|Description:||1. Chrysosplenol D, an efflux pump inhibitor that can potentiate the activity of commercially important antibiotics and antimalarials.|
2. Chrysosplenol D can suppress lipopolysaccharide (LPS)-induced release of IL-1 beta, IL-6 and MCP-1, inhibit cell migration, and reduce LPS-induced IκB and c-JUN phosphorylation in Raw264.7 cells, thus, it can inhibit inflammation in vitro and in vivo.
3. Chrysosplenol D, artemetin, and chrysoplenetin have IC50 values at 2.4 - 6.5 × 10(-5)M against P. falciparum in vitro.
4. Chrysosplenol D exerts its anti-proliferative effect on tsFT210 cells through inhibiting cell cycle and inducing apoptosis, it may as a new cell cycle inhibitor.
5. Chrysosplenol-D displays antibacterial and antifungal activities.
|Targets:||NF-kB | JNK | IkB | IL Receptor | IKK|
|Source:||The herbs of Artemisia annua L.|
|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: firstname.lastname@example.org
|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||2.7755 mL||13.8773 mL||27.7546 mL||55.5093 mL||69.3866 mL|
|5 mM||0.5551 mL||2.7755 mL||5.5509 mL||11.1019 mL||13.8773 mL|
|10 mM||0.2775 mL||1.3877 mL||2.7755 mL||5.5509 mL||6.9387 mL|
|50 mM||0.0555 mL||0.2775 mL||0.5551 mL||1.1102 mL||1.3877 mL|
|100 mM||0.0278 mL||0.1388 mL||0.2775 mL||0.5551 mL||0.6939 mL|
Toxicol Appl Pharmacol. 2015 Apr 17.
|Flavonoids casticin and chrysosplenol D from Artemisia annua L. inhibit inflammation in vitro and in vivo.[Pubmed: 25891417]|
|BACKGROUND: The aim of our experiments was to investigate the anti-inflammatory properties of casticin and Chrysosplenol D, two flavonoids present in Artemisia annua L. METHODS: Topical inflammation was induced in ICR mice using croton oil. Mice were then treated with casticin or Chrysosplenol D. Cutaneous histological changes and edema were assessed. ICR mice were intragastrically administrated with casticin or Chrysosplenol D followed by intraperitoneal injection of lipopolysaccharide (LPS). Mouse Raw264.7 macrophage cells were incubated with casticin or Chrysosplenol D. Intracellular phosphorylation was detected, and migration was assessed by trans-well assay. HT-29/NFκB-luc cells were incubated with casticin or Chrysosplenol D in the presence or absence of LPS, and NF-κB activation was quantified. RESULTS: In mice, administration of casticin (0.5, 1 and 1.5μmol/cm2) and Chrysosplenol D (1 and 1.5μmol/cm2) inhibited croton oil-induced ear edema (casticin: 29.39-64.95%; Chrysosplenol D: 37.76-65.89%, all P<0.05) in a manner similar to indomethacin (0.5, 1 and 1.5μmol/cm2; 55.63-84.58%). Casticin (0.07, 0.13 and 0.27mmol/kg) and Chrysosplenol D (0.07, 0.14 and 0.28mmol/kg) protected against LPS-induced systemic inflammatory response syndrome (SIRS) in mice (all P<0.05), in a manner similar to dexamethasone (0.03mmol/kg). Casticin and Chrysosplenol D suppressed LPS-induced release of IL-1 beta, IL-6 and MCP-1, inhibited cell migration, and reduced LPS-induced IκB and c-JUN phosphorylation in Raw264.7 cells. JNK inhibitor SP600125 blocked the inhibitory effect of Chrysosplenol D on cytokine release. CONCLUSIONS: The flavonoids casticin and Chrysosplenol D from A. annua L. inhibited inflammation in vitro and in vivo.|
J Nat Prod. 2008 Nov;71(11):1961-2.
|Direct synthesis of chrysosplenol D.[Pubmed: 18855445]|
|An aldol condensation and an Algar-Flynn-Oyamada oxidative cyclization were key steps in the direct synthesis of Chrysosplenol D, an efflux pump inhibitor that can potentiate the activity of commercially important antibiotics and antimalarials.|
Plant Cell Rep. 1992 Nov;11(12):637-40.
