| Bioactivity | 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[1]. | ||||||||||||
| Invitro | SRI-41315 exhibits target cell cytotoxicity (CC50) values >50 µM in both FRT and 16BE14o- cells[1].SRI-41315 shows improved potency and efficacy in FRT cells that translated to 16HBE14o- cells[1].SRI-41315 (5 µM, 20 h) depletes eRF1 levels through a proteasome-mediated degradation pathway[1]. Western Blot Analysis[1] Cell Line: | ||||||||||||
| Name | SRI-41315 | ||||||||||||
| CAS | 1613509-49-1 | ||||||||||||
| Formula | C22H19N3O2 | ||||||||||||
| Molar Mass | 357.41 | ||||||||||||
| Appearance | Solid | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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| Reference | [1]. Sharma J, et al. A small molecule that induces translational readthrough of CFTR nonsense mutations by eRF1 depletion. Nat Commun. 2021 Jul 16;12(1):4358. |
SRI-41315
CAS: 1613509-49-1 F: C22H19N3O2 W: 357.41
SRI-41315 induces a prolonged pause at stop codons and suppresses PTCs (premature termination codons) associated with cy
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