SRI-41315 (C09-1170-701)

SRI-41315 induces a prolonged pause at stop codons and suppresses PTCs (premature termination codons) associated with cystic fibrosis in immortalized and primary human bronchial epithelial cells, restoring CFTR (cystic fibrosis transmembrane conductance regulator) expression and function. SRI-41315 suppresses PTCs by reducing the abundance of the termination factor eRF1. SRI-41315 also potentiates aminoglycoside-mediated readthrough, leading to synergistic increases in CFTR activity.In VitroSRI-41315 exhibits target cell cytotoxicity (CC50) values >50 µM in both FRT and 16BE14o- cells. SRI-41315 shows improved potency and efficacy in FRT cells that translated to 16HBE14o- cells. SRI-41315 (5 µM, 20 h) depletes eRF1 levels through a proteasome-mediated degradation pathway. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Western Blot AnalysisCell Line: CFTR-G542X 16HBEge G542X cells Concentration: 5 µM Incubation Time: 20 h Result: Depleted eRF1 levels through a proteasome-mediated degradation pathway. SRI-41315-mediated eRF1 degradation was prevented by the addition of (S)-MG132 but not the neddylation inhibitor MLN4924.Form:Solid. Specifications and Purity: 99%. Molecular Formula: C22H19N3O2. Molecular Weight: 357.41.