Acetylation or pegylation of the molecule and grafting of the bindingmotif intoa stablescaffoldstructure. Such modifications might improve the metabolic properties of the peptide, increase its affinity and binding capacity on the target structure and lead to enhanced tumor-to-organ ratios, which is of high importance for the development of in vivo targeting and imaging strategies. In conclusion, peptides with affinity for the tumor associated carbonic anhydrase IX can be used as lead structures for targeting of imaging agents in hypoxic tumor sites. The evaluation of the newly identified peptide CaIX-P1 indicates that the peptide might be a promising candidate, which could be used as lead structure for the development of new tracers with affinity for human carbonic anhydrase IX. Based on the results of the in vitro experiments the hypothesis of a specific binding to the target can be generated. However, the organ distribution studies demonstrate low tumor-to-blood ratios, which is disadvantageous for the clinical use of the native ligand for imaging purposes. Therefore, further studies are needed in order to improve the serum stability of CaIX-P1, optimize its binding efficacy and lead to generation of peptide-based ligands, which can be used for targeting human carbonic anhydrase IX and tumor hypoxia. Macrophage migration inhibitory, the earliest identified cyokine, was originally described as produced by activated T cells and capable of stopping the random migration of macrophages in vitro. Presently, MIF is recognized as a pleiotropic cytokine that functions as a pivotal mediator of acute and chronic inflammation and is synthesized by a variety of cell types and organs. MIF is constitutively expressed by urothelial cells and mediates inflammation in the bladder. Inflammatory stimuli elicit MIF release from the urothelium into the bladder lumen and upregulation of MIF expression by the bladder in general and urothelium in particular. Released luminal MIF binds and activates receptors for MIF expressed by urothelial cells to induce a cascade of other inflammatory cytokines to be produced by the bladder and urothelium. Therefore, release of urothelial preformed MIF and activation of MIF production in the bladder by inflammatory stimuli are key elements in MIF-mediated bladder inflammation. Understanding the triggers evoking urothelial MIF release is an important component of understanding how cystitis is developed or maintained. Protease activated receptors are a unique class of receptors that carry their own ligands tethered to the receptor complex. Proteases clip and free the tethered ligand to bind to the receptor and mediate PI-103 signal transduction. To date, four different PAR receptors have been identified and they are implicated in mediating inflammation and pain, among other functions. Thrombin is a serine protease with high affinity for PAR1 and much lower affinity for PAR4 receptors.