Moreover, ESI-09 treatment in wild-type (WT) mice infected with R. australis resulted in notably milder disease manifestations and significantly improved survival rates^[2].

This antagonist demonstrates enhanced efficacy in comparison to cAMP, displacing 8-NBD-cAMP binding with an apparent IC50 of 10 μM, and effectively inhibiting cAMP-mediated GEF activity of both EPAC2 and EPAC1. Additionally, ESI-09 dose-dependently suppresses 007-AM-stimulated Akt phosphorylation at T308 and S473, indicating its role in modulating key signaling pathways^[1].

Beyond its anticancer potential, ESI-09 has been shown to significantly reduce both intracellular and total bacterial counts in human umbilical vein endothelial cells (HUVECs) post-infection with R. australis at a multiplicity of infection (MOI) of 10, compared to controls. This demonstrates its utility in infectious disease models, particularly in reducing bacterial burden^[2].