There is an urgent need to understand the molecular determinants of growing bacterial resistance to carbapenems caused by -lactamases. Identification of factors contributing to carbapenemase activity may facilitate understanding of the basis for resistance mediated by such enzymes, and so provide a basis for antibiotic (re)design in order to overcome this growing clinical problem. Crystal structures in the PDB provide insight into active site interactions in the acyl-enzyme state, but the details of why some enzymes are able to efficiently hydrolyze carbapenems, rather than forming stable acyl-enzymes, are unclear. Answering this question requires analysis of reactivity of the acyl-enzymes.