FLI-06 was discovered in a screen designed to monitor the trafficking and processing of a ligand-independent Notch-enhanced GFP reporter. It disrupts the Golgi apparatus in a manner distinct from that of brefeldin A and inhibited general secretion at a step before exit from the ER which was accompanied by a tubule-to-sheet morphological transition of the ER and is thus a novel agent acting at an early stage in secretory traffic (EC50=2.3 M).1 Abolishes MFAP5-dependent transcriptional programs which are upregulated in intrahepatic cholangiocarcinoma.2 Suppresses proliferation and induces apoptosis in esophogeal squamous cell carcinoma cells.3
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