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product name Budesonide


Description: Budesonide is a glucocorticoid steroid for the treatment of asthma, non-infectious rhinitis, and for treatment and prevention of nasal polyposis. Additionally, it is used for Crohns disease (inflammatory bowel disease). Budesonide has shown the potent glucocorticoid activity and little mineralocorticoid activity. In addition, Budesonide has been reported to have a wide range of inhibitory activities against multiple cells types and mediators involved in allergic and nonallergic-mediated inflammatory. 

References: J Immunol. 1999 Nov 15;163(10):5624-32; Vascul Pharmacol. 2005 Aug;43(2):101-11.



Molecular Weight (MW)

430.53
Formula

C25H34O6
CAS No.

51333-22-3
Storage

-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)

DMSO: 86 mg/mL (199.7 mM)
Water: <1 mg/mL
Ethanol: 19 mg/mL (44.1 mM)
Solubility (In vivo)

 
Synonyms

 

other peoduct :References PubMed ID::http://www.ncbi.nlm.nih.gov/pubmed/19422622

In Vitro

In vitro activity: Budesonide effectively inhibits production of eotaxin and RANTES protein although Budesonide inhibits the expression of chemokine mRNA to a variable extent in the human bronchial epithelial cell line BEAS-2B and in primary human bronchial epithelial cells. Budesonide inhibits both RANTES- and eotaxin promoter-driven reporter gene activity in the human bronchial epithelial cell line BEAS-2B and in primary human bronchial epithelial cells. Budesonide also selectively accelerates the decay of eotaxin and MCP-4 mRNA in the human bronchial epithelial cell line BEAS-2B and in primary human bronchial epithelial cells. Budesonide time- and protein synthesis-dependently reduces VEGF secretion and VEGF mRNA expression in both cell types and these effects are inhibited by mifepristone (RU 486), a glucocorticoid receptor antagonist, suggesting that Budesonide reduces VEGF secretion and expression through its glucocorticoid receptor-mediated action. Budesonide causes a dose-dependent, almost total, inhibition of swine dust-induced IL-6 and IL-8 release from epithelial cells and LPS-induced IL-6 and TNF-alpha from alveolar macrophages.


Kinase Assay


Cell Assay

In Vivo Budesonide totally prevents the increased production of TNF-alpha, interleukin (IL)-1beta, IL-6, and monocyte chemoattractive protein (MCP)-1 after LPS challenge at both low (2.5 mg/mL/kg) and high (50 mg/mL/kg) concentrations in rats. Budesonide exerts its effects of chemoprevention through growth arrest via Mad2/3 and through apoptosis via Bim/Blk and, by inference, caspase-8/9 in A/J mice. 
Animal model  
Formulation & Dosage  
References J Immunol. 1999 Nov 15;163(10):5624-32; Vascul Pharmacol. 2005 Aug;43(2):101-11.

A-443655

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Author: Sodium channel