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].

Product Specifications

CAS Number

[60297-37-2]

UNSPSC

12352005

Target

Akt; Cannabinoid Receptor; Ferroptosis; mTOR; p38 MAPK; PI3K; VEGFR

Type

Natural Products

Related Pathways

Apoptosis; GPCR/G Protein; MAPK/ERK Pathway; Neuronal Signaling; PI3K/Akt/mTOR; Protein Tyrosine Kinase/RTK

Applications

Neuroscience-Neuromodulation

Field of Research

Neurological Disease

Assay Protocol

https://www.medchemexpress.com/auriculasin.html

Purity

99.1

Solubility

10 mM in DMSO

Smiles

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

Molecular Formula

C25H24O6

Molecular Weight

420.45

References & Citations

[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.