KYL is an EphA4 receptor tyrosine kinase inhibitor with a Kd of 0.8 µM. KYL inhibits EphA4-EphrinA5 interactions with an IC50 of 6.34 µM. Through EphA4 inhibition, KYL can prevent dendritic spine reduction, the blocking of LTP induction and neuronal apoptosis caused by amyloid- beta oligomers (A betaOs). EphA4-/- neurons or sh-EphA4-transfected neurons showed reduced synaptotoxicity by A betaOs. EphA4/c-Abl activation is a key-signalling event that mediates the synaptic damage induced by A betaOs.
