Hederagenin

Hederagenin is a triterpenoid saponin with orally active and antitumor activity. Hederagenin can inhibit the expression of iNOS, COX-2, and NF-κB in cells induced by LPS stimulation. Hederagenin also increases ROS production in cancer cells, disrupts mitochondrial membrane potential, and induces apoptosis. Hederagenin also sensitizes cancer cells to Cisplatin (HY-17394) and Paclitaxel (HY-B0015), enhancing induced apoptosis. Hederagenin can also bind to SKP2, with K_D = 67.9 μM. Hederagenin also has preventive potential against alcoholic liver injury^{[1][2][3][4][5][6][7]}. In Vitro:Hederagenin (1 μM, 2 μM; 48 h) disrupts mitochondrial membrane potential, increases intracellular reactive oxygen species (ROS) content, and has a cytotoxic effect on cancer cells^[4].
Hederagenin (1 μM, 2 μM; 48 h) induces apoptosis in human colon cancer LoVo cells, upregulates apoptosis-related proteins (Bax), and reduces apoptosis inhibitory proteins (Bcl-2, Bcl-xL, and Survivin) levels^[4].
Hederagenin (50 μM; 4 h) also blocks autophagic flux-induced ROS accumulation and enhances the cytotoxicity of Cisplatin and Paclitaxel in lung cancer cells^[5].
In Vivo:Hederagenin (25 mg/kg; po; 11 d) alone did not affect tumor growth in NCI-H1299 xenograft mice. However, it has a synergistic effect with Cisplatin (1 mg/kg) to inhibit tumor growth^[4].
Hederagenin (50 mg/kg; po; once daily for 21 days) exerts anti-inflammatory and anti-apoptotic activities and reduces liver damage induced by 25% ethanol in mice^[5].