Auriculasin 

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]}.

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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

420.45

C₂₅H₂₄O₆

60297-37-2

Solid

White to off-white

O=C1C(C(O)=C(C=CC(C)(C)O2)C2=C3C/C=C(C)\C)=C3OC=C1C4=CC=C(O)C(O)=C4

Room temperature in continental US; may vary elsewhere.

-20°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

• [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.  [Content Brief]

  [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.  [Content Brief]

  [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.  [Content Brief]

  [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.  [Content Brief]

  [5]. Dizamatova A, et al. A New Prenylated Isoflavonoid From Limonium leptophyllum. Natural Product Communications. May 2019.