To eliminate the undesirable edematogenic effect of the lutemizing hormone-releasing hormone (LH- Since the isolation and structural elucidation of hypothalamic luteinizing hormone-releasing hormone (LH-RH) more than 2000 analogs have been synthesized, in view of their expected medical applications (1). Chronic administration of potent LH-RH agonists leads to the inhibition of pituitary and gonadal functions (2-6). While repeated administration of LH-RH agonists is required to lower the levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and sex steroids, similar effects can be obtained with single administration of LH-RH antagonists (7). Competitive antagonists of LH-RH were developed by multiple modification of the parent molecule,

The chemokine receptor CXCR3 and associated CXC chemokines have been extensively investigated in several inflammatory and autoimmune diseases as well as in tumor development. Recent studies have indicated the role of these chemokines also in cardiovascular diseases. We aimed to present current knowledge regarding the role of CXCR3-binding chemokines in the pathogenesis of atherosclerosis and during acute myocardial infarction.

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