Kamebakaurin

Kamebakaurin is an orally active diterpenoid compound that can be isolated from Isodon excia (Maxin.). Kamebakaurin can inhibit NF-κB activation by directly targeting the DNA-binding activity of p50. Kamebakaurin can induce apoptosis and cell cycle arrest in tumor cells. Kamebakaurin has anti-inflammatory and anti-tumor activities^[1][2][3]. In Vitro: Kamebakaurin (0-10 μg/mL; 8.5 h) can inhibit the expression of NF-κB reporter genes and DNA-binding activities induced by TNF-α, Phorbol 12-myristate 13-acetate (HY-18739), and LPS (HY-D1056) in a dose-dependent manner in various cells such as Jurkat and THP-1^[1].
Kamebakaurin (0-10 μg/mL; 3.5-48 h) can inhibit the expression of TNF-α-induced NF-κB target genes and induce apoptosis, significantly enhancing caspase-8 activity in MCF-7 cells^[1].
Kamebakaurin (0-30 μM; 12 h) can significantly inhibit the accumulation of hypoxia-induced HIF-1α protein in the cell nucleus of HCT116 cells, as well as inhibit the expression of HIF-1α target genes VEGF and EPO, and can induce cell cycle arrest^[2]. In Vivo: Kamebakaurin (15-50 mg/kg; oral administration; every other day; 40 days) exhibits anti-tumor activity in a mouse model of colon cancer^[2].
Kamebakaurin (100 mg/kg; oral administration; 7 days) can inhibit Acetaminophen (APAP) (HY-66005)-induced hepatotoxicity when used for pretreatment in C57BL/6J mice^[3].