(hCysLT2R) based on a β-galactosidase complementation system. The EC50 values for LTC4 and LTD4 are consistent with previous literature values determined based on radio-labelling affinity assays for hCysLT2R. Activity of a synthetic analogue of LTC4, N-Methyl LTC4 (NMLTC4), gave an EC50 value of 8.5 nM. Also described in this thesis, is the synthesis of a cysLT2R selective antagonist, 3-{[(3- carboxycyclohexyl)amino]carbonyl}-4-{3-{4-(4-phenoxybutoxy)phenyl}- propoxy}benzoic acid. Through the in vitro assay system, this selective antagonist showed a dose-dependent inhibition (IC50 value of 86 nM) when CysLT2R was stimulated with 30 nM of LTD4. Both the selective agonist (NMLTC4) as well as the selective cysLT2R antagonist were also tested in vivo in a localized vascular ear inflammation assay. Results show NMLTC4 is able to promote vascular leakage through stimulation of cysLT2R, and this extravasation can be significantly attenuated by the cysLT2R antagonist. / Thesis (Master, Biochemistry) -- Queen's University, 2011-06-29 22:31:03.11