tretinoin

small molecule

12.1 Mechanism of Action Although tretinoin activates three members of the retinoic acid (RAR) nuclear receptors (RARα, RARβ, and RARγ) which may act to modify gene expression, subsequent protein synthesis, and epithelial cell growth and differentiation, it has not been established whether the clinical effects of tretinoin are mediated through activation of retinoic acid receptors and/or other mechanisms. The exact mechanism of action of topical tretinoin for treatment of acne vulgaris is unknown. Current evidence suggests that topical tretinoin decreases cohesiveness of follicular epithelial cells with decreased microcomedone formation. Additionally, tretinoin stimulates mitotic activity and increased turnover of follicular epithelial cells causing extrusion of the comedones.

Retinoic acid receptor alpha, Retinoic acid receptor beta, Retinoic acid receptor gamma, Retinoic acid receptor RXR-beta, Retinoic acid receptor RXR-gamma, Retinoic acid receptor RXR-alpha, Cellular retinoic acid-binding protein 1, Retinoic acid receptor responder protein 1, Aldehyde dehydrogenase 1A1, Retinal dehydrogenase 2, Retinoic acid-induced protein 3, Lipocalin-1, Odorant-binding protein 2a, Retinol-binding protein 4, [Pyruvate dehydrogenase (acetyl-transferring)] kinase isozyme 4, mitochondrial, Carcinoembryonic antigen

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acne vulgaris — FDA

vitiligo, acne vulgaris

2026-04-19