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Dermex
Clobetasol Propionate
Description:
Clobetasol Propionate (Dermex®) ointment and cream is a synthetic corticosteriod, for topical dermatologic use.
Clobetasol Propionate (Dermex®) ointment and cream is a synthetic corticosteriod, for topical dermatologic use.
Indications:
Initial control of all forms of hyperacute eczema in all age groups (in children for no longer than a few days); chronic hyperkeratotic eczema of the hands and feet and patches of chronic lichen simplex; chronic hyperkeratotic psoriasis of any area of the body; severe acute photosensitivity; hypertrophic lichen planus; localized bullous disorders; keloid scarring; pretibial myxoedema; vitiligo; suppression of reaction after cryotherapy.
Initial control of all forms of hyperacute eczema in all age groups (in children for no longer than a few days); chronic hyperkeratotic eczema of the hands and feet and patches of chronic lichen simplex; chronic hyperkeratotic psoriasis of any area of the body; severe acute photosensitivity; hypertrophic lichen planus; localized bullous disorders; keloid scarring; pretibial myxoedema; vitiligo; suppression of reaction after cryotherapy.
Mode of Action:
Like other topical corticosteroids, clobetasol propionate has anti-inflammatory, antipruritic and vasoconstrictive properties. The mechanism of the anti-inflammatory activity of the topical steroids, in general, is unclear. However, corticosteroids are thought to act by induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. 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.
Like other topical corticosteroids, clobetasol propionate has anti-inflammatory, antipruritic and vasoconstrictive properties. The mechanism of the anti-inflammatory activity of the topical steroids, in general, is unclear. However, corticosteroids are thought to act by induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. 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.
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