| Synonyms |
(3R,5aS,6R,8aS,9R,12S,12aR)-Octahydro-3,6,9-trimethyl-3,12-epox12H-pyrano[4,3-j]-1,2-benzodioxepin-10(3H)-one; Artemisine; Arteannuin; Huanghuahaosu; QHS; Qinghaosu; (+)-Artemisinin |
| IUPAC Name |
(1R,4S,5R,8S,9R,12S,13R)-1,5,9-trimethyl-11,14,15,16-tetraoxatetracyclo[10.3.1.04,13.08,13]hexadecan-10-one |
| Molecular Weight |
282.33 |
| Molecular Formula |
C15H22O5 |
| Canonical SMILES |
CC1CCC2C(C(=O)OC3C24C1CCC(O3)(OO4)C)C |
| InChI |
InChI=1S/C15H22O5/c1-8-4-5-11-9(2)12(16)17-13-15(11)10(8)6-7-14(3,18-13)19-20-15/h8-11,13H,4-7H2,1-3H3/t8-,9-,10+,11+,13-,14-,15-/m1/s1 |
| InChIKey |
BLUAFEHZUWYNDE-NNWCWBAJSA-N |
| Boiling Point |
389.9°C at 760 mmHg |
| Melting Point |
156-157°C |
| Flash Point |
172°C |
| Purity |
98% by HPLC |
| Density |
1.24 g/cm3 |
| Solubility |
Soluble in chloroform, acetone, ethyl ether, ethyl acetate, insoluble in water |
| Appearance |
White Solid |
| Storage |
Store at 2-8°C |
| Complexity |
452 |
| Exact Mass |
282.146729 |
| Index Of Refraction |
1.533 |
| In Vitro |
Artemisinin induced a G1 cell cycle arrest in cultured human Ishikawa endometrial cancer cells and downregulated cyclin-dependent kinase-2 (CDK2) and CDK4 transcript and protein levels. Analysis of CDK4 promoter-luciferase reporter constructs showed that the artemisinin ablation of CDK4 gene expression was accounted for by the loss of CDK4 promoter activity. Chromatin immunoprecipitation demonstrated that artemisinin inhibited nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) subunit p65 and p50 interactions with the endogenous Ishikawa cell CDK4 promoter. Coimmunoprecipitation revealed that artemisinin disrupts endogenous p65 and p50 nuclear translocation through increased protein-protein interactions with IκB-α, an NF-κB inhibitor, and disrupts its interaction with the CDK4 promoter, leading to a loss of CDK4 gene expression. Artemisinin treatment stimulated the cellular levels of IκB-α protein without altering the level of IκB-α transcripts. Finally, expression of exogenous p65 resulted in the accumulation of this NF-κB subunit in the nucleus of artemisinin-treated and artemisinin-untreated cells, reversed the artemisinin downregulation of CDK4 protein expression and promoter activity, and prevented the artemisinin-induced G1 cell cycle arrest. |
| In Vivo |
Artemisinin inhibited cell proliferation of estrogen receptor negative breast cancer cells with fewer efficacies in comparison to estrogen receptor positive ones. At the same time, cell viability and proliferation of normal breast epithelial MCF10A cells was un-affected. Artemisinin strongly inhibited cancer cell migration and invasion. Along with orphan nuclear receptors (ERRα, ERRβ and ERRγ), artemisinin altered the ERα/ERβ/PR/Her expression status of MCF-7 cells. The expression of genes involved in the signaling pathways associated with proliferation, migration, invasion and apoptosis was significantly altered which cooperatively resulted into reduced growth promoting activities of breast cancer cells. Interestingly, artemisinin exhibited inhibitory effect on histone deacetylases (HDACs). |
| PSA |
53.99000 |
| Target |
HCV; Parasite; Akt; Ferroptosis |
| Vapor Pressure |
0.0±0.9 mmHg at 25°C |
| XLogP3-AA |
2.8 |
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