Excisanin ACAS# 78536-37-5 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 78536-37-5 | SDF | Download SDF |
| PubChem ID | 11772488 | Appearance | Powder |
| Formula | C20H30O5 | M.Wt | 350.44 |
| Type of Compound | Diterpenoids | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| Chemical Name | (1R,2R,4R,8S,9R,10S,12S,13R,16R)-2,8,12,16-tetrahydroxy-5,5,9-trimethyl-14-methylidenetetracyclo[11.2.1.01,10.04,9]hexadecan-15-one | ||
| SMILES | CC1(CCC(C2(C1CC(C34C2CC(C(C3O)C(=C)C4=O)O)O)C)O)C | ||
| Standard InChIKey | NFENNPKUXFGPST-WEMBNSTNSA-N | ||
| Standard InChI | InChI=1S/C20H30O5/c1-9-15-10(21)7-12-19(4)11(18(2,3)6-5-13(19)22)8-14(23)20(12,16(9)24)17(15)25/h10-15,17,21-23,25H,1,5-8H2,2-4H3/t10-,11+,12-,13-,14+,15+,17+,19+,20-/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. | ||
| Description | 1. Excisanin A can inhibit invasion by suppressing MMP-2 and MMP-9 expression, it may be a potential anti-metastatic chemotherapeutic agent for the treatment of breast cancer. 2. ExcisaninA may be a potent inhibitor of AKT signaling pathway in tumor cells. 3. Excisanin A shows comparable inhibitory effects on the LPS-induced production of NO and PGE2, and activation of NF-kappaB without affecting cell viability. 3. Excisanin A induces apoptosis in colon cancer cell line SW620 as determined by Annexin V staining, the cleavage of caspase-3 and the proteolytic degradation of poly (ADP-ribose) polymerase (PARP). |
| Targets | MMP(e.g.TIMP) | FAK | PI3K | Akt | GSK-3 | Wnt/β-catenin | NO | PARP | JNK | Caspase | NF-kB | PGE |
Excisanin A Dilution Calculator
Excisanin A Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.8536 mL | 14.2678 mL | 28.5356 mL | 57.0711 mL | 71.3389 mL |
| 5 mM | 0.5707 mL | 2.8536 mL | 5.7071 mL | 11.4142 mL | 14.2678 mL |
| 10 mM | 0.2854 mL | 1.4268 mL | 2.8536 mL | 5.7071 mL | 7.1339 mL |
| 50 mM | 0.0571 mL | 0.2854 mL | 0.5707 mL | 1.1414 mL | 1.4268 mL |
| 100 mM | 0.0285 mL | 0.1427 mL | 0.2854 mL | 0.5707 mL | 0.7134 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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A new abietane diterpenoid from Isodon inflexus.[Pubmed:19023532]
Arch Pharm Res. 2008 Nov;31(11):1381-4.
A new ent-abietane diterpenoid, 3alpha,6beta-dihydroxy-7,17-dioxo-ent-abieta-15(16)-ene (1), and three known ent-kaurane diterpenids, kamebacetal A (2), kamebakaurin (3), and Excisanin A (4), and a known triterpenoid, ursolic acid (5), were isolated from the aerial parts of Isodon inflexus. Their chemical structures were determined by extensive analysis of spectroscopic data including 1D-and 2D-NMR experiments. All isolates (1-5) were evaluated for their potential to inhibit LPS-induced nitric oxide production in RAW264.7 cells. Of these, compounds 1-4 inhibited the production of NO with IC(50) values ranging from 1.0 to 26.5 microM.
A diterpenoid compound, excisanin A, inhibits the invasive behavior of breast cancer cells by modulating the integrin beta1/FAK/PI3K/AKT/beta-catenin signaling.[Pubmed:24044886]
Life Sci. 2013 Nov 4;93(18-19):655-63.
AIM: Excisanin A, a diterpenoid compound purified from Isodon macrocalyxin D, has anti-cancer properties with little toxicity. In this study, the anti-invasive effects of Excisanin A on breast cancer cells and its molecular mechanism of action were investigated. MAIN METHODS: MTT, wound healing, transwell chamber and cell adhesion assays were utilized to investigate the effects of Excisanin A on MDA-MB-231 and SKBR3 cells. Western blotting, real-time PCR, RNA interference and luciferase reporter assays were employed to determine the molecular mechanism of action of Excisanin A. KEY FINDINGS: Treating MDA-MB-231 and SKBR3 cells with 10-40muM Excisanin A significantly inhibited cell migration and invasion and suppressed the mRNA and protein levels of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) in a dose-dependent manner. Excisanin A efficiently abolished integrin beta1 expression and reduced the phosphorylation of the downstream kinases focal adhesion kinase (FAK) and Src. Excisanin A inhibited the phosphorylation of phosphoinositide 3-kinase (PI3K), AKT and glycogen synthase kinase 3 beta (GSK3beta) and down-regulated beta-catenin expression and the luciferase activity of the transcription factor LEF-1. Moreover, treating breast cancer cells with siRNA targeting integrin beta1 inhibited cell invasion and migration. SIGNIFICANCE: These results demonstrated that Excisanin A inhibited invasion by suppressing MMP-2 and MMP-9 expression; the integrin beta1/FAK/PI3K/AKT/beta-catenin signaling pathway was involved in this process. Therefore, Excisanin A might be a potential anti-metastatic chemotherapeutic agent for the treatment of breast cancer.
