Desocort0.25%
Cream
Desoximetasone
Incepta Pharmaceuticals Ltd.
Product Code : 4704
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Medicine overview
Indications of Desocort 0.25%
Desocort 0.25% Emollient Cream indicated for the relief of the inflammatory and pruritic manifestations of corticosteroid-inflammatory and pruritic manifestations of corticosteroid
Theropeutic Class
Other Topical corticosteroids
Pharmacology
The precise mechanism of the antiinflammatory activity of topical steroids in the treatment of steroid-responsive dermatoses, in general, is uncertain. However, corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. This is achieved first by the drug binding to the glucocorticoid receptors which then translocates into the nucleus and binds to DNA causing various activations and repressions of genes. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2.
Dosage & Administration of Desocort 0.25%
Apply a thin film of Desocort 0.25% Emollient Cream to the affected skin areas twice daily. Rub in gently
Dosage of Desocort 0.25%
Apply a thin film of Desocort 0.25% Emollient Cream to the affected skin areas twice daily. Rub in gently
Contraindications
Topical corticosteroids are contraindicated in those patients with a history of hypersensitivity to any of the components of the preparation.
Pregnancy & Lactation
Pregnancy Category C
Overdose Effects of Desocort 0.25%
Topically applied corticostero systemic effects
Drug Classes
Other Topical corticosteroids
Mode Of Action
The precise mechanism of the antiinflammatory activity of topical steroids in the treatment of steroid-responsive dermatoses, in general, is uncertain. However, corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. This is achieved first by the drug binding to the glucocorticoid receptors which then translocates into the nucleus and binds to DNA causing various activations and repressions of genes. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2.
Pregnancy
Pregnancy Category C
Disclaimer
The information provided is accurate to our best practices, but it does not replace professional medical advice. We cannot guarantee its completeness or accuracy. The absence of specific information about a drug should not be seen as an endorsement. We are not responsible for any consequences resulting from this information, so consult a healthcare professional for any concerns or questions.
