Dehydroeburicoic acidCAS# 6879-05-6 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 6879-05-6 | SDF | Download SDF |
| PubChem ID | 15250826 | Appearance | Powder |
| Formula | C31H48O3 | M.Wt | 468.7 |
| Type of Compound | Triterpenoids | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| Chemical Name | (2R)-2-[(3S,5R,10S,13R,14R,17R)-3-hydroxy-4,4,10,13,14-pentamethyl-2,3,5,6,12,15,16,17-octahydro-1H-cyclopenta[a]phenanthren-17-yl]-6-methyl-5-methylideneheptanoic acid | ||
| SMILES | CC(C)C(=C)CCC(C1CCC2(C1(CC=C3C2=CCC4C3(CCC(C4(C)C)O)C)C)C)C(=O)O | ||
| Standard InChIKey | ONFPYGOMAADWAT-OXUZYLMNSA-N | ||
| Standard InChI | InChI=1S/C31H48O3/c1-19(2)20(3)9-10-21(27(33)34)22-13-17-31(8)24-11-12-25-28(4,5)26(32)15-16-29(25,6)23(24)14-18-30(22,31)7/h11,14,19,21-22,25-26,32H,3,9-10,12-13,15-18H2,1-2,4-8H3,(H,33,34)/t21-,22-,25+,26+,29-,30-,31+/m1/s1 | ||
| 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. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | 1. Dehydroeburicoic acid treatment resulted in a marked decrease of tumor weight and size without any significant decrease in mice body weights. 2. Dehydroeburicoic acid induces necrotic cell death that involves Ca(2+) overload, mitochondrial dysfunction, and calpain activation in human glioblastomas. 3. Dehydroeburicoic acid and Eburicoic acid have antioxidant and anti-inflammatory activities by the decrease of inflammatory cytokines and an increase of antioxidant enzyme activity, can protect the liver from CCl4-induced hepatic damage. |
| Targets | SOD | NO | TNF-α | NOS | COX | P450 (e.g. CYP17) | IL Receptor | Calcium Channel |
Dehydroeburicoic acid Dilution Calculator
Dehydroeburicoic acid Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.1336 mL | 10.6678 mL | 21.3356 mL | 42.6712 mL | 53.339 mL |
| 5 mM | 0.4267 mL | 2.1336 mL | 4.2671 mL | 8.5342 mL | 10.6678 mL |
| 10 mM | 0.2134 mL | 1.0668 mL | 2.1336 mL | 4.2671 mL | 5.3339 mL |
| 50 mM | 0.0427 mL | 0.2134 mL | 0.4267 mL | 0.8534 mL | 1.0668 mL |
| 100 mM | 0.0213 mL | 0.1067 mL | 0.2134 mL | 0.4267 mL | 0.5334 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. | |||||
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Analgesic and anti-inflammatory bioactivities of eburicoic acid and dehydroeburicoic acid isolated from Antrodia camphorata on the inflammatory mediator expression in mice.[Pubmed:23495748]
J Agric Food Chem. 2013 May 29;61(21):5064-71.
Eburicoic acid (TR1) and Dehydroeburicoic acid (TR2), an active ingredient from Antrodia camphorata (AC) solid-state culture, were evaluated for analgesic and anti-inflammatory effects. Treatment with TR1 and TR2 significantly inhibited a number of acetic acid-induced writhing responses and formalin-induced pain in the late phase. In the anti-inflammatory test, TR1 and TR2 decreased paw edema at the fourth and fifth hour after lambda-carrageenan (Carr) administration and increased the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) in the paw edema tissue. We also demonstrated that TR1 and TR2 significantly attenuated the malondialdehyde (MDA), nitric oxide (NO), tumor necrosis factor (TNF-alpha), and interleukin-1beta (IL-1beta) levels in either edema paw or serum at the fifth hour after Carr injection. Western blotting revealed that TR1 and TR2 decreased Carr-induced inducible nitric oxide synthase (iNOS) and cycloxyclase (COX-2) expressions at the fifth hour in paw edema. Treatment with TR1 and TR2 also diminished neutrophil infiltration into the paw edema at the fifth hour. The present study suggests that the anti-inflammatory mechanisms of TR1 and TR2 might be related to the decrease of inflammatory cytokines and an increase of antioxidant enzyme activity.
