Supplementary key wordsCysteinyl-leukotrienes (cysteinyl-LT) (i.e., LTC 4 , LTD 4 , and LTE 4 ) are members of a large family of biologically active lipid mediators rapidly generated at sites of infl ammation from arachidonic acid via the 5-lipoxygenase (5-LO) pathway ( 1 ). They are synthesized by infl ammatory cells, such as eosinophils, basophils, mast cells, and alveolar macrophages, in response to different immune and infl ammatory stimuli ( 2 ). Beyond their well-recognized role in asthma and immune disorders, cysteinyl-LTs are increasingly regarded as signifi cant infl ammatory factors in cancer, gastrointestinal, and cardiovascular diseases ( 3 ). In the past few years, the use of LT receptor antagonists as cardiovascular drugs has become a matter of considerable interest ( 4-6 ), as the presence of 5-LO, FLAP, and LT receptors transcripts has been shown in atherosclerotic lesions at various stages of development in human aorta, coronary arteries, and carotid arteries ( 3 ).The effects of cysteinyl-LTs are mediated through two offi cially recognized receptor subtypes: CysLT 1 and CysLT 2 ( 2, 3 ), which belong to the G-protein-coupled receptor (GPCR) gene superfamily and particularly to the purine receptor cluster (within the ␦ group) of the rhodopsin family ( 7 ). Over the years, several data in the literature suggested the existence of additional CysLT receptor (CysLT-R) subtypes in humans ( 3 ), and very recently new pharmacological targets have been identifi ed for cysteinylLTs, namely, two possible new receptor entities ( 8, 9 ) and a CysLT 1 /CysLT 2 heterodimer ( 10 ).