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. In FLI-06–treated cells, no APPCTF accumulates despite strongly reduced Aβ secretion, suggesting that it acts upstream of α-secretase and β-secretase cleavage. 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].
In Vivo:
Fields:
FLI-06 is a novel potent and selective small molecule intercepting Notch signaling and the early secretory pathway (EC50 ~2.3 μM).
Specificity:
Target:Notch. Fields: FLI-06 is a novel potent and selective small molecule intercepting Notch signaling and the early secretory pathway (EC50 ~2.3 μM).
Source:
Rabbit
Dilution:
EC50: 2.3 μM (Notch signaling)[1]
Concentration:
>98%
Storage Stability:
2 years -20°C Powder, 2 weeks4°C in DMSO,6 months-80°C in DMSO
MolecularWeight(Da):
438.52
References:
[1]. Kramer A, et al. Small molecules intercept Notch signaling and the early secretory pathway. Nat Chem Biol. 2013 Nov;9(11):731-8.