Astellas Pharma disclosed preclinical data showing tumor growth inhibition for ASP‑4396, a CRBN‑based proteolysis targeting chimera (PROTAC) designed to degrade KRAS G12D. The preclinical package reported mutant‑selective engagement and anti‑tumor activity in model systems, positioning the program as a new entry in efforts to drug the historically intractable KRAS oncogene. KRAS G12D is a frequent oncogenic driver across multiple solid tumors; a degrader approach seeks to remove the protein entirely rather than inhibit its activity. Translational hurdles include demonstrating selectivity versus wild‑type KRAS, optimizing delivery and exposure, and establishing a therapeutic window. Astellas’ data will accelerate attention on degrader libraries and E3 ligase selection strategies in precision oncology.