Research Paper On Budesonide
Budesonide
Structure:
Chemical Formula : C25H34O6
Molecular Weight : 430.534 g/mol
IUPAC : 16,17-(butylidenebis(oxy))-11,21-dihydroxy-, (11-β,16-α)-pregna-1,4-diene-3,20-dione
Description : Budesonide is a glucocorticoid used in the management of asthma, the treatment of various skin disorders, and allergic rhinitis. [PubChem] The extended release oral tablet, marketed as Uceris, was FDA approved on January 14, 2013 for the management of ulcerative colitis. Budesonide is provided as a mixture of two epimers (22R and 22S). Interestingly, the 22R form is two times more active than the 22S epimer. The two forms do not interconvert.
Solubulity :. Soluble in DMSO (100 mM), ethanol (50 mM), chloroform,
Half life :Following IV administration of budesonide, the elimination half-life is 2.0 to 3.6 hours. This value does not differ between healthy adults and patients with Crohn’s disease.
Mechanism of action : Budesonide is an anti-inflammatory corticosteroid that exhibits potent glucocorticoid activity and weak mineralocorticoid activity. The precise mechanism of corticosteroid actions on inflammation in asthma, Crohn's disease, or ulcerative colitis is not …show more content…
known. Inflammation is an important component in the pathogenesis of asthma. Corticosteroids have been shown to have a wide range of inhibitory activities against multiple cell types (eg, mast cells, eosinophils, neutrophils, macrophages, and lymphocytes) and mediators (eg, histamine, eicosanoids, leukotrienes, and cytokines) involved in allergic and non-allergic-mediated inflammation. These anti-inflammatory actions of corticosteroids may contribute to their efficacy in the aforementioned diseases. Because budesonide undergoes significant first-pass elimination, the both oral preparations are formulated as an extended release tablet. As a result, budesonide release is delyaed until exposure to a pH ≥ 7 in the small intestine.
Formoterol
Structure:
Chemical formula : C19H24N2O4
Molecular Weight : 344.405 g/mol
IUPAC :rac-(R,R)-N-[2-hydroxy-5-[1-hydroxy-2-[1-(4-methoxy phenyl) propan-2-ylamino]ethyl] phenyl] formamide
Category : Sympathomimetics Adrenergic beta-2 Receptor Agonists BronchodilatorAgents
Description : Formoterol is a long-acting (12 hours) beta2-agonist used in the management of asthma and/or chronic obstructive pulmonary disease (COPD). Inhaled formoterol works like other beta2-agonists, causing bronchodilatation through relaxation of the smooth muscle in the airway so as to treat the exacerbation of asthma.
Pharmacodynamics : Formoterol is a long-acting selective beta2-adrenergic receptor agonist (beta2-agonist).
Inhaled formoterol fumarate acts locally in the lung as a bronchodilator. In vitro studies have shown that formoterol has more than 200-fold greater agonist activity at beta2-receptors than at beta1- receptors. Although beta2-receptors are the predominant adrenergic receptors in bronchial smooth muscle and beta1-receptors are the predominant receptors in the heart, there are also beta2-receptors in the human heart comprising 10%-50% of the total beta-adrenergic receptors. The precise function of these receptors has not been established, but they raise the possibility that even highly selective beta2- agonists may have cardiac
effects.
Mechanism of Action: The pharmacologic effects of beta2-adrenoceptor agonist drugs, including formoterol, are at least in part attributable to stimulation of intracellular adenyl cyclase, the enzyme that catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-3', 5'-adenosine monophosphate (cyclic AMP). Increased cyclic AMP levels cause relaxation of bronchial smooth muscle and inhibits the release of pro-inflammatory mast-cell mediators such as histamine and leukotrienes. Formoterol also inhibits histamine-induced plasma albumin extravasation in anesthetized guinea pigs and inhibits allergen-induced eosinophil influx in dogs with airway hyper-responsiveness. The relevance of these in vitro and animal findings to humans is unknown.
Absorption: Rapidly absorbed into plasma following administration by oral inhalation. It is likely that the majority of the inhaled formoterol delivered is swallowed and then absorbed from the gastrointestinal tract.
Metabolism: Metabolized primarily by direct glucuronidation at either the phenolic or aliphatic hydroxyl group and O-demethylation followed by glucuronide conjugation at either phenolic hydroxyl groups. Minor pathways involve sulfate conjugation of formoterol and deformylation followed by sulfate conjugation. The most prominent pathway involves direct conjugation at the phenolic hydroxyl group. The second major pathway involves O-demethylation followed by conjugation at the phenolic 2'-hydroxyl group. Four cytochrome P450 isozymes (CYP2D6, CYP2C19, CYP2C9 and CYP2A6) are involved in the O-demethylation of formoterol.
