The primary therapeutic effect of Betamethasone dipropionate is due to the anti-inflammatory activity which is nonspecific. Topically applied glucocorticoids like Betamethasone dipropionate binds with receptor proteins in the cytoplasm of target cells. This leads to the formation of phospholipase A2inhibitory proteins, collectively called lipocortins. Phospholipase A2 is known to catalyse the conversion of membrane phospholipids to Arachidonic acid. Arachidonic acid binds with cyclo-oxygenase to form highly inflammatory prostaglandins, PGE2. Lipocortins inhibits phopholipase A2,and thereby controls the biosynthesis of potent mediators of inflammation like prostaglandin E2(PGE2) and leukotrienes, kinins, histamine, liposomal enzymes and the complement system. When applied to inflamed area of skin Betamethasone dipropionate inhibits the migration of leukocytes into the area by reversing vascular dilatation and permeability. The clinical result is a decrease in edema (swelling), erythema and pruritus. Betamethasone dipropionate falls under the category of very potent corticosteroids with a vasconstrictor potency index of 1660. Due to double esterification at positions 17&21, Betamethasone becomes very lipophilic thereby offering better penetration.

Salicylic Acid in STERNON –S is a Keratolytic agent causing desquamation of stratum corneum, thereby ensuring better penetration of Betamethasone Dipropionate. The mechanism of action of topical salicylic acid may include two pathway, both leading to desquamation of corneocytes. Salicylic acid reduces intercellular cohesiveness of the horny cells by dissolving the intercellular cement material. Salicylic acid also reduces the pH of the stratum corneum, thereby increasing hydration and softening.