To examine the protein spatial and temporal changes upon carfilzomib-mediated proteasome inhibition in cardiac cells, we produced human iPSC-derived cardiomyocytes using a standard small molecule based protocol. Cardiomyocyte identity was confirmed by morphology, observation of contraction, and the presence of GFP tagged MLC-2a in the reporter line. We then applied the SPLAT protocol to untreated and carfilzomib-exposed iPSC-cardiomyocytes.