Betamethasone Pharmacology 

Betamethasone
Betamethasone
Potent glucocorticoid, Anti-inflammatory, immunosuppressent.
Potent glucocorticoid, Anti-inflammatory, immunosuppressent.
The drug exerts it`s pharmacological action by penetrating and binding to cytoplasmic receptor protein and causes a structural change in steroid receptor complex. This structural change allows it`s migration in to the nucleus and then binding to specific sites on the DNA which leads to transcription of specific m-RNA and which ultimately regulates protein synthesis. It exerts highly selective glucocorticoid action. It stimulates the enzymes needed to decrease the inflammatory response.
The drug exerts anti-inflammatory and immunosuppressant actions as follows: – 1) Induce lipocortins in macrophages, endothelium, and fibroblasts which inhibits phospholipase A2 and thus decreases the production of Prostaglandins, leukotriens (LT), and platelet activating factor, 2) Causes negative regulation of genes for cytokines in macrophages, endothelial cells and lymphocytes and thus decreases the production of interleukins (IL-1, IL-2, IL-3, IL-6), TNF-alpha, GM-CSF (granulocyte macrophage colony stimulating factor), Gama interferon and suppresses fibroblast proliferation and T-lymphocyte functions and interferes chemotaxis. 3) Decreases the production of acute phase reactants from macrophages and endothelial cells and interferes complement function. 4) Decreases the production of ELAM-1(Endothelial leukocyte adhesion molecule-1) and ICAM- 1(intracellular adhesion molecule-1) in endothelial cells. 5) Inhibit IgE mediated histamine and LT-C4 release from basophiles and the effects of antigen-antibody reaction is not mediated 6) Reduces the production of
collagenase and stromolysin and thus prevents tissue destruction.
The drug exerts it`s pharmacological action by penetrating and binding to cytoplasmic receptor protein and causes a structural change in steroid receptor complex. This structural change allows it`s migration in to the nucleus and then binding to specific sites on the DNA which leads to transcription of specific m-RNA and which ultimately regulates protein synthesis. It exerts highly selective glucocorticoid action. It stimulates the enzymes needed to decrease the inflammatory response.
The drug exerts anti-inflammatory and immunosuppressant actions as follows: – 1) Induce lipocortins in macrophages, endothelium, and fibroblasts which inhibits phospholipase A2 and thus decreases the production of Prostaglandins, leukotriens (LT), and platelet activating factor, 2) Causes negative regulation of genes for cytokines in macrophages, endothelial cells and lymphocytes and thus decreases the production of interleukins (IL-1, IL-2, IL-3, IL-6), TNF-alpha, GM-CSF (granulocyte macrophage colony stimulating factor), Gama interferon and suppresses fibroblast proliferation and T-lymphocyte functions and interferes chemotaxis. 3) Decreases the production of acute phase reactants from macrophages and endothelial cells and interferes complement function. 4) Decreases the production of ELAM-1(Endothelial leukocyte adhesion molecule-1) and ICAM- 1(intracellular adhesion molecule-1) in endothelial cells. 5) Inhibit IgE mediated histamine and LT-C4 release from basophiles and the effects of antigen-antibody reaction is not mediated 6) Reduces the production of
collagenase and stromolysin and thus prevents tissue destruction.
Absorption: Well absorbed orally, Distribution: Distributed in to muscle, liver, kidney, skin, and intestine. It crosses the placenta and also secreted in breast milk, Metabolism: Metabolized in liver in to inactive metabolites by glucuronide and sulfate conjugation. Excretion: Metabolites are excreted mainly through urine and a small amount is excreted through faeces.
Topical:-Absorption: It is absorbed in to the systemic circulation and the amount is depending on the potency,
amount applied and the nature of the skin at the site of application. Absorption increases at the site of skin damage, inflammation or occlusion
Absorption: Well absorbed orally, Distribution: Distributed in to muscle, liver, kidney, skin, and intestine. It crosses the placenta and also secreted in breast milk, Metabolism: Metabolized in liver in to inactive metabolites by glucuronide and sulfate conjugation. Excretion: Metabolites are excreted mainly through urine and a small amount is excreted through faeces.
Topical:-Absorption: It is absorbed in to the systemic circulation and the amount is depending on the potency,
amount applied and the nature of the skin at the site of application. Absorption increases at the site of skin damage, inflammation or occlusion
Absorption: Well absorbed orally, Distribution: Distributed in to muscle, liver, kidney, skin, and intestine. It crosses the placenta and also secreted in breast milk, Metabolism: Metabolized in liver in to inactive metabolites by glucuronide and sulfate conjugation. Excretion: Metabolites are excreted mainly through urine and a small amount is excreted through faeces.
Topical:-Absorption: It is absorbed in to the systemic circulation and the amount is depending on the potency,
amount applied and the nature of the skin at the site of application. Absorption increases at the site of skin damage, inflammation or occlusion
Absorption: Well absorbed orally, Distribution: Distributed in to muscle, liver, kidney, skin, and intestine. It crosses the placenta and also secreted in breast milk, Metabolism: Metabolized in liver in to inactive metabolites by glucuronide and sulfate conjugation. Excretion: Metabolites are excreted mainly through urine and a small amount is excreted through faeces.
Topical:-Absorption: It is absorbed in to the systemic circulation and the amount is depending on the potency,
amount applied and the nature of the skin at the site of application. Absorption increases at the site of skin damage, inflammation or occlusion
3 to 25 days
3 to 25 days
36 to 54 hours
36 to 54 hours