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11-Keto-beta-boswellic acid

11-Keto-beta-boswellic acid

Catalog No. BCN2298
Size Price Stock
5mg $198 In stock
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Quality Control of 11-Keto-beta-boswellic acid

Chemical structure

11-Keto-beta-boswellic acid

Biological Activity of 11-Keto-beta-boswellic acid

1. 11-Keto-beta-boswellic acid (KBA), one of the active constituents in the gum resin of Boswellia serrata, possesses significant anti-inflammatory activity.
2. 11-Keto-beta-boswellic acid exerts multi-focal action in cancer cells while it required 10-fold higher the concentration to produce cytotoxicity in normal human PBMC and gingival cell line, and therefore, may find usefulness in the management of human leukemia.

11-Keto-beta-boswellic acid Dilution Calculator

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Chemical Properties of 11-Keto-beta-boswellic acid

Cas No. 17019-92-0 SDF Download SDF
Type of Compound Triterpenoids Appearance White powder
Formula C30H46O4 M.Wt 470.68
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other courier with RT , or blue ice upon request.

Preparing Stock Solutions of 11-Keto-beta-boswellic acid

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.1246 mL 10.6229 mL 21.2459 mL 42.4917 mL 53.1146 mL
5 mM 0.4249 mL 2.1246 mL 4.2492 mL 8.4983 mL 10.6229 mL
10 mM 0.2125 mL 1.0623 mL 2.1246 mL 4.2492 mL 5.3115 mL
50 mM 0.0425 mL 0.2125 mL 0.4249 mL 0.8498 mL 1.0623 mL
100 mM 0.0212 mL 0.1062 mL 0.2125 mL 0.4249 mL 0.5311 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Preparation of 11-Keto-beta-boswellic acid

This product is isolated and purified from the herbs of Boswellia carterii Birdw.

References on 11-Keto-beta-boswellic acid

Biotransformation of 11-keto-β-boswellic acid by Cunninghamella blakesleana.[Pubmed: 23962801]

11-Keto-beta-boswellic acid (KBA), as one of the active constituents in the gum resin of Boswellia serrata, possesses significant biological activities including anti-inflammatory activity. However, its extensive metabolism and low polarity has limited the systemic availability of 11-Keto-beta-boswellic acid. The present research was aimed to obtain and explore the various possible derivatives of 11-Keto-beta-boswellic acid through biotransformation by Cunninghamella blakesleana AS 3.970. A total of ten transformed compounds were isolated and purified, and their chemical structures were characterized as 7β-hydroxy-11-keto-β-boswellic acid; 7β, 15α-dihydroxy-11-keto-β-boswellic acid ; 7β, 16β-dihydroxy-11-keto-β-boswellic acid; 7β, 16α-dihydroxy-11-keto-β-boswellic acid; 7β, 22β-dihydroxy-11-keto-β-boswellic acid; 7β, 21β-dihydroxy-11-keto-β-boswellic acid; 7β, 20β-dihydroxy-11-keto-β-boswellic acid; 7β, 30-dihydroxy-11-keto-β-boswellic acid; 3α, 7β-dihydroxy-11-oxours-12-ene-24, 30-dioic acid and 3α, 7β-dihydroxy-30-(2-hydroxypropanoyloxy)-11-oxours-12-en-24-oic acid by various spectroscopic methods. The biotransformation processes include hydroxylation, oxidation and esterification. Primary structure-activity relationships (SAR) of inhibitory effects on NO production in RAW 264.7 macrophage cells are discussed.

A novel cyano derivative of 11-keto-β-boswellic acid causes apoptotic death by disrupting PI3K/AKT/Hsp-90 cascade, mitochondrial integrity, and other cell survival signaling events in HL-60 cells.[Pubmed: 21751262]

Intervention of apoptosis is a promising strategy for discovery of novel anti-cancer therapeutics. In this study, we examined the ability of a novel cyano derivative of 11-Keto-beta-boswellic acid , that is, butyl 2-cyano-3,11-dioxours-1,12-dien-24-oate (BCDD) to induce apoptosis in cancer cells. BCDD inhibited cell proliferation with 48 h IC(50) of 0.67 µM in HL-60, 1 µM in Molt4, and 1.5 µM in THP1 cells. The mechanism of cell death was investigated in HL-60 cells where it caused apoptosis by acting against several potential apoptosis suppressive targets. It inhibited phosphatidylinositol-3-kinase (PI3K)/AKT activity, NF-κB, Hsp-90, and survivin which may enhance the sensitivity of cells to apoptosis. Also, BCDD decreased the activity of Bid and Bax in cytosol, caused ΔΨ(mt) loss, releasing pro-apoptotic cytochrome c, SMAC/DIABLO leading to caspase-9-mediated down stream activation of caspase-3, ICAD, and PARP1 cleavage. Translocation of apoptotis-inducing factor (AIF) from mitochondria to the nucleus indicated some caspases-independent apoptosis. Though it upregulated DR-5 and caspase-8, the caspase inhibitor yet had no effect on apoptosis as against 75% inhibition by caspase-9 inhibitor. Attempts were made to examine any acclaimed role of AIF in the activation of caspase-8 using siRNA where it had no effect on caspase-8 activity while the Bax-siRNA inhibited caspase-3 activation suggesting predominance of intrinsic signaling. Our studies thus demonstrated that BCDD exerts multi-focal action in cancer cells while it required 10-fold higher the concentration to produce cytotoxicity in normal human PBMC and gingival cell line, and therefore, may find usefulness in the management of human leukemia.


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