Background:

IC50: 1.5 μM

3-acetyl-11-keto-β-Boswellic Acid, as known as AKBA, is a pentacyclic triterpene that suppresses 5-lipoxygenase in a selective, nonredox, enzyme-directed, and noncompetitive manner. Also, AKBA inhibits topoisomeraseⅠ and NF-κB signaling. AKBA has been studied for potential use in the control of inflammatory diseases, including arthritis and cancer.

In vitro: AKBA exerted a time- and concentration -dependent cytotoxicity on androgen-independent prostate cancer cells. AKBA blocked proliferation and elicited apoptosis in the chemoresistant and androgen-independent human PC-3 prostate cancer cells by the release of mitochondrial cytochrome c and DNA fragmentation. Also, AKBA concentration-dependently inhibited NF-κB signaling, yet it did not directly affect the NF-κB binding to DNA. Additionally, AKBA suppressed inhibitor κB kinase and NF-κB-dependent antiapoptotic gene products in PC-3 cells [1].

In vivo: PC-3 xenotransplanted male NMRI/nu-nu mice were injected intraperitoneally at 100 μmol/kg daily for three weeks. AKBA dampened growth and proliferation of PC-3 xenografts in nude mice and elicited apoptosis. Moreover, compared with the control group, AKBA reduced the tumor volume and the invasiveness of the tumor into the surrounding tissues [1].

Reference:
[1].  Syrovets, T., Gschwend, J., Buchele, B., Laumonnier, Y., Zugmaier, W., Genze, F., & Simmet, T. Inhibition of IκB Kinase Activity by Acetyl-boswellic Acids Promotes Apoptosis in Androgen-independent PC-3 Prostate Cancer Cells in Vitro and in Vivo. Journal of Biological Chemistry. 2004; 280(7): 6170-6180.