ScFvs are a small functional form of an antibody, only consisting of the variable regions of the antibody��s heavy and light chain fused together via a short linker molecule, and can be produced in bacteria at low costs. The specificity of its target binding is unique, and target affinity is comparable to clinically used gpIIb/IIIa antagonists. The small size of the LIBSscFv allows for good accessibility and OB 24 hydrochloride penetration of the thrombus as well as rapid blood pool clearance via the kidney of non-bound labeled protein. Fortunately, cross-reactivity with mouse platelets allows the assessment of the LIBS-antibody as a probe for molecular imaging in mouse models. Nuclear imaging techniques have been used for years to detect molecular receptors in oncology and encounter broad clinical acceptance. Therefore, nuclear imaging of activated platelets would be a first step towards clinical application. A transfer from bench to bedside would be certainly challenging but worthwhile with regards to the therapeutic benefits. While the risk of immunogenicity is extremely low, selective targeting of activated platelets provides pathophysiologic information which allows for individual risk stratification and will help to guide therapeutic strategies. Favorable non-radioactive molecular imaging techniques such as MRI with MPIOs for the detection of activated platelets have also been evaluated by our group. These techniques are certainly promising, however have not yet reached the level of clinical applicability due to potential toxicity of the contrast-giving molecules. A possible limitation of the animal model applied in our study for further functional evaluation of 111Indium-LIBS is the need of the carotid artery to be directly exposed for the reliable and reproducible induction of wall-adherent thrombosis. Thereby, a wound area reaching from the skin surface towards the artery is created, allowing non-specific radiotracer deposition in edematous tissue but also specific binding to activated platelets involved into hemostasis. This is the reason for the high signal background in the wound area seen in both animal groups, after injection of 111In-control but also with 111In-LIBS. However, the uptake signal caused by specific binding of 111In-LIBS at the carotid artery thrombosis is still sufficient to obtain a highly significant signal. The reason for applying this model in our study in spite of these disadvantages is its reproducibility, which is an important prerequisite in a proof-of-concept-study. We are currently evaluating alternative animal models to overcome this limitation. Conclusions We describe the P1075 construction of a radioligand based on a singlechain antibody specifically targeting activated platelets in an in vivo mouse model of wall-adherent non-occlusive thrombosis in the carotid artery, which imitates the surface of an inflamed or ruptured plaque. In all approaches applying in vitro, ex vivo and in vivo techniques, the 111In-LIBS radiotracer enabled the sensitive detection of wall-adherent activated platelets, such as found in atherothrombosis or plaque inflammation.