Falcarindiol

Falcarindiol, an orally active polyacetylenic oxylipin, activates PPARγ and increases the expression of the cholesterol transporter ABCA1 in cells. Falcarindiol induces apoptosis and autophagy. Falcarindiol has anti-inflammatory, antifungal, anticancer and antidiabetic properties^[1][2]. Falcarindiol is a click chemistry reagent, itcontains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups. In Vitro: Falcarindiol (3, 6, 12, 24 μM; for 24 hours) significantly decreases cell viability of MDA-MB-231 and MDA-MB-468 cells. Cell viability of MCF-10A cells is unchanged until the dose of Falcarindiol reaches to 24 uM. Falcarindiol preferentially induces cell death in breast cancer cells^[1].
Falcarindiol (6 uM; for 2 hours) induces autophagy and causes significant level of LC3-I converted to LC3-II in MDA-MB-231, MDA-MB-468 and SKBR3 cells^[1].
Falcarindiol (6 uM; for 2, 4, 8, 24 hours) increases the level of GRP78 in MDA-MB-231 cells in dose- and time-dependent manner^[1].
Falcarindiol (1-20 μM) has no effect on hMSCs and HT-29 cell viability. Falcarindiol with only concentrations above 50 μM exhibits a toxic effect on the cells^[2].
Falcarindiol (5 μM; 10 min, 1 h and 24 h) causes a significant upregulation on PPARγ2 expression at 24 h^[2].
In Vivo: Falcarindiol (7 μg/g; diet) increases ABCA1 expression in neoplastic tissue in five weeks old male rats^[2].