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Piperlongumine

  Cat. No.:  DC9691   Featured
Chemical Structure
20069-09-4
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More than 5000 active chemicals with high quality for research!
Field of application
Piperlongumine induces cell death and increases the level of reactive oxygen species (ROS) in cancer cells with both wild-type and normal p53.
Chemicals PropertiesBiological activity COA & MSDSRelated productsDatasheet
Cas No.: 20069-09-4
Chemical Name: 5,6-Dihydro-1-[(2E)-1-oxo-3-(3,4,5-trimethoxyphenyl)-2-propen-1-yl]-2(1H)-pyridinone
SMILES: COC1=CC(=CC(=C1OC)OC)/C=C/C(=O)N2CCC=CC2=O
Formula: C17H19NO5
M.Wt: 317.34
Purity: >98%
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description: Piperlongumine is a natural alkaloid isolated from Piper longum Linn[1], possesses ant-inflammatory, antibacterial, antiangiogenic, antioxidant, antitumor, and antidiabetic activities[2]. Piperlongumine induces ROS, and induces apoptosis in cancer cell lines[1]. Piperlongumine shows anti-cardiac fibrosis activity, suppresses myofibroblast transformation via suppression of the ERK1/2 signaling pathway[2].
Target: ERK1 ERK2
In Vivo: Piperlongumine (30 mg/kg/day, i.p. for 3 weeks) exhibits potent anti-tumor effect in athymic nude mice bearing L3.6pL cells without body weight loss[1].
In Vitro: Piplartine (5, 10, and 15 μM) significantly decreases cell proliferation of 786-O, SKBR3, Panc1, A549, and L3.6pL cancer cells after treatment for 24 and 48 hours, induces apoptosis and ROS in these cell lines at 5 and 10 μM after 3 or 9 h of treatment[1]. Piplartine (5 or 10 μM) induces cleaved PARP and downregulates Sp1, Sp3, Sp4, and Sp-regulated genes[1]. Piplartine (20 μM) decreases the viability of cardiac fibroblasts (CFs). Piplartine (0-10 μM) suppresses myofibroblast transformation via suppression of the ERK1/2 signaling pathway[2].
References: [1]. Karki K, et al. Piperlongumine Induces Reactive Oxygen Species (ROS)-Dependent Downregulation of Specificity Protein Transcription Factors. [2]. Wu X, e,t al. Piperlongumine inhibits angiotensin II-induced extracellular matrix expression in cardiac fibroblasts. J Cell Biochem. 2018 Dec;119(12):10358-10364
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
2018-0101
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