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premature termination codons

" in MedChemExpress (MCE) Product Catalog:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-150090
    SRI-41315
    1 Publications Verification

    		 CFTR Inflammation/Immunology
    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 .
    SRI-41315
  • HY-150089
    SRI-37240

    		CFTR Inflammation/Immunology
    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 .
    SRI-37240
  • HY-143792
    HTT-D3

    		Huntingtin P-glycoprotein Neurological Disease
    HTT-D3 is an orally active, blood-brain barrier penetrant splicing modulator of huntingtin (HTT). HTT-D3 promotes the inclusion of a pseudo-exon containing a premature termination codon into HTT pre-mRNA, triggers nonsense-mediated mRNA degradation and reduces HTT protein levels. HTT-D3 induces dose-dependent, comparable reductions in mutant HTT protein in both the brain and peripheral tissues of transgenic mouse models. HTT-D3 can be used for the research of Huntington's disease .
    HTT-D3
  • HY-177569
    NVS1.1

    		Eukaryotic Initiation Factor (eIF) Others
    NVS1.1 is a potent, orally active and brain-penetrant readthrough promoter. NVS1.1 triggers the degradation of eRF1 by activating the ribosome-related quality control pathways (involving GCN1, RNF14, and RNF25), thereby facilitating the reading through of premature termination codons. NVS1.1 can be used for the research of genetic diseases caused by nonsense mutations .
    NVS1.1
  • HY-177963
    NV914

    		DNA Methyltransferase Inflammation/Immunology
    NV914 is an inhibitor of FTSJ1 (tryptophan tRNA-specific 2'-O-methyltransferase) that inhibits the methyltransferase activity of FTSJ1, induces translational readthrough of premature termination codons, and enables genes carrying nonsense mutations to synthesize full-length proteins. NV914 belongs to translational readthrough-inducing compounds (TRIDs). NV914 exhibits translational readthrough activity against nonsense mutations in in vitro systems, does not induce readthrough of natural termination codons, and restores CFTR protein expression. NV914 shows favorable acute oral tolerance in mice, with low health risks and good safety profiles. NV914 is applicable to research related to cystic fibrosis and Shwachman-Diamond syndrome .
    NV914
  • HY-177757
    NVS2.1

    		Eukaryotic Initiation Factor (eIF) Others
    NVS2.1 is a potent, orally active and brain-penetrant readthrough promoter. NVS2.1 triggers the degradation of eRF1 by activating the ribosome-related quality control pathways (involving GCN1, RNF14, and RNF25), thereby facilitating the reading through of premature termination codons. NVS2.1 can be used for the research of genetic diseases caused by nonsense mutations .
    NVS2.1

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