low price 51333-22-3 in stockBest price Budesonide CAS NO.51333-22-3

Budesonide (brand name: Pulmicort) is a synthetic corticosteroid medication. It is indicated for the maintenance and prophylactic treatment of asthma. It is also used for the long-term management of chronic obstructive pulmonary disease (COPD). It is also useful for the treatment of inflammatory bowel disease including Crohn’s disease, ulcerative colitis and microscopic colitis, and also for treating allergic rhinitis. It exhibits potent glucocorticoid activity and weak mineralocorticoid activity in vivo. It is effective in inhibiting the activities of multiple cell types and mediators participating in either allergic or non-allergic-mediated inflammation.

Budesonide is a glucocorticoid and an agonist of glucocorticoid receptors (EC₅₀ = 45.7 pM in a transactivation assay). It is selective for glucocorticoid over mineralocorticoid receptors (EC₅₀ = 7,620 pM). Budesonide inhibits LPS-induced TNF-α release from human peripheral blood mononuclear cells (PBMCs; IC₅₀ = 0.96 nM). It reduces levels of IL-1β and eotaxin in the lungs and the number of eosinophils and neutrophils in bronchoalveolar lavage fluid (BALF) in a rat model of ovalbumin-induced airway inflammation when administered at a dose of 3 mg/kg. Intracolonic administration of budesonide decreases colon wet weight and colonic myeloperoxidase (MPO) activity in a rat model of oxazolone-induced colitis. Formulations containing budesonide have been used in the treatment of Crohn's disease, ulcerative colitis, allergic rhinitis, and asthma.

Budesonide is composed of a 1:1 mixture of epimers of the 16,17-butylacetal, creating a chiral center. The 22R-epimer binds to the GR with higher affinity than does the 22S-epimer (Table 33.5). The butyl acetal chain provided the highest potency for the homologous acetal chains. Its rate of topical uptake into epithelial tissue is more than 100 times faster than that for hydrocortisone and dexamethasone. Approximately 85% of the IV administered dose of budesonide undergoes extensive first-pass hepatic metabolism by CYP3A4 to its primary metabolites, 6β-hydroxybudesonide and 16α-hydroxyprednisolone, which have approximately 1/100 the potency of budesonide. This is an important inactivation step in limiting budesonide's systemic effect on adrenal suppression.

The exact mechanism of action of budesonide in the treatment of Crohn's disease is not fully understood. However, being a glucocorticosteroid, budesonide has a high local anti-inflammatory effect.