Acetyl oleanolic acid chloride
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| Category | Enzyme inhibitors |
| Catalog number | BBF-05567 |
| CAS | 7372-21-6 |
| Molecular Weight | 517.18 |
| Molecular Formula | C32H49ClO3 |
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Description
It has inhibitory activity against S. pneumoniae, and this activity is stronger than Oleanolic acid.
Specification
| Synonyms | Olean-12-en-28-oyl chloride, 3-(acetyloxy)-, (3β)-; Olean-12-en-28-oyl chloride, 3-(acetyloxy)-, (3beta)- |
| IUPAC Name | (3S,4aR,6aR,6bS,8aS,12aS,14aR,14bR)-8a-(chlorocarbonyl)-4,4,6a,6b,11,11,14b-heptamethyl-1,2,3,4,4a,5,6,6a,6b,7,8,8a,9,10,11,12,12a,14,14a,14b-icosahydropicen-3-yl acetate |
Reference Reading
1. Evaluation of the antibacterial activity of the methylene chloride extract of Miconia ligustroides, isolated triterpene acids, and ursolic acid derivatives
Wilson R Cunha, Geilton X de Matos, Maria Goreti M Souza, Marcos G Tozatti, Márcio L Andrade e Silva, Carlos H G Martins, Rosangela da Silva, Ademar A Da Silva Filho Pharm Biol. 2010 Feb;48(2):166-9. doi: 10.3109/13880200903062648.
The methylene chloride extract of Miconia ligustroides (DC.) Naudin (Melastomataceae), the isolated compounds ursolic and oleanolic acids and a mixture of these acids, and ursolic acid derivatives were evaluated against the following microorganisms: Bacillus cereus (ATCC 14579), Vibrio cholerae (ATCC 9458), Salmonella choleraesuis (ATCC 10708), Klebsiella pneumoniae (ATCC 10031), and Streptococcus pneumoniae (ATCC 6305). The microdilution method was used for determination of the minimum inhibitory concentration (MIC) during evaluation of the antibacterial activity. The methylene chloride extract showed no activity against the selected microorganisms. Ursolic acid was active against B. cereus, showing a MIC value of 20 microg/mL. Oleanolic acid was effective against B. cereus and S. pneumoniae with a MIC of 80 microg/mL in both cases. The mixture of triterpenes, ursolic and oleanolic acids, did not enhance the antimicrobial activity. However, the acetyl and methyl ester derivatives, prepared from ursolic acid, increased the inhibitory activity for S. pneumoniae.
2. In vitro trypanocidal activity of triterpenes from miconia species
Wilson Roberto Cunha, Camila Martins, Daniele da Silva Ferreira, Antonio Eduardo Miller Crotti, Norberto Peporine Lopes, Sérgio Albuquerque Planta Med. 2003 May;69(5):470-2. doi: 10.1055/s-2003-39719.
The bioassay-guided fractionation of methylene chloride extracts of Miconia fallax DC. and Miconia stenostachya DC. led to the isolation of five triterpene acids. The triterpenes ursolic acid, oleanolic acid and gypsogenic acid were active against blood trypomastigote forms of Trypanosoma cruzi. In contrast, the acetyl and methyl ester derivatives were not found to potentiate the trypanocidal activity. These results suggest the importance of the polar groups for activity.
3. Depletion of intracellular glutathione contributes to JNK-mediated death receptor 5 upregulation and apoptosis induction by the novel synthetic triterpenoid methyl-2-cyano-3, 12-dioxooleana-1, 9-dien-28-oate (CDDO-Me)
Ping Yue, Zhongmei Zhou, Fadlo R Khuri, Shi-Yong Sun Cancer Biol Ther. 2006 May;5(5):492-7. doi: 10.4161/cbt.5.5.2565. Epub 2006 May 2.
The novel synthetic triterpenoid methyl-2-cyano-3, 12-dioxooleana-1, 9-dien-28-oate (CDDO-Me) induces apoptosis in human cancer cells, showing potential as a cancer therapeutic agent. We previously demonstrated that CDDO-Me induces a c-Jun N-terminal kinase (JNK)-mediated DR5 expression and apoptosis. This study revealed the mechanism by which CDDO-Me induces JNK activation and subsequent DR5 upregulation and apoptosis. To determine whether CDDO-Me activates JNK and induces DR5 expression and apoptosis via oxidative stress by inducing the generation of reactive oxygen species (ROS), we examined the effects of various antioxidants on JNK activation, DR5 upregulation, and apoptosis induction by CDDO-Me. Thiol antioxidants, including N-acetyl-L-cycteine (NAC), glutathione (GSH) and dithiothrietol (DTT), abrogated CDDO-Me-induced apoptosis. In contrast, nonthiol antioxidants, including butylated hydroxyanisole (BHA), Trolox, mannitol, and Mn(II) tetra(4-benoic acid) porphyrin chloride (MnTBAP), failed to do so, with the exception of vitamin C (Vit C). Accordingly, only thiol antioxidants blocked JNK activation induced by CDDO-Me. CDDO-Me reduced intracellular levels of GSH; this reduction was abrogated only by thiol antioxidants and Vit C. However, CDDO-Me did not promote ROS generation. These results suggest that depletion of intracellular GSH, but not ROS generation, contributes to CDDO-Me-induced JNK activation and apoptosis, at least in our systems. Furthermore, these thiol antioxidants abrogated CDDO-Me-induced DR5 expression, whereas the GSH-depleting agent diethylmaleate also upregulated DR5 expression at concentrations that deplete intracellular GSH, demonstrating that GSH depletion can cause DR5 upregulation. Collectively, we conclude that CDDO-Me activates the JNK pathway via depletion of intracellular GSH, leading to DR5 upregulation and induction of apoptosis.
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
