AN-465

AN-465 (20 μM) reduces the expression levels of METTL3 and VP1 in EV71-infected cells^[1].
In the AN-465 (20 µM) treatment group, red CY3-labeled EV71-2C localizes predominantly in the cytoplasm, and the same is true for green FITC-labeled METTL3^[1].
AN-465 exhibits significant antiviral activity against EV71 in RD cells with favorable safety profiles^[1].
AN-465 (20 µM; 24 h) significantly reduces the viral loads of EV71 and CV-A6 in RD cells and PBMCs; the copy numbers of intracellular and extracellular viral nucleic acids decrease synchronously, and the reduction magnitude of intracellular viral particles is significantly greater than that of extracellular viral particles^[1].
AN-465 (20 µM) protects cells from EV71-induced ultrastructural damage and inhibits the assembly of viral particles^[1].
AN-465 (20 µM) inhibits m6A modification of cellular and viral RNAs, with a preferential impact on immunomodulatory pathways and the EV71 2C region^[1].
AN-465 (5-20 µM; 24 h) inhibits EV71 replication by downregulating METTL3 and NF-κB pathway genes and disrupting the EV71-2C/METTL3 interaction^[1].
AN-465 (5-40 µM; 12-48 h) exhibits low cytotoxicity against human PBMCs within the tested concentration range^[1].
AN-465 effectively inhibits the methyltransferase activity of METTL3 with an IC₅₀ of 1.782 µM, confirming its potential as a METTL3 inhibitor^[1].
AN-465 exhibits strong binding affinity for the METTL3 protein, with a K_D of 8.75 µM^[1].
AN-465 (20 µM) attenuates apoptosis and restores autophagic flux in EV71-infected RD cells^[1].

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