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Overview
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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].
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