|Source:||The roots of Cudrania tricuspidata Bureau.|
|Biological Activity or Inhibitors:||1. Cudratricusxanthone A inhibits lipopolysaccharide-induced neuroinflammation through inhibition of NF-κB and p38 MAPK pathways in BV2 microglia.
2. Cudratricusxanthone A has potent anti-proliferative, antioxidative, and monoamine oxidase inhibitory effects.
3. Cudratricusxanthone A possesses anti-cancer activities and provide a basis for developing effective therapeutic agents to inhibit growth and metastasis of breast cancer.
4. Cudratricusxanthone A reversibly inhibits CYP1A2, 2C8, and 2C9.
5. Cudratricusxanthone A protects pancreatic beta cells from cytokines-mediated toxicity through the inhibition of NF-κB and STAT pathways.
6. Cudratricusxanthone A has antiplatelet, anticoagulant, and profibrinolytic activities, thus, it possesses antithrombotic activities.
7. Cudratricusxanthone A exhibits the significant hepatoprotective effect on nitrofurantoin-induced cytotoxicity in human liver-derived Hep G2 cells.
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: email@example.com
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||2.5225 mL||12.6126 mL||25.2251 mL||50.4503 mL||63.0628 mL|
|5 mM||0.5045 mL||2.5225 mL||5.045 mL||10.0901 mL||12.6126 mL|
|10 mM||0.2523 mL||1.2613 mL||2.5225 mL||5.045 mL||6.3063 mL|
|50 mM||0.0505 mL||0.2523 mL||0.5045 mL||1.009 mL||1.2613 mL|
|100 mM||0.0252 mL||0.1261 mL||0.2523 mL||0.5045 mL||0.6306 mL|
Molecules. 2016 Sep 16;21(9).
|A Prenylated Xanthone, Cudratricusxanthone A, Isolated from Cudrania tricuspidata Inhibits Lipopolysaccharide-Induced Neuroinflammation through Inhibition of NF-κB and p38 MAPK Pathways in BV2 Microglia.[Pubmed: 27649130]|
|Cudrania tricuspidata Bureau (Moraceae) is an important source of traditional Korean and Chinese medicines used to treat neuritis and inflammation. Cudratricusxanthone A (1), a prenylated xanthone, isolated from C. tricuspidata, has a variety of biological and therapeutic activities. The goal of this study was to examine the effects of compound 1 on neuroinflammation and characterize its mechanism of action in lipopolysaccharide (LPS)-stimulated BV2 microglia. Cudratricusxanthone A (1) suppressed the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 enzymes and decreased the production of iNOS-derived nitric oxide and COX-2-derived prostaglandin E2 in LPS-stimulated mouse BV2 microglia. The compound also decreased tumor necrosis factor-α, interleukin (IL)-1β, and IL-12 production; inhibited the phosphorylation and degradation of IκB-α; and blocked the nuclear translocation of p50 and p65 in mouse BV2 microglia induced by LPS. Cudratricusxanthone A (1) had inhibitory effects on nuclear factor kappa B DNA-binding activity. Additionally, it inhibited the p38 mitogen-activated protein kinase signaling pathway. Our data suggests that Cudratricusxanthone A (1) may be a useful therapeutic agent in the treatment of neurodegenerative diseases caused by neuroinflammation.|
J Ethnopharmacol. 2016 Dec 24;194:57-62.
|Cudraticusxanthone A isolated from the roots of Cudrania tricuspidata inhibits metastasis and induces apoptosis in breast cancer cells.[Pubmed: 27586822 ]|
|The roots of Cudrania tricuspidata is a deciduous tree found in Korea, China, and Japan. C. tricuspidata contains an abundance of various minerals, B vitamins, and flavonoids to help prevent diverse cancers. Cudratricusxanthone A (CTXA), a compound isolated from the roots of C. tricuspidata, has potent anti-proliferative, antioxidative, and monoamine oxidase inhibitory effects. RESULTS: The results show that CTXA gradually reduced viability of the two breast cancer cell lines and induced apoptosis in a concentration-dependent manner. Moreover, CTXA effectively blocked breast cancer cell migration and invasion. CTXA decreased the expression of matrix metalloproteinase-9, extracellular regulated kinases 1 and 2 and phosphorylation of the inhibitor IκBα in the MCF-7 and MDA-MB-231 cell lines. CONCLUSIONS: Collectively, these results indicate that CTXA possesses anti-cancer activities and provide a basis for developing effective therapeutic agents to inhibit growth and metastasis of breast cancer.|
Food Chem Toxicol. 2015 Jul;81:171-5.
