PeptideDB

Budesonide

CAS: 51333-22-3 F: C25H34O6 W: 430.53

Budesonide, an inhaled glucocortical steroid, is an orally active glucocorticoid receptor agonist. Budesonide decreases
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Bioactivity Budesonide, an inhaled glucocortical steroid, is an orally active glucocorticoid receptor agonist. Budesonide decreases the size of lung tumors, reverses DNA hypomethylation and modulates mRNA expression of genes. Budesonide is an anti-inflammatory agent used for asthma[1][2][3].
Invitro Budesonide is selective for human glucocorticoid receptor (hGR; EC50=45.7 pM) over mineralocorticoid receptors (EC50=7,620 pM) in CV-1 cells[1]. Budesonide (30 min prior to LPS) suppresses the activation of the NLRP3 inflammasome by LPS (100 ng/mL) plus ATP (5 mM) in macrophages (RAW 264.7 cells)[2].
In Vivo Budesonide (2.0 mg/kg; orally via their diet; at 2, 7 and 21 days prior to killing) decreases the size of lung tumors[3]. Budesonide (0.5 mg/kg; intranasal administration 1 h before LPS injection (5 mg/kg)) pretreatment dramatically attenuates pathological injury and reduces pathological scores in mice with ALI in adult male C57BL/6 mice[2]. Animal Model:
Name Budesonide
CAS 51333-22-3
Formula C25H34O6
Molar Mass 430.53
Appearance Solid
Transport Room temperature in continental US; may vary elsewhere.
Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Reference [1]. Claudia Grossmann, et al. Transactivation via the Human Glucocorticoid and Mineralocorticoid Receptor by Therapeutically Used Steroids in CV-1 Cells: A Comparison of Their Glucocorticoid and Mineralocorticoid Properties. Eur J Endocrinol. 2004 Sep;151(3): [2]. Liang Dong, et al. Intranasal Application of Budesonide Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Suppressing Nucleotide-Binding Oligomerization Domain-Like Receptor Family, Pyrin Domain-Containing 3 Inflammasome Activation in Mice. J Imm [3]. Michael A Pereira, et al. Modulation by Budesonide of DNA Methylation and mRNA Expression in Mouse Lung Tumors. Int J Cancer. 2007 Mar 1;120(5):1150-3.