Half life: 10 hours
Structure:
Chemical Formula : C25H34O6
Molecular Weight : 430.534 g/mol
IUPAC : 16,17-(butylidenebis(oxy))-11,21-dihydroxy-, (11-β,16-α)-pregna-1,4-diene-3,20-dione
Description : Budesonide is a glucocorticoid used in the management of asthma, the treatment of various skin disorders, and allergic rhinitis. [PubChem] The extended release oral tablet, marketed as Uceris, was FDA approved on January 14, 2013 for the management of ulcerative colitis. Budesonide is provided as a mixture of two epimers (22R and 22S). Interestingly, the 22R form is two times more active than the 22S epimer. The two forms do not interconvert.
Solubulity :. Soluble in DMSO (100 mM), ethanol (50 mM), chloroform,
Half life :Following IV administration of budesonide, the elimination half-life is 2.0 to 3.6 hours. This value does not differ between healthy adults and patients with Crohn’s disease.
Mechanism of action : Budesonide is an anti-inflammatory corticosteroid that exhibits potent glucocorticoid activity and weak mineralocorticoid activity. The precise mechanism of corticosteroid actions on inflammation in asthma, Crohn's disease, or ulcerative colitis is not …show more content…
known. Inflammation is an important component in the pathogenesis of asthma. Corticosteroids have been shown to have a wide range of inhibitory activities against multiple cell types (eg, mast cells, eosinophils, neutrophils, macrophages, and lymphocytes) and mediators (eg, histamine, eicosanoids, leukotrienes, and cytokines) involved in allergic and non-allergic-mediated inflammation. These anti-inflammatory actions of corticosteroids may contribute to their efficacy in the aforementioned diseases. Because budesonide undergoes significant first-pass elimination, the both oral preparations are formulated as an extended release tablet. As a result, budesonide release is delyaed until exposure to a pH ≥ 7 in the small intestine.
Formoterol
Structure:
Chemical formula : C19H24N2O4
Molecular Weight : 344.405 g/mol
IUPAC :rac-(R,R)-N-[2-hydroxy-5-[1-hydroxy-2-[1-(4-methoxy phenyl) propan-2-ylamino]ethyl] phenyl] formamide
Category : Sympathomimetics Adrenergic beta-2 Receptor Agonists BronchodilatorAgents
Description : Formoterol is a long-acting (12 hours) beta2-agonist used in the management of asthma and/or chronic obstructive pulmonary disease (COPD). Inhaled formoterol works like other beta2-agonists, causing bronchodilatation through relaxation of the smooth muscle in the airway so as to treat the exacerbation of asthma.
Pharmacodynamics : Formoterol is a long-acting selective beta2-adrenergic receptor agonist (beta2-agonist).
Inhaled formoterol fumarate acts locally in the lung as a bronchodilator. In vitro studies have shown that formoterol has more than 200-fold greater agonist activity at beta2-receptors than at beta1- receptors. Although beta2-receptors are the predominant adrenergic receptors in bronchial smooth muscle and beta1-receptors are the predominant receptors in the heart, there are also beta2-receptors in the human heart comprising 10%-50% of the total beta-adrenergic receptors. The precise function of these receptors has not been established, but they raise the possibility that even highly selective beta2- agonists may have cardiac
effects.
Mechanism of Action: The pharmacologic effects of beta2-adrenoceptor agonist drugs, including formoterol, are at least in part attributable to stimulation of intracellular adenyl cyclase, the enzyme that catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-3', 5'-adenosine monophosphate (cyclic AMP). Increased cyclic AMP levels cause relaxation of bronchial smooth muscle and inhibits the release of pro-inflammatory mast-cell mediators such as histamine and leukotrienes. Formoterol also inhibits histamine-induced plasma albumin extravasation in anesthetized guinea pigs and inhibits allergen-induced eosinophil influx in dogs with airway hyper-responsiveness. The relevance of these in vitro and animal findings to humans is unknown.
Absorption: Rapidly absorbed into plasma following administration by oral inhalation. It is likely that the majority of the inhaled formoterol delivered is swallowed and then absorbed from the gastrointestinal tract.
Metabolism: Metabolized primarily by direct glucuronidation at either the phenolic or aliphatic hydroxyl group and O-demethylation followed by glucuronide conjugation at either phenolic hydroxyl groups. Minor pathways involve sulfate conjugation of formoterol and deformylation followed by sulfate conjugation. The most prominent pathway involves direct conjugation at the phenolic hydroxyl group. The second major pathway involves O-demethylation followed by conjugation at the phenolic 2'-hydroxyl group. Four cytochrome P450 isozymes (CYP2D6, CYP2C19, CYP2C9 and CYP2A6) are involved in the O-demethylation of formoterol.
Half life: 10 hours