EGA

EGA is an inhibitor that selectively targets the endosomal trafficking pathways. EGA targets the proteins involved in the endosomal trafficking pathways through which multiple toxins and viruses enter cells. EGA exerts its activity by inhibiting the trafficking from early endosomes to late endosomes, blocking the entry of multiple acid-dependent bacterial toxins and viruses into mammalian cells and delaying the lysosomal targeting and degradation of EGFR^[1]. In Vitro:EGA (12 μM; pretreated for 1 hour) in RAW 264.7 macrophages inhibits the cytotoxicity mediated by anthrax lethal toxin (LT) and increases cell viability, with an IC50 of 1.7 μM^[1].
EGA (20 μM; pretreated for 1 hour) in BMDMs inhibits LT - mediated caspase-1 activation^[1].
EGA (25 μM; pretreated for 1 hour) in RAW 264.7 cells inhibits PA pore formation^[1].
EGA (20 μM; treated for 60 minutes) in HeLa cells slows down the degradation of EGFR induced by high-dose EGF^[1].
EGA (20 μM; pretreated for 1 hour) in HeLa cells protects cells from diphtheria toxin (DT) and Pseudomonas aeruginosa exotoxin A (ExoA)^[1].
EGA (12.5 μM; pretreated for 1 hour) in CHO-pgsA745 cells inhibits Hd-CDT-mediated cytotoxicity but has no inhibitory effect on Ec-CDT-mediated cytotoxicity^[1].
EGA (20 μM; pretreated for 1 hour) in HeLa cells inhibits the infection of VSV-G pseudotyped lentivirus but does not inhibit the infection of NiV-G pseudotyped lentivirus^[1].
EGA (20 μM; pretreated for 1 hour) in Vero cells reduces the number of cells infected with recombinant GFP-expressing LCMV^[1].
EGA (0.5-15 μM; treated 1 hour before, simultaneously with, or 1 hour after infection) in HeLa cells transfected with the Flu gLuc reporter inhibits influenza virus infection. It can completely inhibit when treated 1 hour before and simultaneously with infection, and has partial protection when treated 1 hour after infection^[1].