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3-ACETYL-11-KETO-BETA-BOSWELLIC ACID

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3-ACETYL-11-KETO-BETA-BOSWELLIC ACID Basic information

Product Name:
3-ACETYL-11-KETO-BETA-BOSWELLIC ACID
Synonyms:
  • BOSWELLIC ACID, ACETYL KETO
  • 3-O-ACETYL-11-KETO-BETA-BOSWELLIC ACID
  • 3-ACETYL-11-KETO-BETA-BOSWELLIC ACID
  • 3-ACETYL-11-KETONE-BETA-ACETYLBOSWELLIC ACID
  • AKBA
  • AK-BETABA
  • ACETYL-11-KETO-B-BOSWELLIC ACID, 3
  • ACETYL-11-KETO-BETA-BOSWELLIC ACID
CAS:
67416-61-9
MF:
C32H48O5
MW:
512.73
Product Categories:
  • Pharmaceuticals
  • Miscellaneous Natural Products
Mol File:
67416-61-9.mol
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3-ACETYL-11-KETO-BETA-BOSWELLIC ACID Chemical Properties

Melting point:
271℃
Boiling point:
600.3±55.0 °C(Predicted)
Density 
1.13±0.1 g/cm3(Predicted)
storage temp. 
Sealed in dry,Store in freezer, under -20°C
solubility 
Chloroform (Sparingly), Methanol (Slightly)
pka
4.28±0.70(Predicted)
color 
White to Off-White
LogP
7.418 (est)
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Safety Information

Risk Statements 
36/37/38
Safety Statements 
26
WGK Germany 
3
HS Code 
2918300000
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3-ACETYL-11-KETO-BETA-BOSWELLIC ACID Usage And Synthesis

Description

3-acetyl-11-keto-β-Boswellic acid is a naturally occurring pentacyclic triterpene isolated from the gum resin exudate from the stem of the tree B. serrata (frankincense). It selectively inhibits 5-lipoxygenase (IC50 = 1.5 μM) in an enzyme-directed, nonredox, and noncompetitive manner. 3-acetyl-11-keto-β-Boswellic acid and other members of the boswellic acid family have been studied for potential use in the control of inflammatory diseases, including arthritis and cancer.

Uses

3-Acetyl-11-keto-β-boswellic Acid (AKBA), be used in the place of the non-steroidal anti-inflammatory drug. AKBA, also inhibits human gastric carcinoma growth through modulation of the Wnt/β-catenin signaling pathway. It can be used as an anticancer agent.

Definition

ChEBI: 3-Acetyl-11-keto-beta-boswellic acid is a triterpenoid.

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].

IC 50

1.5 μm

References

[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.

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