetylation in vivo and in vitro bysodium butyrate. The Journal of Biological Chemisty 253(10), 3364-3366 (1978).
[2]. Sealy, L., and Chalkley, R. The e?ect of sodium butyrate on histone modi?cation. Cell 14, 115-121(1978).
[3]. Davie, J.R. Inhibition of histone deacetylase activity by butyrate. Journal of Nutrition 133,2485-2493 (2003).
[4]. Monneret, C. Inhibition of histone deacetylase activity by butyrate. European Journal of MedicinalChemistry 40, 1-13 (2005).
[5]. Joseph, J., Mudduluru, G., Antony, S., et al. Expression pro?ling of sodium butyrate (NaB)-treatedcells: identi?cation of regulation of genes related to cytokine signaling and cancer metastasis by NaB.Oncogene 23, 6304-6315 (2004).
Caution: Producthasnot been fully validated for medical applications. For research use only.
Tel: (626) 353-8530 Fax: (626) 353-8530 E-mail: tech@glpbio.com
Address: 10292 Central Ave. #205, Montclair, CA, USA
3www.glpbio.com
共分享92篇相关文档