We selected a RIPK2 PROTAC 1 and an anti-HER2 monoclonal antibody (mAb), trastuzumab, as our model system to demonstrate selective RIPK2 degradation in HER2+ cells only. Dysregulation of RIPK2mediated pathways is associated with inflammatory bowel disease, severe pulmonary sarcoidosis, multiple sclerosis, and cancer. We hypothesised that the ability to degrade RIPK2 only in cells which express cancer biomarkers would provide the basis for cell selective targeting.