|In vitro inhibition of human cytochrome P450 by cudratricusxanthone A.[Pubmed: 25936586 ]|
|Cudratricusxanthone A (CTXA) isolated from the roots of Cudrania tricuspidata Bureau (Moraceae) has several biological activities, including hepatoprotective, neuroprotective, anti-inflammatory, monoamine oxidase inhibitory, and antithrombotic activities. In this study, we investigated the potential herb-drug interaction of CTXA and nine cytochrome P450 (CYP) isoforms in pooled human liver microsomes (HLMs) using a cocktail probe assay. CTXA reversibly inhibited the CYP1A2-catalyzed phenacetin O-deethylation, CYP2C8-catalyzed paclitaxel 6-hydroxylation, and CYP2C9-catalyzed diclofenac 4'-hydroxylation with half-maximal inhibitory concentration (IC50) values of 3.9, 4.7, and 2.9 μM, respectively. The IC50 values did not change under different preincubation conditions. CTXA showed marked dose-dependent, but not time-dependent, inhibition of CYP1A2 and 2C9 activities in HLMs. Dixon plots showed typical competitive inhibition of CYP1A2 and CYP2C9 with Ki values of 1.3 and 1.5 μM, respectively. Further, CTXA inhibited CYP2C8 in a non-competitive manner with a Ki value of 2.2 μM. Our results showed that CTXA reversibly inhibits CYP1A2, 2C8, and 2C9.|
Int Immunopharmacol. 2014 Jul;21(1):26-33.
|Cudratricusxanthone A protect pancreatic beta cells from cytokines-mediated toxicity through the inhibition of NF-κB and STAT pathways.[Pubmed: 24768584 ]|
|Cudratricusxanthone A (CTXA) has an isoprenylated xanthone skeleton that is known to exert a variety of biological activities, including anti-inflammatory, neuroprotective, hepatoprotective, anti-proliferative, and mono-amine oxidase inhibitory effects. In this study, we investigated the effect of CTXA on IL-1β (5 ng/ml) and IFN-γ (100 U/ml)-induced β-cell damage. Pre-treatment with CTXA increased the viability and reactive oxygen species (ROS) inhibition of cytokine-treated RINm5F cells at concentrations of 1-10 μM. CTXA prevented nitric oxide (NO) production, and this effect was correlated with reduced levels of protein and mRNA expression of inducible nitric oxide synthase (iNOS). The molecular mechanism by which CTXA inhibits iNOS gene expression appeared to involve the inhibition of NF-κB activation. Moreover, pancreatic β-cells treated with cytokines upregulated the phosphorylation of STAT-1, STAT-3 and STAT-5; however, pretreatment with CTXA attenuated these effects. Additionally, in a second set of experiments in which rat islets were used, the protective effects of CTXA in rat islets were essentially the same as those observed when RINm5F cells were used. CTXA prevented cytokines-induced NO production, iNOS expression, JAK/STAT activation, and NF-κB activation and inhibition of glucose-stimulated insulin secretion (GSIS). Collectively, these results suggest that CTXA can be used for the prevention of functional β-cell damage.|
Arch Pharm Res. 2014 Aug;37(8):1069-78.
|Antiplatelet, anticoagulant, and profibrinolytic activities of cudratricusxanthone A.[Pubmed: 24234914]|
|Cudratricusxanthone A (CTXA), a natural bioactive compound extracted from the roots of Cudrania tricuspidata Bureau, is known to possess hepatoprotective, antiproliferative and anti-inflammatory activities. However, antiplatelet, anticoagulant, and profibrinolytic properties have not been studied. The anticoagulant activities of CTXA were measured by monitoring activated partial thromboplastin-time (aPTT), prothrombin time (PT), and the activities of cell-based thrombin and activated factor X (FXa). The effects of CTXA on the expressions of plasminogen activator inhibitor type 1 (PAI-1) and tissue-type plasminogen activator (t-PA) were also tested in tumor necrosis factor-α (TNF-α) activated human umbilical vein endothelial cells. Our data showed that CTXA inhibited thrombin-catalyzed fibrin polymerization and platelet aggregation, prolonged aPTT and PT significantly and inhibited the activities and production of thrombin and FXa. CTXA prolonged in vivo bleeding time and inhibited TNF-α induced PAI-1 production. Furthermore, PAI-1/t-PA ratio was significantly decreased by CTXA. Collectively, these results indicate that CTXA possesses antithrombotic activities and suggest that the current study could provide bases for the development of new anticoagulant agents.|
Arch Pharm Res. 2005 Jan;28(1):44-8.
|Hepatoprotective constituents of Cudrania tricuspidata.[Pubmed: 15742807]|
|Phytochemical investigation of the MeOH extract of the root barks of Cudrania tricuspidata Bureau (Moraceae), as guided by hepatoprotective activity in vitro, furnished four isoprenylated xanthones, Cudratricusxanthone A (1), cudraxanthone L (2), cudratricusxanthone E (3), and macluraxanthone B (4). All of these compounds showed the significant hepatoprotective effect on tacrine-induced cytotoxicity in human liver-derived Hep G2 cells. Compounds 1, 2, and 4 also exhibited the significant hepatoprotective effect on nitrofurantoin-induced cytotoxicity in human liver-derived Hep G2 cells.|