|Antimalarial activity of Artemisia annua flavonoids from whole plants and cell cultures.[Pubmed: 24213368 ]|
|Cell suspension cultures developed from Artemisia annua exhibited antimalarial activity against Plasmodium faldparum in vitro both in the n-hexane extract of the plant cell culture medium and in the chloroform extract of the cells. Trace amounts of the antimalarial sesquiterpene lactone artemisinin may account for the activity of the n-hexane fraction but only the methoxylated flavonoids artemetin, chrysoplenetin, Chrysosplenol D and cirsilineol can account for the activity of the chloroform extract. These purified flavonoids were found to have IC50 values at 2.4 - 6.5 × 10(-5)M against P. falciparum in vitro compared with an IC50 value of about 3 × 10(-8)M for purified artimisinin. At concentrations of 5 × 10(-6)M these flavonoids were not active against P. falciparum but did have a marked and selective potentiating effect on the antiplasmodial activity of artemisinin.|
Nat Prod Res. 2014;28(11):812-8.
|A new α-glucosidase inhibitor from Achillea fragrantissima (Forssk.) Sch. Bip. growing in Egypt.[Pubmed: 24666348]|
|chondrillasterol (1), quercetin-3,6,7-trimethyl ether (Chrysosplenol D) (2), isovitexin-4'-methyl ether (3) and isovitexin (4). The structure of the new compound (5) was elucidated on the basis of its spectral data, including HR-FAB-MS, UV, (1)H NMR, (13)C NMR, (1)H-(1)H COSY, HSQC and HMBC. The new compound (5) exhibited the most significant α-glucosidase inhibitory activity (IC₅₀ 1.5 ± 0.09 μg/mL). Under the assay conditions, all the tested compounds were more potent than the positive control acarbose (IC50 224 ± 2.31 μg/mL).|
J Asian Nat Prod Res. 2005 Aug;7(4):615-26.
|Flavonoids from Vitex trifolia L. inhibit cell cycle progression at G2/M phase and induce apoptosis in mammalian cancer cells.[Pubmed: 16087636 ]|
|Six flavonoids, persicogenin (1), artemetin (2), luteolin (3), penduletin (4), vitexicarpin (5) and Chrysosplenol D (6), have been isolated for the first time as new cell cycle inhibitors from Vitex trifolia L., a Chinese folk medicine used to treat cancers, through a bioassay-guided separation procedure. They were identified by spectroscopic methods. The inhibitory effects of 1-6 on the proliferation of mammalian cancer cells have been evaluated by the SRB (sulforhodamine B) method and their effects on cell cycle and apoptosis investigated by flow cytometry with the morphological observation under light microscope and by agarose-gel electrophoresis to detect internucleosomal DNA fragmentation. Compounds 1-6 inhibited the proliferation of mouse tsFT210 cancer cells with the IC50s (microg ml(-1)) > 100 (inhibition rate at 100 microg ml(-1), 47.9%) for 1, >100 (inhibition rate at 100 microg ml(-1), 49.6 %) for 2, 10.7 for 3, 19.8 for 4, 0.3 for 5, and 3.5 for 6. Flow cytometric investigations for 1-6 demonstrated that 1-5 mainly inhibited cell cycle at the G2/M phase in a dose-dependent manner with a weak induction of apoptosis on the tsFT210 cells, while 6 induced mainly apoptosis of the same tsFT210 cells also in a dose-dependent manner together with a weak inhibition of the cell cycle at the G0/G1 and G2/M phases, demonstrating that 1-6 exert their anti-proliferative effect on tsFT210 cells through inhibiting cell cycle and inducing apoptosis. In contrast to the cell cycle G2/M phase inhibitory main effect on tsFT210 cells, 5 induced mainly apoptosis on human myeloid leukemia K562 cells with a weak inhibition of the cell cycle at the G2/M phase. The present result provides flavonoids 1-6 as new cell cycle inhibitors and 1 and 4 as new anticancer flavonoids, which not only provide the first example of cell cycle G2/M phase inhibitory and apoptosis-inducing constituents of V. trifolia L. but also explain the use of Vitex trifolia L. by Chinese people to treat cancers.|
Phytochemistry, 1989, 28(9):2323-7.
|Antimicrobial flavonoids from Psiadia trinervia and their methylated and acetylated derivatives.[Reference: WebLink]|
|From a dichloromethane extract and a hydrolysed methanolic extract from the leaves of Psiadia trinervia, 13 3-methylated flavonols have been isolated. Their structures were established by the usual spectroscopic methods (UV, EIMS, 1H and 13C NMR). Ayanin, casticin, chrysosplenol-D and 5,7,4′-trihydroxy-3,8-dimethoxyfiavone were responsible for the antifungal activity found in the preliminary screening. Chrysosplenol D, isokaempferide, 5,7,4′- trihydroxy-3,3′-dimethoxyflavone and 5,7,4′-trihydroxy-3,8-dimethoxyflavone displayed antibacterial activity. Twenty-nine derivatives were prepared by permethylation and selective methylation of the free hydroxyl group at C-5. The antimicrobial activities of the isolates and derivatives were determined by bioautographic assays using C. cucumerinum and B. cereus as test organisms.|