Pemphigus vulgaris (PV) is an IgG-mediated autoimmune disease of stratified squamous epithelia, such as the skin and oral mucosa. IgG autoantibodies are raised against cell-cell adhesion molecules found in desmosomes. The characteristic autoantibodies are desmoglein 1 and desmoglein 3. The pathophysiological effect of these antibodies causes the keratinocytes to separate, a process called acantholysis, resulting in intraepithelial split formation. Subsequently, the clinical picture of the disease predominantly manifests in blistering of the skin and/or the mucous membranes, erosion formation, bleeding and dysphagia. The mainstay of the treatment is based on general immunosuppression: The systemic administration of steroids and latterly monoclonal antibodies, show severe side effects. Hence, further understanding of the fundamental pathogenesis of PV is essential to identify and test more precise treatment options for the disease. My project aims to further identify the role of kinases in intracellular signalling cascades in PV. Therefore, I investigate the dose-dependent effects of seven kinase inhibitors on the development of acantholysis. The experimentally induced PV skin specimens are prepared and harvested within the scope of the human skin organ culture model, previously established within the Hundt lab (Imke Burmester et al., 2019). The model mimics the intraepidermal split formation of PV by injecting a single chain variable fragment. The overall aim is to determine, whether and if so at which concentration effectively, the kinase inhibitors successfully minimize acantholysis compared to the controls. The skin samples are further assessed histologically to quantify the effect.