Exchange protein activated by cAMP (Epac) proteins mediate cAMP signaling independent of protein kinase A (PKA). CE3F4 is an uncompetitive inhibitor of Epac1 activity toward its effector Rap1 in vitro (IC50 = 23 μM) and in cells.. It has no effect on PKA activity. CE3F4 blocks Epac1-induced autophagy in cardiomyocytes stimulated with isoprenaline and blocks the activation of transient receptor potential canonical (TRPC) channels by the Epac activator 8-pCPT.