SRI-41315, a chemical compound, effectively addresses premature termination codons (PTCs) associated with cystic fibrosis in immortalized and primary human bronchial epithelial cells. It induces a prolonged pause at stop codons, resulting in the restoration of cystic fibrosis transmembrane conductance regulator (CFTR) expression and function. This compound achieves PTC suppression by reducing the abundance of the termination factor eRF1. Additionally, SRI-41315 synergistically enhances CFTR activity by potentiating aminoglycoside-mediated readthrough [1].
