Puquitinib is a selective Akt inhibitor that effectively disrupts the PI3K/AKT/mTOR signaling pathway, promoting autophagy in nasopharyngeal carcinoma cells. This compound demonstrates a dose-dependent antiproliferative effect on CNE-2 cells, which is accompanied by increased autophagosome and autolysosome formation as confirmed by fluorescence and electron microscopy. Puquitinib enhances the conversion of LC3-I to LC3-II and elevates beclin 1 levels while decreasing p62 expression. Additionally, it induces apoptosis in CNE-2 cells, highlighting the interplay between autophagy and apoptosis in mediating cell death processes relevant to cancer research.
Puquitinib is a selective Akt inhibitor that effectively disrupts the PI3K/AKT/mTOR signaling pathway, promoting autophagy in nasopharyngeal carcinoma cells. This compound demonstrates a dose-dependent antiproliferative effect on CNE-2 cells, which is accompanied by increased autophagosome and autolysosome formation as confirmed by fluorescence and electron microscopy. Puquitinib enhances the conversion of LC3-I to LC3-II and elevates beclin 1 levels while decreasing p62 expression. Additionally, it induces apoptosis in CNE-2 cells, highlighting the interplay between autophagy and apoptosis in mediating cell death processes relevant to cancer research.
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