SRI-37240是一种有效的提前终止密码子 (PTCs) 抑制剂。SRI-37240 抑制 CFTR 的无义突变。在 HEK293T 细胞中，SRI-37240 改变 PTCs 的细胞翻译终止。当与 G418 使用联合时，SRI-37240 还能恢复原发性支气管上皮细胞的 CFTR 功能。

SRI-37240 is a potent premature termination codons (PTCs) inhibitor. SRI-37240 suppresses CFTR nonsense mutations. SRI-37240 alters cellular translation termination at PTCs in HEK293T cells. SRI-37240 can also restore CFTR function in primary bronchial epithelial cells when combination with G418.

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Premature termination codons, CFTR

SRI-37240 (1, 3, 10 and 30 μM; 48 h) induces concentration-dependent increases in CFTR-dependent (Forskolin-stimulated and sensitive to the inhibitor CFTRInh-172) chloride conductance.
SRI-37240 (10 μM; 72 h) significantly increases the amount of full-length, fully glycosylated form of CFTR protein, and the unprocessed, immature form of full-length CFTR protein in 16HBEge cells when co-treated with G418 (100 μM).
SRI-37240 (10?μM; 24 h) alters cellular translation termination at PTCs in HEK293T cells, also increases global densities of ribosomes at normal stop codons without affecting densities of ribosomes in 3-UTRs.
SRI-37240 (10?μM; 72 h) restores CFTR function in primary bronchial epithelial cells when combination with G418. has not independently confirmed the accuracy of these

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[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.

In Vitro: DMSO : 11.36 mg/mL (29.47 mM; ultrasonic and warming and heat to 60°C)配制储备液