CDDO-EACAS# 932730-51-3 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 932730-51-3 | SDF | Download SDF |
| PubChem ID | 44159258 | Appearance | Powder |
| Formula | C33H46N2O3 | M.Wt | 518.73 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | CDDO ethyl amide; TP319; RTA 405 | ||
| Solubility | DMSO : ≥ 34 mg/mL (65.54 mM) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | (4aS,6aR,6bS,8aR,12aS,14aR,14bS)-11-cyano-N-ethyl-2,2,6a,6b,9,9,12a-heptamethyl-10,14-dioxo-1,3,4,5,6,7,8,8a,14a,14b-decahydropicene-4a-carboxamide | ||
| SMILES | CCNC(=O)C12CCC(CC1C3C(=O)C=C4C(C3(CC2)C)(CCC5C4(C=C(C(=O)C5(C)C)C#N)C)C)(C)C | ||
| Standard InChIKey | RZRQJICXYQPEQJ-YKEYHJQHSA-N | ||
| Standard InChI | InChI=1S/C33H46N2O3/c1-9-35-27(38)33-14-12-28(2,3)18-21(33)25-22(36)16-24-30(6)17-20(19-34)26(37)29(4,5)23(30)10-11-31(24,7)32(25,8)13-15-33/h16-17,21,23,25H,9-15,18H2,1-8H3,(H,35,38)/t21-,23-,25-,30-,31+,32+,33-/m0/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. | ||
CDDO-EA Dilution Calculator
CDDO-EA Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 1.9278 mL | 9.6389 mL | 19.2779 mL | 38.5557 mL | 48.1946 mL |
| 5 mM | 0.3856 mL | 1.9278 mL | 3.8556 mL | 7.7111 mL | 9.6389 mL |
| 10 mM | 0.1928 mL | 0.9639 mL | 1.9278 mL | 3.8556 mL | 4.8195 mL |
| 50 mM | 0.0386 mL | 0.1928 mL | 0.3856 mL | 0.7711 mL | 0.9639 mL |
| 100 mM | 0.0193 mL | 0.0964 mL | 0.1928 mL | 0.3856 mL | 0.4819 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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CDDO-EA is an NF-E2 related factor 2/antioxidant response element (Nrf2/ARE) activator.
In Vitro:CDDO-EA potently activates Nrf2/ARE in a cell culture model of ALS and in the G93A SOD1 mouse model of ALS[1]. CDDO-EA is a potent inducer of apoptosis in A549 lung cancer cells, as shown both by PARP cleavage and Annexin staining. CDDO-EA is more potent than CDDO itself as inducers of heme oxygenase-1 (HO-1). In RAW264.7 macrophage-like cells, CDDO-EA is 7-fold more potent than CDDO as suppressors of the ability of IFN-γ to induce iNOS[2].
In Vivo:The survival analysis shows that G93A mice treated with CDDO-EA, compared to G93A littermate controls, lives significantly longer. CDDO-EA treatment increases the life-span by 20.6 days from 124.05±3.7 days to 144.72±8.1 days (16.6%) (p<0.001). In CDDO-EA-treated G93A mice, the age of death is 141.4±5.2 days and the duration from the age of onset to the age of death is 57.6±7.6 days, which means that the age of death from onset is prolonged by 17.5 days (43%)[1].
References:
[1]. Neymotin A, et al. Neuroprotective effect of Nrf2/ARE activators, CDDO ethylamide and CDDO trifluoroethylamide, in a mouse model of amyotrophic lateral sclerosis. Free Radic Biol Med. 2011 Jul 1;51(1):88-96.
[2]. Liby K, et al. The synthetic triterpenoids CDDO-methyl ester and CDDO-ethyl amide prevent lung cancer induced by vinyl carbamate in A/J mice. Cancer Res. 2007 Mar 15;67(6):2414-9.
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The Synthetic Triterpenoid RTA 405 (CDDO-EA) Halts Progression of Liver Fibrosis and Reduces Hepatocellular Carcinoma Size Resulting in Increased Survival in an Experimental Model of Chronic Liver Injury.[Pubmed:26443840]
Toxicol Sci. 2016 Jan;149(1):111-20.
UNLABELLED: Patients with cirrhosis have an increased risk of developing liver cancer and a higher rate of mortality. Cirrhosis currently has no known cure, and patients may benefit from new agents aimed at alleviating their complications and slowing down the rate of disease progression. Therefore, the effects of the orally bioavailable synthetic triterpenoid 2-cyano-3,12-dioxooleana- 1,9(11)-dien-28-oate-ethyl amide (CDDO-EA, RTA 405), which has potent antioxidative and antiinflammatory properties, was evaluated in a chronic carbon tetrachloride (CCl(4))-induced model of liver cirrhosis and hepatocellular carcinoma (HCC). Mice were injected with CCl(4) (to induce fibrosis and cirrhosis) or placebo biweekly for 12 weeks followed by CDDO-EA in the diet for 18 weeks with continued biweekly injections of CCl(4). Chronic CCl(4) administration resulted in cirrhosis, ascites, and HCC formation, associated with increased serum transforming growth factor-beta1, hepatic hydroxyproline content, and increased serum bilirubin. CDDO-EA, whose administration commenced after establishment of liver fibrosis, decreased liver fibrosis progression, serum bilirubin, ascites, and HCC formation and markedly increased overall survival. CDDO-EA also attenuated -TNFalpha (tumor necrosis factor-alpha), alpha-SMA (alpha smooth muscle actin), augmented -IL-10 levels, and improved histologic and serologic markers of fibrosis. CONCLUSIONS: CDDO-EA mitigates the progression of liver fibrosis induced by chronic CCl(4) administration, which is associated with the induction of antifibrogenic genes and suppression of profibrogenic genes.
Protective effect of CDDO-ethyl amide against high-glucose-induced oxidative injury via the Nrf2/HO-1 pathway.[Pubmed:28343048]
Spine J. 2017 Jul;17(7):1017-1025.
BACKGROUND CONTEXT: Intervertebral disc degeneration (IDD) is the main cause of low back pain, and nucleus pulposus (NP) cell apoptosis is an important risk factor of IDD. However, the molecular mechanism of this disease remains unknown. PURPOSE: To assess the potential protective effect of CDDO-ethyl amide (EA) against high-glucose-induced oxidative stress injury in NP cells and to investigate the mechanism of antioxidative effects and apoptotic inhibition. STUDY DESIGN/SETTING: To find new molecule to inhibit intervertebral disc degeneration. METHODS: Viability, reactive oxygen species (ROS) levels, and apoptosis were examined in NP cells. The protein expression levels of HO-1 and Nrf2 were measured through Western blot RESULTS: CDDO-EA elicited cytoprotective effects against NP cell apoptosis and ROS accumulation induced by high glucose. CDDO-EA treatment increased the HO-1 and Nrf2 expression abrogated by HO-1, Nrf2, and mitogen-activated protein kinase inhibitors. CONCLUSIONS: The phosphorylation and nuclear translocation of Nrf2 are crucial for HO-1 overexpression induced by CDDO-EA, which is essential for the cytoprotection against high-glucose-induced oxidative stress in NP cells.
