Halobetasol Propionate is the propionate salt form of halobetasol, a synthetic corticosteroid with anti-inflammatory, antipruritic, and vasoconstrictor activities. Halobetasol, a topical steroid, diffuses across cell membranes to interact with cytoplasmic corticosteroid receptors located in both the dermal and intradermal cells, thereby activating gene expression of anti-inflammatory proteins mediated via corticosteroid receptor response element. Specifically, this agent induces phospholipase A2 inhibitory proteins, which inhibit the release of arachidonic acid, thereby inhibiting the biosynthesis of potent mediators of inflammation, such as prostaglandins and leukotrienes. As a result, halobetasol reduces edema, erythema, and pruritus through its cutaneous effects on vascular dilation and permeability. The initial interaction, however, is due to the drug binding to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes.

Fluticasone propionate, a medium-potency synthetic corticosteroid, is used topically to relieve inflammatory and pruritic symptoms of dermatoses and psoriasis, intranasally to manage symptoms of allergic and non-allergic rhinitis, and orally for the treatment of asthma. Fluticasone proprionate is marketed under several different brand names such as Flonase®. Fluticasone propionate is also available as a combination product of azelastine hydrochloride and fluticasone propionate called Dymista™. Dymista™ is indicated in patients over 12 years old for symptomatic relief of seasonal allergic rhinitis. Fluticasone propionate binds to the glucocorticoid receptor. Unbound corticosteroids cross the membranes of cells such as mast cells and eosinophils, binding with high affinity to glucocorticoid receptors (GR). The results include alteration of transcription and protein synthesis, a decreased release of leukocytic acid hydrolases, reduction in fibroblast proliferation, prevention of macrophage accumulation at inflamed sites, reduction of collagen deposition, interference with leukocyte adhesion to the capillary wall, reduction of capillary membrane permeability and subsequent edema, reduction of complement components, inhibition of histamine and kinin release, and interference with the formation of scar tissue. In the management of asthma, the glucocorticoid receptor complexes down-regulates proinflammatory mediators such as interleukin-(IL)-1, 3, and 5, and up-regulates anti-inflammatory mediators such as IkappaB [inhibitory molecule for nuclear factor kappaB1], IL-10, and IL-12. The antiinflammatory actions of corticosteroids are also thought to involve inhibition of cytosolic phospholipase A2 (through activation of lipocortin-1 (annexin)) which controls the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.

CLOBETASOL, a derivative of prednisolone with high glucocorticoid activity and low mineralocorticoid activity. Absorbed through the skin faster than fluocinonide, it is used topically in the treatment of psoriasis but may cause marked adrenocortical suppression. For short-term topical treatment of the inflammatory and pruritic manifestations of moderate to severe corticosteroid-responsive dermatoses of the scalp. Like other topical corticosteroids, clobetasol has anti-inflammatory, antipruritic, and vasoconstrictive properties. It is a very high potency topical corticosteroid that should not be used with occlusive dressings. Topical corticosteroids share anti-inflammatory, antipruritic, and vasoconstrictive properties. The mechanism of the anti-inflammatory activity of topical steroids is unclear. However, corticosteroids are thought to act by the 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. Initially, however, clobetasol, like other corticosteroids, bind to the glucocorticoid receptor, which complexes, enters the cell nucleus and modifies genetic transcription (transrepression/transactivation).

Josamycin propionate, a tasteless josamycin derivative suitable for the preparation of pediatric oral suspension. After oral administration Josamycin propionate underwent metabolic transformation to Josamycin, semi-synthetic 16-membered ring macrolide, that acts via protein synthesis inhibition.

Ticabesone Propionate is Ticabesone ester patented by Syntex, Inc. as an anti-inflammatory agent. Ticabesone Propionate shows potent antiinflammatory activity silver nitrate-induced inflammation in the rat cornea.

Cloticasone propionate is an ester of an antiinflammation steroid cloticasone.