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4-Methylumbelliferone(Hymecromone 4-MU)
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
4-Methylumbelliferone(Hymecromone 4-MU)图片
CAS NO:90-33-5
规格:≥98%
包装与价格:
包装价格(元)
500mg电议
1g电议
2g电议
5g电议
10g电议
50g电议

产品介绍
理化性质和储存条件
Molecular Weight (MW)176.17
FormulaC10H8O3
CAS No.90-33-5
Storage-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)DMSO: 35 mg/mL (198.7 mM)
Water: <1 mg/mL
Ethanol: 35 mg/mL (198.7 mM)
SMILESO=C1C=C(C)C2=CC=C(O)C=C2O1
SynonymsHymecromone; 4-MU; 4MU; 4 MU
实验参考方法
In Vitro

In vitro activity: 4-Methylumbelliferone (MU), an inhibitor of HA synthesis, has been studied as a potential anti-tumor drug on account of inhibiting the growth of primary tumors and distant metastasis of tumor cells. The mechanism still needs to be clarified, although several studies revealed that the anticancer effects of MU are mediated by inhibition of HA signal pathway. In a previous study the regulation of HA synthesis was demonstrated by ceramide, and now show how MU activated NSMase2 generates ceramides and mediates MU modulated inhibition of HA synthesis (cell migration and invasion, and apoptosis of tumor cells). Using a HA enriched mouse oligodendroglioma cell line G26-24, it was found that MU elevated the activity of NSMase2 and enhanced ceramide levels, which in turn potentiated phosphatase PP2A activity. Further, the activated PP2A decreased phosphorylation of Akt, reduced activities of HA synthase2 (HAS2) and calpains, and blocked both the synthesis of HA, and the migration and invasion of G26-24 tumor cells. In addition, MU mediated ceramide induced activation of p53 and caspase-3, decreased SIRT1 expression and deduced G26-24 viability. The mechanism of the MU anticancer therefore initially involves NSMase2/ceramide/PP2A/AKT/HAS2/caspase-3/p53/SIRT1 and the calpain signaling pathway, indicating that ceramides play a important role in the ability of a tumor to become aggressively metastatic and grow.


Cell Assay: 4-Methylumbelliferone (MU), an inhibitor of HA synthesis, has been studied as a potential anti-tumor drug on account of inhibiting the growth of primary tumors and distant metastasis of tumor cells. The mechanism still needs to be clarified, although several studies revealed that the anticancer effects of MU are mediated by inhibition of HA signal pathway. In a previous study the regulation of HA synthesis was demonstrated by ceramide, and now show how MU activated NSMase2 generates ceramides and mediates MU modulated inhibition of HA synthesis (cell migration and invasion, and apoptosis of tumor cells). Using a HA enriched mouse oligodendroglioma cell line G26-24, it was found that MU elevated the activity of NSMase2 and enhanced ceramide levels, which in turn potentiated phosphatase PP2A activity. Further, the activated PP2A decreased phosphorylation of Akt, reduced activities of HA synthase2 (HAS2) and calpains, and blocked both the synthesis of HA, and the migration and invasion of G26-24 tumor cells. In addition, MU mediated ceramide induced activation of p53 and caspase-3, decreased SIRT1 expression and deduced G26-24 viability. The mechanism of the MU anticancer therefore initially involves NSMase2/ceramide/PP2A/AKT/HAS2/caspase-3/p53/SIRT1 and the calpain signaling pathway, indicating that ceramides play a important role in the ability of a tumor to become aggressively metastatic and grow

In Vivo
Animal model
Formulation & Dosage
References

Biochim Biophys Acta. 2016 Feb;1861(2):78-90.