Macranthoidin B

Macranthoidin B (Macranthoiside I) is an orally active triterpene saponin. Macranthoidin B inhibits epithelial-mesenchymal transition in endometriosis via the COX‑2/PGE2 pathway, and also induces tumor cell apoptosis and inhibits their proliferation by regulating metabolism and increasing ROS levels. Macranthoidin B can be used in studies related to endometriosis, colorectal cancer and hepatocellular carcinoma^[1][2][3]. In Vitro:Macranthoidin B (0-500 μM; 24 h) inhibits migration and invasion of primary endometriotic stromal cells and HEC1-B endometrial cancer cells, and suppresses epithelial-mesenchymal transition and the COX-2/PGE2 pathway^[1].
Macranthoidin B (20-400 μM; 24-48 h) reduces the viability of HCT-116 colorectal cancer cells in a dose-dependent manner, induces cell apoptosis, and promotes ROS generation^[2].
Macranthoidin B (20-400 μM; 48 h) dose-dependently promotes ROS production in HCT-116 colorectal cancer cells^[2].
Macranthoidin B (20-400 μM; 48 h) dose-dependently downregulates the mRNA expression of antioxidant enzymes MnSOD and GSH-Px in HCT-116 colorectal cancer cells^[2].
Macranthoidin B (100-400 μM; 24 h) inhibits the proliferation of Hepa1-6 cells in a dose-dependent manner and increases intracellular ROS levels^[3].
Macranthoidin B (100-400 μM; 24 h) dose-dependently induces oxidative stress in Hepa1-6 cells, which is characterized by a significant increase in MDA levels and significant decreases in GSH levels, SOD activity and GSH-Px activity at all tested concentrations^[3]. In Vivo:Macranthoidin B (3-27 mg/kg; p.o.; daily; 28 days) inhibits the growth of ectopic lesions in a rat autotransplantation endometriosis model^[1].
Macranthoidin B (16 mg/kg; i.p.; once daily; for 3 consecutive weeks) significantly inhibits the growth of colorectal cancer xenografts in nude mice by inducing tumor cell apoptosis^[2].