Hepatoprotective effects of eburicoic acid and dehydroeburicoic acid from Antrodia camphorata in a mouse model of acute hepatic injury.[Pubmed:23871054]
Food Chem. 2013 Dec 1;141(3):3020-7.
The hepatoprotective effects of eburicoic acid (TR1) and Dehydroeburicoic acid (TR2) from Antrodia camphorata (AC) against carbon tetrachloride (CCl4)-induced liver damage were investigated in mice. TR1 and TR2 was administered intraperitoneally (i.p.) for 7 days prior to the administration of CCl4. Pretreatment with TR1 and TR2 prevented the elevation of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and liver lipid peroxides in CCl4-treated mice. The activities of antioxidant enzymes [catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx)], nitric oxide (NO) production, and tumour necrosis factor-alpha (TNF-alpha) were decreased after the treatment with TR1 and TR2 in CCl4-treated mice. Western blotting revealed that TR1 and TR2 significantly decreased inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expressions and increased the expression of cytochrome P4502E1 (CYP2E1) in CCl4-treated mice. Therefore, we speculate that TR1 and TR2 protect the liver from CCl4-induced hepatic damage via antioxidant and anti-inflammatory mechanisms.
Antileukemia component, dehydroeburicoic acid from Antrodia camphorata induces DNA damage and apoptosis in vitro and in vivo models.[Pubmed:22516893]
Phytomedicine. 2012 Jun 15;19(8-9):788-96.
Antrodia camphorata (AC) is a native Taiwanese mushroom which is used in Asian folk medicine as a chemopreventive agent. The triterpenoid-rich fraction (FEA) was obtained from the ethanolic extract of AC and characterized by high performance liquid chromatography (HPLC). FEA caused DNA damage in leukemia HL 60 cells which was characterized by phosphorylation of H2A.X and Chk2. It also exhibited apoptotic effect which was correlated to the enhancement of PARP cleavage and to the activation of caspase 3. Five major triterpenoids, antcin K (1), antcin C (2), zhankuic acid C (3), zhankuic acid A (4), and Dehydroeburicoic acid (5) were isolated from FEA. The cytotoxicity of FEA major components (1-5) was investigated showing that Dehydroeburicoic acid (DeEA) was the most potent cytotoxic component. DeEA activated DNA damage and apoptosis biomarkers similar to FEA and also inhibited topoisomerase II. In HL 60 cells xenograft animal model, DeEA treatment resulted in a marked decrease of tumor weight and size without any significant decrease in mice body weights. Taken together, our results provided the first evidence that pure AC component inhibited tumor growth in vivo model backing the traditional anticancer use of AC in Asian countries.
Dehydroeburicoic acid induces calcium- and calpain-dependent necrosis in human U87MG glioblastomas.[Pubmed:19848398]
Chem Res Toxicol. 2009 Nov;22(11):1817-26.
Dehydroeburicoic acid (DeEA) is a triterpene purified from medicinal fungi such as Antrodia camphorate, the crude extract of which is known to exert cytotoxic effects against several types of cancer cells. We aim to test the hypothesis that DeEA possesses significant cytotoxic effects against glioblastomas, one of the most frequent and malignant brain tumors in adults. 3-(4,5-Dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase release assays indicated that DeEA inhibited the proliferation of the human glioblastoma cell U87MG. In addition, Annexin V and propidium iodide staining showed that DeEA treatment led to a rapid increase of glioblastomas in the necrotic/late apoptotic fraction, whereas cell cycle analysis revealed that DeEA failed to significantly enhance the population of U87MG cells in the hypodiploid (sub-G1) fraction. Using electron microscopy, we found that DeEA induced significant cell enlargements, massive cytoplasmic vacuolization, and loss of mitochondrial membrane integrity. DeEA treatment triggered an intracellular Ca(2+) increase, and DeEA-induced cell death was significantly attenuated by BAPTA-AM but not ethylenediaminetetraacetic acid or ethylene glycol tetraacetic acid. DeEA instigated a reduction of both mitochondrial transmembrane potential and intracellular ATP level. Moreover, DeEA induced proteolysis of alpha-spectrin by calpain, and DeEA cytotoxicity in U87MG cells was caspase-independent but was effectively blocked by calpain inhibitor. Interestingly, DeEA also caused autophagic response that was prevented by calpain inhibitor. Taken together, these results suggest that in human glioblastomas, DeEA induces necrotic cell death that involves Ca(2+) overload, mitochondrial dysfunction, and calpain activation.
