Auriculasin is an anticancer agent that inhibits VEGFR2, PI3K/AKT/mTOR, MAPK. Auriculasin can inhibit cell proliferation, induce cell apoptosis, and inhibit angiogenesis, and promotes mitochondrial oxidative stress and ferroptosis. Auriculasin is also active at the cannabinoid receptor CB1 with an IC50 of 8.92 μM. Auriculasin can be used in cancer research, especially related diseases such as prostate cancer and non-small cell lung cancer, as well as research on the development of anti-angiogenic drugs [1] [2] [3] [4] [5].
In Vivo, Auriculasin (5, 10 μg/mL; subcutaneous injection; single dose) reduces hemoglobin content, endothelial cell accumulation and VEGF expression and inhibited angiogenesis in the C57BL/6 mouse model[1]. Auriculasin (5, 10 mg/kg; oral gavage; once every 2 days; 21 days) reduces tumor size, weight and volume in the nude mouse LNCaP prostate cancer xenograft model without significant toxicity[3].
In Vitro, Auriculasin (2.5-10 μM; 6-24 h) inhibits the proliferation of human umbilical vein endothelial cells (HUVECs) in a dose- and time-dependent manner[1]. Auriculasin (5-10 μM; 12 h) inhibits VEGF-induced migration and invasion of HUVECs[1]. Auriculasin (5-10 μM; 6 h) inhibits the formation of capillary-like structures in HUVECs[1]. Auriculasin (5-10 μM; 6 days) inhibits microvascular sprouting in rat aortic rings[1]. Auriculasin (5-10 μM; 24 h or 30 min-1 h) downregulates the expression of Bcl-2, Bcl-XL, and VEGF in HUVECs, and inhibits the phosphorylation of VEGFR2 and its downstream Akt, mTOR, etc.[1]. Auriculasin (2.5-10 μM; 24 h) inhibits the viability of RC-58T/h/SA#4 primary prostate cancer cells, and the effect is more significant when combined with TRAIL, and has low toxicity to RWPE-1 prostate epithelial cells[2]. Auriculasin (5 μM) combined with TRAIL (100 ng/mL; 24 h) induces apoptosis of RC-58T/h/SA#4 cells[2]. Auriculasin (1-10 μM; 24 h) reduces the viability of LNCa P prostate cancer cells and has no effect on RWPE-1 cells[3]. Auriculasin (1-5 μM; 24 h) induces apoptosis of LNCaP cells, which is manifested by an increase in the sub-G1 population and DNA fragmentation[3]. Auriculasin (2.5-5 μM; 12-24 h) increases ROS generation in LNCaP cells[3]. Auriculasin reduces NSCLC A549 cell viability and promotes mitochondrial oxidative stress and ferroptosis[4].
References:
[1]. Cho HD, et al. Effects of auriculasin on vascular endothelial growth factor (VEGF)-induced angiogenesis via regulation of VEGF receptor 2 signaling pathways in vitro and in vivo. Food Chem Toxicol. 2018 Nov;121:612-621.
[2]. Cho HD, et al. Auriculasin sensitizes primary prostate cancer cells to TRAIL-mediated apoptosis through up-regulation of the DR5-dependent pathway. Food Chem Toxicol. 2019 Apr;126:223-232.
[3]. Cho HD, et al. Auriculasin-induced ROS causes prostate cancer cell death via induction of apoptosis. Food Chem Toxicol. 2018 Jan;111:660-669.
[4]. Wang X, et al. Auriculasin induces mitochondrial oxidative stress and drives ferroptosis by inhibiting PI3K/Akt pathway in non-small cell lung cancer. Naunyn Schmiedebergs Arch Pharmacol. 2025 Jan;398(1):967-977.
[5]. Dizamatova A, et al. A New Prenylated Isoflavonoid From Limonium leptophyllum. Natural Product Communications. May 2019.
In Vivo, Auriculasin (5, 10 μg/mL; subcutaneous injection; single dose) reduces hemoglobin content, endothelial cell accumulation and VEGF expression and inhibited angiogenesis in the C57BL/6 mouse model[1]. Auriculasin (5, 10 mg/kg; oral gavage; once every 2 days; 21 days) reduces tumor size, weight and volume in the nude mouse LNCaP prostate cancer xenograft model without significant toxicity[3].
In Vitro, Auriculasin (2.5-10 μM; 6-24 h) inhibits the proliferation of human umbilical vein endothelial cells (HUVECs) in a dose- and time-dependent manner[1]. Auriculasin (5-10 μM; 12 h) inhibits VEGF-induced migration and invasion of HUVECs[1]. Auriculasin (5-10 μM; 6 h) inhibits the formation of capillary-like structures in HUVECs[1]. Auriculasin (5-10 μM; 6 days) inhibits microvascular sprouting in rat aortic rings[1]. Auriculasin (5-10 μM; 24 h or 30 min-1 h) downregulates the expression of Bcl-2, Bcl-XL, and VEGF in HUVECs, and inhibits the phosphorylation of VEGFR2 and its downstream Akt, mTOR, etc.[1]. Auriculasin (2.5-10 μM; 24 h) inhibits the viability of RC-58T/h/SA#4 primary prostate cancer cells, and the effect is more significant when combined with TRAIL, and has low toxicity to RWPE-1 prostate epithelial cells[2]. Auriculasin (5 μM) combined with TRAIL (100 ng/mL; 24 h) induces apoptosis of RC-58T/h/SA#4 cells[2]. Auriculasin (1-10 μM; 24 h) reduces the viability of LNCa P prostate cancer cells and has no effect on RWPE-1 cells[3]. Auriculasin (1-5 μM; 24 h) induces apoptosis of LNCaP cells, which is manifested by an increase in the sub-G1 population and DNA fragmentation[3]. Auriculasin (2.5-5 μM; 12-24 h) increases ROS generation in LNCaP cells[3]. Auriculasin reduces NSCLC A549 cell viability and promotes mitochondrial oxidative stress and ferroptosis[4].
References:
[1]. Cho HD, et al. Effects of auriculasin on vascular endothelial growth factor (VEGF)-induced angiogenesis via regulation of VEGF receptor 2 signaling pathways in vitro and in vivo. Food Chem Toxicol. 2018 Nov;121:612-621.
[2]. Cho HD, et al. Auriculasin sensitizes primary prostate cancer cells to TRAIL-mediated apoptosis through up-regulation of the DR5-dependent pathway. Food Chem Toxicol. 2019 Apr;126:223-232.
[3]. Cho HD, et al. Auriculasin-induced ROS causes prostate cancer cell death via induction of apoptosis. Food Chem Toxicol. 2018 Jan;111:660-669.
[4]. Wang X, et al. Auriculasin induces mitochondrial oxidative stress and drives ferroptosis by inhibiting PI3K/Akt pathway in non-small cell lung cancer. Naunyn Schmiedebergs Arch Pharmacol. 2025 Jan;398(1):967-977.
[5]. Dizamatova A, et al. A New Prenylated Isoflavonoid From Limonium leptophyllum. Natural Product Communications. May 2019.