KRAS protein regulates many important cellular functions including cellular multiplication. The KRAS G12D mutation causes KRAS to function improperly and is present in approximately 40% of pancreatic adenocarcinoma cases. In this project, we set out to design a protein to bind to KRAS with a G12D mutation and prevent it from functioning abnormally. To achieve this, we used a novel combination of four algorithms: RFdiffusion, ProteinMPNN, Alphafold2, and Rosetta to generate five protein designs optimized to bind to KRAS G12D. Our designs are excellent candidates for in vitro and in vivo evaluations to test their ability to bind to KRAS G12D and treat pancreatic cancer.