Bacteria have evolved several mechanisms to promote their survival, which sometimes come at the cost of human health. They use toxins known as virulence factors to cause the symptoms associated with infections. They also form communities called biofilm, which allow them to thrive and resist attacks by the host's immune system. Conventional antibiotics fail to penetrate the biofilm matrix. The expression of virulence factors and formation of biofilm are both regulated by a phenomenon known as quorum sensing. Quorum sensing is a form of cell-to-cell communication, which allows bacteria to coordinate gene expression via the secretion of signaling molecules, known as autoinducers, and the subsequent detection of these molecules. The ultimate goal of this dissertation was to identify new small molecules that would be used to disrupt quorum sensing in bacteria. AI-2, which is a universal quorum sensing autoinducer, found in over 60 bacterial species, was targeted. In this study a new facile synthesis of AI-2 was achieved and this new methodology was adapted to the synthesis of a library of analogs. These analogs were screened for their ability to modulate AI-2 mediated quorum sensing in Vibrio harveyi, Escherichia coli, Salmonella typhimurium and Pseudomonas aeruginosa. It was found that AI-2 analogs were able to cause synergistic agonism of bioluminescence in V. harveyi. Furthermore, several analogs were able to repress quorum sensing in E. coli yet very few analogs were active in the homologous quorum sensing system of S. typhimurium. These analogs were processed by the AI-2 processing enzymes in E. coli. Finally some AI-2 analogs were found to inhibit quorum sensing in P. aeruginosa in pure culture as well as in mixed cultures. These findings will provide the framework for the development of new small molecules which are able to modulate quorum sensing and thus act as tools in the inhibition of bacterial virulence and biofilm formation.