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首页-小分子抑制剂&激动剂-Others-Other Targets-KI-DX-014
KI-DX-014

Chemical Structure : KI-DX-014

CAS No.: 1309288-83-2

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KI-DX-014

货号: PC-25281Not For Human Use, Lab Use Only.

KI-DX-014 is a specific small-molecule compound capable of inhibiting the interaction of DDX21 with RNA with IC50 of 3.31 uM, directly binds to DDX21-C-terminal domain (HC+CTD) with Kd of 15.9 uM, allosterically attenuates DDX21 ATPase activity.

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纯度 & COA & 质检文件 纯度: >98% (HPLC) Select Batch:

    生物&药学活性

    KI-DX-014 is a specific small-molecule compound capable of inhibiting the interaction of DDX21 with RNA with IC50 of 3.31 uM, directly binds to DDX21-C-terminal domain (HC+CTD) with Kd of 15.9 uM, allosterically attenuates DDX21 ATPase activity.
    KI-DX-014 inhibits DDX21's C-terminal domain interaction with RNA.
    KI-DX-014 does not impair the ability of the DDX21 to unwind an RNA duplex, shows no inhibitory activity against U15 binding
    KI-DX-014 specifically inhibits the binding of structured RNAs, such as 7SK-SL1 and 7SK-SL4, which interact with the CTD of DDX21.
    KI-DX-014 does not inhibit the unwinding activity of DDX21 or its binding to nonstructured RNAs.
    KI-DX-014 affects the ability of DDX21 to undergo phase separation in vitro.
    KI-DX-014 blocks DDX21-dependnet release of P-TEFb from the 7SK snRNP in vitro and Pol II phosphorylation in vivo.
    KI-DX-014 suppresses DDX21-dependent phosphorylation of the Pol II CTD by inhibiting P-TEFb release, leading to developmental defects in zebrafish embryos.
    DDX21 is a member of the DEAD-box protein family, capable of binding and remodeling RNA structures and RNA–protein complexes through ATP hydrolysis.

    物理化学性质&存储条件

    分子量 330.39
    分子式 C17H22N4O3
    外观性状 Solid
    CAS No.
    储存条件
    固体粉末
    -20°C 12 个月; 4°C 6 个月
    配置液
    -80°C 6 个月; -20°C 6 个月
    Shipping
    Solubility

    10 mM in DMSO
    Chemical Name/SMILES

    3-amino-1-((1-(4-methoxyphenyl)-5-methyl-1H-pyrazol-4-yl)methyl)pyrrolidine-3-carboxylic acid

    参考文献

    1. Aiba T, et al. ACS Chem Biol. 2025 Jul 10. doi: 10.1021/acschembio.5c00302.

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