Novel antagonists of CXCR3-binding CXC chemokines, and in particular of human CXCL11, can be obtained by generating mutants of such chemokines in which the binding to glycosaminoglycans (GAGs) is impaired due to non-conservative substitutions of amino acids involved in this interaction. Compounds prepared in accordance with the present invention can be used to block the activity of CXCR3-binding CXC chemokines on CXCR3-expressing cells, thereby providing therapeutic compositions for use in the treatment or prevention of diseases related to excessive activated T cells migration, such as graft rejection and autoimmune diseases, and of diseases needing an increase of vascularization, such as ischemic heart disease.