ExcisaninA, a diterpenoid compound purified from Isodon MacrocalyxinD, induces tumor cells apoptosis and suppresses tumor growth through inhibition of PKB/AKT kinase activity and blockade of its signal pathway.[Pubmed:19372560]
Mol Cancer Ther. 2009 Apr;8(4):873-82.
Isodon diterpenoids have received considerable phytochemical and biological attention for their strong antitumor activity with low toxicity. In this study, ExcisaninA, a diterpenoid compound purified from Isodon MacrocalyxinD, was tested on human Hep3B and MDA-MB-453 cell lines and Hep3B xenograft models. The results showed ExcisaninA could inhibit the proliferation of Hep3B and MDA-MB-453 cells via induction of apoptosis, with the evidence of increasing AnnexinV-positive cells and characteristic morphologic changes of apoptosis in the nucleus. Also, ExcisaninA sensitized Hep3B cells to 5-fluorouracil treatment or MDA-MB-453 cells to ADM treatment in vitro. In Hep3B xenograft models, ExcisaninA at 20 mg/kg/d remarkably decreased the xenograft tumor size and induced tumor cells apoptosis using transferase-mediated FITC-12-dUTP nick-end labeling assay. More importantly, we found that ExcisaninA could inhibit AKT activity and block its signal pathway in vitro and in vivo. And treatment with ExcisaninA significantly reduced the number of viable cells in Hep3B/myr-AKT1 cells more than that in control cells. Together, ExcisaninA might be a potent inhibitor of AKT signaling pathway in tumor cells. These data provide validation for the development of ExcisaninA to treat cancers displaying elevated levels of AKT.
Acetylcholinesterase expression mediated by c-Jun-NH2-terminal kinase pathway during anticancer drug-induced apoptosis.[Pubmed:16715131]
Oncogene. 2006 Nov 9;25(53):7070-7.
It has been shown that acetylcholinesterase (AChE) expression was induced during apoptosis and the anti-sense oligonucleotides and siRNA of AChE may prevent apoptosis in various cell types. However, the mechanisms underlying AChE upregulation remain elusive. We demonstrated here that c-Jun NH2-terminal kinase (JNK) could mediate AChE expression. In this study, both etoposide and Excisanin A, two anticancer agents, induced apoptosis in colon cancer cell line SW620 as determined by Annexin V staining, the cleavage of caspase-3 and the proteolytic degradation of poly (ADP-ribose) polymerase (PARP). The results showed that both the agents upregulated AChE in SW620 cells. In the meantime, JNK was also activated and the expression and phosphorylation of c-Jun increased in SW620 cells exposed to the two agents. The induced AChE mRNA and protein expression could be blocked by SP600125, a specific inhibitor of SAPK/JNK, and small interfering RNA directed against JNK1/2. Transfection with adenovirus-mediated dominant negative c-Jun also blocked the upregulation of AChE expression. Together, these results suggest that AChE expression may be mediated by the activation of JNK pathway during apoptosis through a c-Jun-dependent mechanism.
Kaurane diterpenes from Isodon japonicus inhibit nitric oxide and prostaglandin E2 production and NF-kappaB activation in LPS-stimulated macrophage RAW264.7 cells.[Pubmed:11488452]
Planta Med. 2001 Jul;67(5):406-10.
A methanolic extract of the whole plant of Isodon japonicus (Labiatae) showed potent inhibition on the LPS-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production in RAW264.7 cells. Four known kaurane diterpenes were isolated by activity-guided fractionation and their structures were identified as kamebanin (1), kamebacetal A (2), kamebakaurin (3), Excisanin A (4). All compounds also inhibited the LPS-induced NF-kappaB activation as assessed by NF-kappaB reporter assay and electrophoretic mobility shift assay (EMSA). Compounds 2-4 showed comparable inhibitory effects on the LPS-induced production of NO and PGE2, and activation of NF-kappaB without affecting cell viability. These results suggest that kaurane diterpenes could exert their inhibitory effects on the production of NO and PGE2 through the suppression of NF-kappaB activation, and be partially responsible for the anti-inflammatory activities of the genus Isodon.
