Cafestol

Cafestol is an orally active diterpenoid and an inhibitor of ERK2. Cafestol has elevated blood lipids, anti-inflammatory, anti-angiogenic and anti-diabetic activities. In addition, Cafestol induces tumor cell apoptosis and autophagy, which can be used in the study of cancer^[1][2][3][4]. In Vitro: Cafestol (0-100 μM; 6-24 h) inhibits PGE₂ production in a dose-dependent manner, with an IC₅₀ of 45.7 μM, and decreases COX-2 mRNA levels in LPS (HY-D1056) treated macrophages^[1].
Cafestol (0-100 μM; 1 h) inhibits AP-1 activation and ERK2 activity in LPS (HY-D1056) treated macrophages^[1].
Cafestol (0-80 μM; 6-24 h) inhibits the proliferation, migration and lumen formation of human umbilical vein endothelial cells by inhibiting the phosphorylation of FAK, Akt and the production of NO^[2].
Cafestol (20-80 μM; 24-72 h) inhibits the proliferation of HCT116 cells and induces autophagy through LKB1/AMPK/ULK1 pathway^[3]. In Vivo: Cafestol (40-80 mg/kg; oral gavage ; 20 days) has antitumor effect in xenografted mouse model of colon cancer^[3].
Cafestol (0.4-1.1 mg/day; feed administration; 10 weeks) shows antidiabetic activity in KKAy mice^[4].