Anti-inflammatory Properties
Properties of AKBA
Specification of BosPure
Mechanism Proposed for AKBA
Comparison of BosPure vs Other Boswellia Serrata Extracts
Clinical Studies on BosPure


Acetyl-11-Keto-β-Boswellic Acid (AKBA) is the most active, followed by Acetyl-α-Boswellic Acid & Acetyl-β-Boswellic Acid and then followed by β-Boswellic Acid. The keto group might be important for apoptotic property and the presence of acetyl group may strongly enhance the effect.

In another recent study1, acetyl boswellic acids were shown to inhibit proliferation and elicit cell death in chemoresistant androgen-independent PC-3 prostate cancer cells in vitro and in vivo. Induction of apoptosis was demonstrated in cultured PC-3 cells by several parameters. At the molecular level these compounds inhibit constitutively activated NFκB signaling by intercepting IKK. Signaling through interferon-stimulated response element remained unaffected, suggesting specificity for IKK inhibition. In addition, expression of cyclin D1, a crucial cell cycle regulator, was reduced as well. Both compounds tested were active in vivo, but AKBA proved far superior. Indeed, topical application of water-soluble AKBA-gamma cyclodextrin on PC-3 tumors xenografted onto chick chorioallantoic membranes induced concentration-dependent inhibition of proliferation as well as apoptosis. Similarly, in nude mice carrying PC-3 tumors, systemic application of AKBA-gamma cyclodextrin inhibited tumor growth and triggered apoptosis in the absence of detectable systemic toxicity. Thus, AKBA and related compounds acting on IKK might provide a novel approach for treatment of chemoresistant human tumors.

Cytotoxic effect of a 1:1 mixture of acetyl-α- and β-boswellic acids was investigated recently2 in 6 human myeloid leukemia cell lines (NB4, SKNO-1, K562, U937, ML-1, HL-60). More than 50% of the cells underwent apoptosis after treatment with 20 μg/mL boswellic acids for 24 h. The apoptosis process was p53-dependent. The acetyl boswellic acids induced Bid cleavage and decreased mitochondrial membrane potential without production of hydrogen peroxide. Caspase inhibitors blocked the boswellic acid-induced apoptosis. The mRNAs of death receptors 4 and 5 (DR4 and DR5) were induced in leukemia cells undergoing apoptosis after acetyl boswellic acid treatment. Apoptosis induced by acetyl boswellic acids is believed to proceed through activation of caspase-8 by induced expression of DR4 and DR5 and the activated caspase-8 may either directly activate caspase-3 by cleavage, or indirectly by cleaving Bid, which in turn decreases the mitochondria membrane potential.

Acetyl-11-Keto-β-Boswellic Acid demonstrates multifaceted bioactivities such as:

• 5-Lipoxygenase inhibition
• Human leukocyte elastase inhibition
• Topoisomerase inhibition
• Calcium mobilization
• MAP kinase activation
• Caspase activation
• IKK inhibition leading to inhibition of constitutively activated NFκB

1. Xia L, Cheen D, Han R, et al. Boswellic acid acetate induces apoptosis through caspase-mediated pathways in myeloid leukemia cells, Mol. Cancer Ther., 2005, 4:361-88.
2. Syrovets T, Gschwend JE, Buchele B, et al. Inhibition of IkappaB kinase activity by acetyl boswellic acids promotes apoptosis in androgen-independent PC-3 prostate cancer cells in vitro and in vivo, J. Biol. Chem., 2005, 280:6170-80.

These activities are preserved in BosPure, a mixture of Acetyl-Keto-β-Boswellic Acid, Acetyl-α-Boswellic Acid and Acetyl-β-Boswellic Acid.

A joint venture with Arjuna Natural Extracts Ltd

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