EGA

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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.