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Product name : FLI-06
Item : CR1783
Price : 100mg, $745; 200mg, $1185
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CAS : 313967-18-9
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Details:
 Chemical Information
M.Wt 438.52 Storage Please store the product under the recommended conditions in the Certificate of Analysis.
Formula C25H30N2O5
CAS No 313967-18-9
Solubility

DMSO



Biological Activity of FLI-06

 

FLI-06 is a novel potent and selective small molecule intercepting Notch signaling and the early secretory pathway (EC50 ~2.3 μM), identified by using automated microscopy to monitor the trafficking and processing of a ligand-independent Notch-GFP fusion reporter.
IC50 value: 2.3 uM (EC50) [1]
Target: Notch signaling
FLI-06 can induce accumulation of the reporter at the plasma membrane by interfering with transport in the secretory pathway. It can also disrupt the Golgi apparatus in a manner distinct from that of brefeldin A and golgicide A. FLI-06 inhibited general secretion at a step before exit from the endoplasmic reticulum (ER), which was accompanied by a tubule-to-sheet morphological transition of the ER, rendering FLI-06 the first small molecule acting at such an early stage in secretory traffic. FLI-06 is a very useful chemical probe to study the inhibition of membrane traffic at pre- ER-exit site (ERES) stages without fusion of ER-Golgi.
 

 

[1]. Kramer A, et al. Small molecules intercept Notch signaling and the early secretory pathway. Nat Chem Biol. 2013 Nov;9(11):731-8.
Abstract
Notch signaling has a pivotal role in numerous cell-fate decisions, and its aberrant activity leads to developmental disorders and cancer. To identify molecules that influence Notch signaling, we screened nearly 17,000 compounds using automated microscopy to monitor the trafficking and processing of a ligand-independent Notch-enhanced GFP (eGFP) reporter. Characterization of hits in vitro by biochemical and cellular assays and in vivo using zebrafish led to five validated compounds, four of which induced accumulation of the reporter at the plasma membrane by inhibiting γ-secretase. One compound, the dihydropyridine FLI-06, disrupted the Golgi apparatus in a manner distinct from that of brefeldin A and golgicide A. FLI-06 inhibited general secretion at a step before exit from the endoplasmic reticulum (ER), which was accompanied by a tubule-to-sheet morphological transition of the ER, rendering FLI-06 the first small molecule acting at such an early stage in secretory traffic. These data highlight the power of phenotypic screening to enable investigations of central cellular signaling pathways.


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