@article{ajbr2013131,
author={AUTHOR = {Kim, Dong-Chan and Rho, Seong-Hwan and Kim, Dongjin and Kim, Sung In and Jang, Chul-Soo and Ryu, Jae Ki and Kim, Byung Weon and Kweon, Chang Oh and Kim, Hyun-kyung and Lee, Suk Jun},
title={Coumarin, a Lead Compound of Warfarin, Inhibits Melanogenesis via Blocking Adenylyl Cyclase},
journal={American Journal of Biomedical Research},
volume={1},
number={3},
pages={43--47},
year={2013},
url={http://pubs.sciepub.com/ajbr/1/3/1},
issn={2328-3955},
abstract={Due to Its multiple biological activities, coumarin (a main ingredient of Cinnamon extracts) has gained attention as potentially useful therapeutics for various diseases. However, the efficacy of coumarin for the use of dermatological health has not been fully explored. To clarify the action mechanism of the skin protecting property of coumarin, we firstly investigated the molecular docking property of coumarin on the mammalian adenylyl cyclase, which is the key enzyme of cAMP-induced melanogenesis in the skin cells. In binding study, the benzopyran moiety of coumarin occupies dual sites of the hydrophobic cleft at the interface of two subunits of adenylyl cyclase. We also examined the involvement of coumarin in alpha-MSH and forskolin induced cAMP signaling within a cell based assay. In addition, we inquired into the inhibitory effect of coumarin on melanogenesis and found that the pretreatment with coumarin inhibited the forskolin-induced melanin contents significantly without annihilating the cell viability. Our results strongly suggest that coumarin directly inhibits the activity of adenylyl cyclase, downregulates forskolin-induced cAMP-production pathway, consequently inhibiting melanogenesis. Thus, coumarin may also be used as an effective inhibitor of hyperpigmentation.},
doi={10.12691/ajbr-1-3-1}
publisher={Science and Education Publishing}
}