Though polar interactions, and hydrogen bonding in particular, is generally known to inhibit SN2 reactions of anionic nucleophiles, we discovered recently that networks of electrostatic interactions that engage ion pairs at both the anionic and cationic components can in fact accelerate ion-pair collapse proceeding through SN2 mechanisms. In that case, rate enhancement was concluded to result from electrostatic preorganization of the salt into a geometry approaching the SN2 reaction trajectory. Though catalysis of SN2 mechanisms between ion pairs is rare, 11c the observation of an ionic resting state bound to a dipolar catalyst in the azetidine opening led us to consider whether similar electrostatic preorganization is the basis for catalysis by 1a. When 1a was replaced by a hydrogen-bond donor lacking an aryl pyrrolidine cation-binding domain (5), no rate acceleration was observed. In fact, 5 proved to be a potent inhibitor of anion delivery, illustrating that cooperativity between the hydrogen-bond donor and aryl pyrrolidine fragments is essential for catalysis of azetidinium ring opening by 1a (Figure ). A computational model of the azetidine opening reaction reveals a network of interactions that stabilize the transition state 1a•3v ‡ more than the ionic intermediate 1a•3v-int (Figure ). However, the uncatalyzed pathway does not proceed through a detectable ionicresting state, so we cannot rule out the possibility that 1a achieves rate acceleration entirely by driving formation of the azetidinium intermediate. While determination of the relative effect of catalyst on the two steps of azetidine opening will require further study, the computational model points to electrostatic pre-organization of the ionpair by 1a playing the critical role. The ability of 1a to leverage hydrogen-bonding interactions in combination with cation stabilization to accelerate anion delivery highlights the potential generality of this principle for catalyzing reactions of persistent ion pairs.