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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 (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].

Falcarindiol (7 µg/g; diet) increases ABCA1 expression in neoplastic tissue in five weeks old male rats[2].

[1]. Tingting Lu, et al. Autophagy contributes to falcarindiol-induced cell death in breast cancer cells with enhanced endoplasmic reticulum stress. PLoS One. 2017 Apr 25;12(4):e0176348.

[2]. Camilla Bertel Andersen, et al. Falcarindiol Purified From Carrots Leads to Elevated Levels of Lipid Droplets and Upregulation of Peroxisome Proliferator-Activated Receptor-γ Gene Expression in Cellular Models. Front Pharmacol. 2020 Aug 28;11:565524.

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