KamebakaurinCAS# 73981-34-7 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 73981-34-7 | SDF | Download SDF |
PubChem ID | 13945489 | Appearance | Powder |
Formula | C20H30O5 | M.Wt | 350.45 |
Type of Compound | Diterpenoids | Storage | Desiccate at -20°C |
Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
SMILES | CC1(CCC(C2(C1CC(C34C2CCC(C3O)C(=C)C4=O)O)CO)O)C | ||
Standard InChIKey | WHSUEVLJUHPROF-BIGDWJEQSA-N | ||
Standard InChI | InChI=1S/C20H30O5/c1-10-11-4-5-12-19(9-21)13(18(2,3)7-6-14(19)22)8-15(23)20(12,16(10)24)17(11)25/h11-15,17,21-23,25H,1,4-9H2,2-3H3/t11-,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. |
||
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. |
||
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 | Kamebakaurin has anti-cancer and anti-inflammatory activities through direct inhibition of DNA-binding activity of nuclear factor-kappa B (NF-κB) p50; it has anti-neuroinflammatory activity via inhibition of c-Jun NH₂-terminal kinase and p38 mitogen-activated protein kinase pathway in activated microglial cells. Kamebakaurin inhibits the expression of hypoxia-inducible factor-1α and its target genes to confer antitumor activity. Kamebakaurin also has the ability to protect the liver from APAP-induced hepatotoxicity, presumably by both inhibiting the inflammatory response and oxidative stress. |
Targets | HIF | Topoisomerase | VEGFR | NF-kB | JNK | p38MAPK | IkB | NO | COX | NOS | IKK |
In vitro | Anti-neuroinflammatory activity of Kamebakaurin from Isodon japonicus via inhibition of c-Jun NH₂-terminal kinase and p38 mitogen-activated protein kinase pathway in activated microglial cells.[Pubmed: 21705843]J Pharmacol Sci. 2011;116(3):296-308.Compelling evidence supports the notion that the majority of neurodegenerative diseases are associated with microglia-mediated neuroinflammation. Therefore, quelling of microglial activation may lead to neuronal cell survival.
|
Kinase Assay | Inhibition of TAK1 by kamebakaurin in dendritic cells.[Pubmed: 23159603 ]Kamebakaurin inhibits the expression of hypoxia-inducible factor-1α and its target genes to confer antitumor activity.[Pubmed: 26781327 ]Oncol Rep. 2016 Apr;35(4):2045-52.Hypoxia-inducible factor 1 (HIF-1), a heterodimeric transcription factor that mediates the adaptation of tumor cells and tissues to the hypoxic microenvironment, has attracted considerable interest as a potential therapeutic target. Kamebakaurin is a diterpenoid compound isolated from Isodon excia (Maxin.) Hara, which has been used for anti-inflammatory activities. However, its antitumor activity along with molecular mechanism has not been reported.
Int Immunopharmacol. 2013 Jan;15(1):138-43.Kamebakaurin (KA) has anti-cancer and anti-inflammatory activities through direct inhibition of DNA-binding activity of nuclear factor-kappa B (NF-κB) p50.
|
Animal Research | Suppressive effect of kamebakaurin on acetaminophen-induced hepatotoxicity by inhibiting lipid peroxidation and inflammatory response in mice.[Pubmed: 28624597]Pharmacol Rep. 2017 Oct;69(5):903-907.Kamebakaurin (KA) is an ent-kaurane diterpenoid known to have anti-inflammatory potential. In the current study, we investigated whether pretreatment with KA could ameliorate acetaminophen (APAP)-induced hepatotoxicity by inhibiting the anti-inflammatory response in mice.
