FLI-06
Notch pathway inhibitor / 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 uM).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
Biochemicals & reagents
313967-18-9
1) Krämer, et al., (2013), Small molecules intercept Notch signaling and the early secretory pathway; Nat. Chem. Biol. 9 731 2) Li et al. (2019) MFAP5 facilitates the aggressiveness of intrahepatic Cholangiocarcinoma by activating the Notch1 signaling pathway: J. Exp. Clin. Cancer Res. 38 476 3) Lu et al. (2018) FLI-06 suppresses proliferation, induces apoptosis and cell cycle arrest by targeting LSD1 and Notch pathway in esophageal squamous cell carcinoma cells; Biomed. Pharmacol. 107 1370
-20°C
TARGET: ER/Golgi -- PATHWAY: Notch; Intracellular transport; Proliferation -- DISEASE AREA: Cancer