For its use in cancer, its mechanism of action is unknown, but on a cellular level, laboratory tests show that<unk>  forces APL cells to differentiate and stops them from proliferating; in people there is evidence that it forces the primary cancerous promyelocytes to differentiate into their final form, allowing normal cells to take over the bone marrow. Recent study shows that ATRA inhibits and degrades active PIN1. For its use in acne,<unk>  (along with other retinoids) are vitamin A derivatives that act by binding to two nuclear receptor families within keratinocytes: the retinoic acid receptors (RAR) and the retinoid X receptors (RXR). These events contribute to the normalization of follicular keratinization and decreased cohesiveness of keratinocytes, resulting in reduced follicular occlusion and microcomedone formation. The retinoid-receptor complex competes for coactivator proteins of AP-1, a key<unk> nscription factor involved in inflammation. Retinoids also down-regulate expression of toll-like receptor (TLR)-2, which has been implicated in the inflammatory response in acne. Moreover,<unk>  and retinoids may enhance the penetration of other topical acne medications. The combination of the 10% benzoyl peroxide and light results in more than 50% degradation of<unk>  in about 2 hours and 95% in 24 hours. This lack of stability in the presence of light and oxidizing agents has led to the development of novel formulations of the drug. When microencapsulated<unk>  is exposed to benzoyl peroxide and light only 1% degradation takes place in about 4 hours and only 13% after 24 hours.
Tretinoin
Alitretinoin
Isotretinoin
Clobetasol
Clobetasol propionate
Ulobetasol propionate
Urodilatin
Bexarotene