U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

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Showing 31 - 40 of 48 results

Status:
Other

Class (Stereo):
CHEMICAL (ACHIRAL)

Status:
Other

Class (Stereo):
CHEMICAL (ACHIRAL)

Status:
Other

Class (Stereo):
CHEMICAL (ACHIRAL)

Status:
Other

Class (Stereo):
CHEMICAL (ACHIRAL)

Status:
Possibly Marketed Outside US
Source:
Canada:VITAMIN A PROPIONATE
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

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.
Status:
First approved in 1990

Class (Stereo):
CHEMICAL (ABSOLUTE)



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.

Showing 31 - 40 of 48 results