Cystic Fibrosis (CF) is one of the most prevalent inherited disorders, characterized by mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene. In human lungs, dysfunctional CFTR leads to a decrease in mucociliary clearance leading to infections and contributing to high mortality. Approved treatments require constant application to alleviate symptoms but do not cure the genetic cause and are often extremely expensive. We present an approach towards correcting the prevalent p.F508del mutation using prime editing delivered via RNA in lipid nanoparticles (LNPs). The LNPs comprised ionizable lipids for endosomal escape, DOTAP for improved lung specificity, PEGylated lipids, and an RNA complexed with chitosan for increased stability. Physicochemical characterization (DLS, cryo-EM, zeta potential) confirmed optimal hydrodynamic size (~100 nm) and stability. Upon testing various editing options, a PE6c prime editor was chosen, in which prime editing guide RNAs (pegRNA) were equipped with silent edits and a protective 3' motif. Correction of a fluorescent reporter plasmid mimicking F508del was achieved in HEK-293 and CFBE41o- bronchial epithelial cells as observed by flow cytometry and microscopy.