research use only
Cat.No.S3846
| Related Targets | Dehydrogenase HSP Transferase P450 (e.g. CYP17) PDE phosphatase Vitamin Carbohydrate Metabolism Mitochondrial Metabolism Drug Metabolite |
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| Other PPAR Inhibitors | T0070907 GW9662 GW6471 WY-14643 (Pirinixic Acid) GSK3787 GW0742 AZ6102 Astaxanthin GSK0660 Oroxin A |
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In vitro |
DMSO
: 68 mg/mL
(197.49 mM)
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In vivo |
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Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.
Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.
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| Molecular Weight | 344.32 | Formula | C18H16O7 |
Storage (From the date of receipt) | |
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| CAS No. | 22368-21-4 | Download SDF | Storage of Stock Solutions |
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| Synonyms | NSC 122413 | Smiles | COC1=C(C=C(C=C1)C2=CC(=O)C3=C(O2)C=C(C(=C3O)OC)O)OC | ||
| In vitro |
Eupatilin has been reported to induce apoptosis in human gastric cancer AGS cells, also triggers differentiation of these cells. Treatment of AGS cells with this compound induces cell cycle arrest at the G1 phase with the concomitant induction of p21cip1, a cell cycle inhibitor. It also markedly induces trefoil factor1(TFF1). This compound dramatically induces redistribution of tight junction proteins such as occludin and ZO-1, and F-actin at the junctional region between cells. It also induces phosphorylation of extracellular signal-regulated kinase 2 and p38 kinase. This chemical is known to inhibit the growth of MCF-10A-ras cells by inhibiting the expression of cell cycle regulators such as cyclinD1, cyclinB1, Cdk2, and Cdc2.
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| In vivo |
Treatment with eupatilin significantly decreases serum alanine aminotransferase and serum aspartate aminotransferase as well as liver histologic changes. This compound also preventes hepatic glutathione depletion and increases malondialdehyde levels induced by Ischemia-reperfusion injury (IRI). It improves the acute hepatic IRI by reducing inflammation and apoptosis. Oral administration of this chemical (10 mg/kg) in a therapeutic paradigm significantly reduces brain infarction and improves neurological functions in tMCAO-challenged mice. Its administration reduces the number of Iba1-immunopositive cells across ischemic brain and induces their morphological changes from amoeboid into ramified in the ischemic core, which is accompanied with reduced microglial proliferation in ischemic brain. This agent suppresses NF-κB signaling activities in ischemic brain by reducing IKKα/β phosphorylation, IκBα phosphorylation, and IκBα degradation.
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References |
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