SML3864
SMG1i
≥95% (HPLC)
别名:
1-[4-[4-[2-[4-Chloro-3-(diethylsulfamoyl)anilino]pyrimidin-4-yl]pyridin-2-yl]phenyl]-3-methylurea, 2-Chloro-N,N-diethyl-5-[[4-[2-[4-[[(methylamino)carbonyl]amino]phenyl]-4-pyridinyl]-2-pyrimidinyl]amino]benzenesulfonamide, NMDi, SMG1 inhibitor 11j, SMG1 inhibitor compound 11j
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生化／生理作用
Potent and selective SMG-1 (hSMG-1; SMG1) kinase inhibitor that blocks nonsense-mediated decay (NMD).
SMG1i is a potent and selective SMG-1 kinase inhibitor (hSMG-1 IC50 = 110 pM) with much reduced potency against mTOR, PI3Kα/γ and CDK1/2 (IC50 = 50 nM, 92/60 nM, 32/7.1 μM, respectively). SMG1i selectively downregulates MDA361 cellular phosphorylation of UPF1 (0.3 -1 μM), but not that of mTOR or AKT substrates (p70s6 K and PI3K). Nonsense-mediated decay (NMD) inhibition by SMG1i (1 µM) is shown to synergize with premature termination codons (PTCs) readthrough agents (G418, gentamicin, and paromomycin) in promoting the expression of CFTR protein in murine cells carrying Cftr G542X nonsense mutation.
SMG1i is a potent and selective SMG-1 kinase inhibitor (hSMG-1 IC50 = 110 pM) with much reduced potency against mTOR, PI3Kα/γ and CDK1/2 (IC50 = 50 nM, 92/60 nM, 32/7.1 μM, respectively). SMG1i selectively downregulates MDA361 cellular phosphorylation of UPF1 (0.3 -1 μM), but not that of mTOR or AKT substrates (p70s6 K and PI3K). Nonsense-mediated decay (NMD) inhibition by SMG1i (1 µM) is shown to synergize with premature termination codons (PTCs) readthrough agents (G418, gentamicin, and paromomycin) in promoting the expression of CFTR protein in murine cells carrying Cftr G542X nonsense mutation.
儲存類別代碼
11 - Combustible Solids
水污染物質分類（WGK）
WGK 3
閃點（°F）
Not applicable
閃點（°C）
Not applicable
Identification of pyrimidine derivatives as hSMG-1 inhibitors
Bioorganic & Medicinal Chemistry Letters, 22(21), 6636-6641 (2012)
Functional Restoration of CFTR Nonsense Mutations in Intestinal Organoids
Journal of Cystic Fibrosis, 21(2), 246-253 (2022)
Daniel R McHugh et al.
International journal of molecular sciences, 22(1) (2021-01-06)
Many heritable genetic disorders arise from nonsense mutations, which generate premature termination codons (PTCs) in transcribed mRNA. PTCs ablate protein synthesis by prematurely terminating the translation of mutant mRNA, as well as reducing mutant mRNA quantity through targeted degradation by
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