|
Kamebakaurin Dilution Calculator
Kamebakaurin Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.8535 mL | 14.2674 mL | 28.5347 mL | 57.0695 mL | 71.3369 mL |
5 mM | 0.5707 mL | 2.8535 mL | 5.7069 mL | 11.4139 mL | 14.2674 mL |
10 mM | 0.2853 mL | 1.4267 mL | 2.8535 mL | 5.7069 mL | 7.1337 mL |
50 mM | 0.0571 mL | 0.2853 mL | 0.5707 mL | 1.1414 mL | 1.4267 mL |
100 mM | 0.0285 mL | 0.1427 mL | 0.2853 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. |
Calcutta University
University of Minnesota
University of Maryland School of Medicine
University of Illinois at Chicago
The Ohio State University
University of Zurich
Harvard University
Colorado State University
Auburn University
Yale University
Worcester Polytechnic Institute
Washington State University
Stanford University
University of Leipzig
Universidade da Beira Interior
The Institute of Cancer Research
Heidelberg University
University of Amsterdam
University of Auckland
TsingHua University
The University of Michigan
Miami University
DRURY University
Jilin University
Fudan University
Wuhan University
Sun Yat-sen University
Universite de Paris
Deemed University
Auckland University
The University of Tokyo
Korea University
- Cilostazol
Catalog No.:BCC2291
CAS No.:73963-72-1
- 7,8-Dimethoxy-1,3-dihydro-2H-3-benzazepin-2-one
Catalog No.:BCC8774
CAS No.:73942-87-7
- Isolimonexic acid
Catalog No.:BCN7141
CAS No.:73904-93-5
- Hispidone
Catalog No.:BCN4293
CAS No.:73891-72-2
- H-His-OMe.2HCl
Catalog No.:BCC2956
CAS No.:7389-87-9
- Foresaconitine
Catalog No.:BCC8173
CAS No.:73870-35-6
- 3-Amino-9H-pyrido[3,4-b]indole
Catalog No.:BCC8617
CAS No.:73834-77-2
- Boc-Glu(OcHex)-OH
Catalog No.:BCC3390
CAS No.:73821-97-3
- Boc-Asp(OcHex)-OH
Catalog No.:BCC3365
CAS No.:73821-95-1
- 2,6-Dimethyl-7-octene-2,3,6-triol
Catalog No.:BCN4292
CAS No.:73815-21-1
- Orientin 2''-O-p-trans-coumarate
Catalog No.:BCN2792
CAS No.:73815-15-3
- S-Sulfo-L-cysteine sodium salt
Catalog No.:BCC6558
CAS No.:7381-67-1
- Ethambutol
Catalog No.:BCC5195
CAS No.:74-55-5
- L-Arginine
Catalog No.:BCN2691
CAS No.:74-79-3
- Mosloflavone
Catalog No.:BCN6796
CAS No.:740-33-0
- p-Hydroxy-cinnamic acid
Catalog No.:BCN5027
CAS No.:7400-08-0
- Enoxacin (Penetrex)
Catalog No.:BCC3775
CAS No.:74011-58-8
- Lancifolin C
Catalog No.:BCN2019
CAS No.:74048-71-8
- Ketanserin
Catalog No.:BCC5050
CAS No.:74050-98-9
- Macamide B
Catalog No.:BCN1366
CAS No.:74058-71-2
- Cudratricusxanthone A
Catalog No.:BCN7649
CAS No.:740810-42-8
- ACV 1
Catalog No.:BCC5989
CAS No.:740980-24-9
- Ketorolac
Catalog No.:BCC5190
CAS No.:74103-06-3
- Ketorolac tromethamine salt
Catalog No.:BCC4431
CAS No.:74103-07-4
Anti-neuroinflammatory activity of Kamebakaurin from Isodon japonicus via inhibition of c-Jun NH(2)-terminal kinase and p38 mitogen-activated protein kinase pathway in activated microglial cells.[Pubmed:21705843]
J Pharmacol Sci. 2011;116(3):296-308. Epub 2011 Jun 25.
Compelling evidence supports the notion that the majority of neurodegenerative diseases are associated with microglia-mediated neuroinflammation. Therefore, quelling of microglial activation may lead to neuronal cell survival. The present study investigated the effects of Kamebakaurin (KMBK), a kaurane diterpene isolated from Isodon japonicus HARA (Labiatae), on the production of pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated cytotoxicity in rat primary microglial cultures and the BV-2 cell line. KMBK significantly inhibited the LPS-induced production of nitric oxide (NO) in a concentration-dependent fashion in activated microglial cells. The mRNA and protein levels of inducible nitric oxide synthase (iNOS) and cyclooxycenase-2 (COX-2) were also decreased dose-dependently. Furthermore KMBK inhibited the JNK and p38 mitogen-activated protein kinases (MAPKs) in LPS-stimulated BV-2 microglial cells. Considering the results obtained, the present study authenticated the potential benefits of KMBK as a therapeutic target in ameliorating microglia-mediated neuroinflammatory diseases.
