Retinyl propionate is a synthetic derivative of a Vitamin A. Upon topical application, retinyl propionate is hydrolyzed by esterases to retinol, which is ultimately converted to retinoic acid. In mouse models, retinyl propionate induced epidermal thickening in mouse tail and promoted collagen formation in UV-irradiated mice. These results encouraged clinical trials of retinyl palmitate against photoaging. Topical retinyl propionate cream (0.15%) did not demonstrate any statistically significant improvement over placebo, but in later studies of combinations of retinyl propionate with climbazole or niacinamide improvements in the appearance of fine lines, wrinkles and age spots were demonstrated.

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.

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).