Inhibition of TAK1 by kamebakaurin in dendritic cells.[Pubmed:23159603]
Int Immunopharmacol. 2013 Jan;15(1):138-43.
Kamebakaurin (KA) has anti-cancer and anti-inflammatory activities through direct inhibition of DNA-binding activity of nuclear factor-kappa B (NF-kappaB) p50. We suggest here another molecular target of KA by the use of lipopolysaccharide-treated dendritic cells. In cell- and enzyme-based assays, KA directly inhibited autophosphorylation and kinase activity of TAK1, followed by the inhibition of TAK1-downstream signaling cascades, such as IKK phosphorylation-IkappaBalpha degradation-nuclear translocation of NF-kappaB, phosphorylation of MEK3/6-p38 mitogen activated protein kinase (MAPK), and MKK4/7-c-Jun N-terminal kinase MAPK. These results demonstrated that TAK1 might be the direct molecular target of KA.
Kamebakaurin inhibits the expression of hypoxia-inducible factor-1alpha and its target genes to confer antitumor activity.[Pubmed:26781327]
Oncol Rep. 2016 Apr;35(4):2045-52.
Hypoxia-inducible factor 1 (HIF-1), a heterodimeric transcription factor that mediates the adaptation of tumor cells and tissues to the hypoxic microenvironment, has attracted considerable interest as a potential therapeutic target. Kamebakaurin is a diterpenoid compound isolated from Isodon excia (Maxin.) Hara, which has been used for anti-inflammatory activities. However, its antitumor activity along with molecular mechanism has not been reported. Kamebakaurin showed potent inhibitory activity against HIF-1 activation induced by hypoxia or CoCl2 in various human cancer cell lines. This compound significantly decreased the hypoxia-induced accumulation of HIF-1alpha protein, whereas it did not affect the expression of topoisomerase-I (Topo-I). Further analysis revealed that Kamebakaurin inhibited HIF-1alpha protein synthesis, without affecting the expression level of HIF-1alpha mRNA or degradation of HIF-1alpha protein. Furthermore, Kamebakaurin prevented hypoxia-induced expression of HIF-1 target genes for vascular endothelial growth factor (VEGF) and erythropoietin (EPO). However, Kamebakaurin caused cell growth inhibition via cell cycle arrest at G1 phase in tumor cells. In vivo studies, we further confirmed the inhibitory effect of Kamebakaurin on the expression of HIF-1alpha proteins, leading to growth inhibition of HCT116 cells in a xenograft tumor model. These results show that Kamebakaurin is an effective inhibitor of HIF-1 and provide new perspectives into its anticancer activity.
Suppressive effect of kamebakaurin on acetaminophen-induced hepatotoxicity by inhibiting lipid peroxidation and inflammatory response in mice.[Pubmed:28624597]
Pharmacol Rep. 2017 Oct;69(5):903-907.
BACKGROUND: Kamebakaurin (KA) is an ent-kaurane diterpenoid known to have anti-inflammatory potential. In the current study, we investigated whether pretreatment with KA could ameliorate acetaminophen (APAP)-induced hepatotoxicity by inhibiting the anti-inflammatory response in mice. METHODS: Seven-week-old C57BL/6J mice were orally administered KA or olive oil emulsion for seven days. Twenty-four hours after the last KA or olive oil administration, the mice were intraperitoneally injected with 400mg/kg APAP or saline under feed deprived condition. The mice from each group were euthanized and bled for plasma analysis 24h after the injection. RESULT: APAP increased plasma levels of hepatic injury markers (i.e., alanine aminotransferase and aspartate aminotransferase), lipid peroxidation, and pro-inflammatory cytokines. Pretreatment with KA reduced the magnitude of APAP-induced increases in plasma levels of hepatic injury markers, lipid peroxidation, and inflammatory response. In addition, KA exhibited antioxidant capacity in a dose-dependent manner, with slight reactive oxygen species scavenging activity. CONCLUSION: Our results indicate that KA has the ability to protect the liver from APAP-induced hepatotoxicity, presumably by both inhibiting the inflammatory response and oxidative stress.