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  • S1460 SP600125 Biological Activity of SP600125: SP600125 is a JNK inhibitor (IC50=40 nM for JNK-1 and JNK-2 and 90 nM for JNK-3). This agent exhibits greater than 300-fold selectivity for JNK against related MAP kinases ERK1 and p38–2, and the serine threonine kinase PKA. [1] SP600125 is a reversible ATP-competitive inhibitor. In cells, SP600125 dose dependently inhibited the phosphorylation of c-Jun, the expression of inflammatory genes COX-2, IL-2, IFN-γ, TNF-α, and prevented the activation and differentiation of primary human CD4 cell cultures. [1] References on SP600125: [1] Brydon L. Bennett et al. Proc Natl Acad Sci U S A. 2001;98(24):13681-6

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    Biological Activity of SP600125: SP600125 is a JNK inhibitor (IC50=40 nM for JNK-1 and JNK-2 and 90 nM for JNK-3). This agent exhibits greater than 300-fold selectivity for JNK against related MAP kinases ERK1 and p38–2, and the serine threonine kinase PKA. [1] SP600125 is a reversible ATP-competitive inhibitor. In cells, SP600125 dose dependently inhibited the phosphorylation of c-Jun, the expression of inflammatory genes COX-2, IL-2, IFN-γ, TNF-α, and prevented the activation and differentiation of primary human CD4 cell cultures. [1] References on SP600125: [1] Brydon L. Bennett et al. Proc Natl Acad Sci U S A. 2001;98(24):13681-6

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    Biological Activity of SP600125: SP600125 is a JNK inhibitor (IC50=40 nM for JNK-1 and JNK-2 and 90 nM for JNK-3). This agent exhibits greater than 300-fold selectivity for JNK against related MAP kinases ERK1 and p38–2, and the serine threonine kinase PKA. [1] SP600125 is a reversible ATP-competitive inhibitor. In cells, SP600125 dose dependently inhibited the phosphorylation of c-Jun, the expression of inflammatory genes COX-2, IL-2, IFN-γ, TNF-α, and prevented the activation and differentiation of primary human CD4 cell cultures. [1] References on SP600125: [1] Brydon L. Bennett et al. Proc Natl Acad Sci U S A. 2001;98(24):13681-6

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    S1460 SP600125 Biological Activity of SP600125: SP600125 is a JNK inhibitor (IC50=40 nM for JNK-1 and JNK-2 and 90 nM for JNK-3). This agent exhibits greater than 300-fold selectivity for JNK against related MAP kinases ERK1 and p38–2, and the serine threonine kinase PKA. [1] SP600125 is a reversible ATP-competitive inhibitor. In cells, SP600125 dose dependently inhibited the phosphorylation of c-Jun, the expression of inflammatory genes COX-2, IL-2, IFN-γ, TNF-α, and prevented the activation and differentiation of primary human CD4 cell cultures. [1] References on SP600125: [1] Brydon L. Bennett et al. Proc Natl Acad Sci U S A. 2001;98(24):13681-6

    Uploaded by

    Selleck Chemicals LLC
    Biological Activity of SP600125: SP600125 is a JNK inhibitor (IC50=40 nM for JNK-1 and JNK-2 and 90 nM for JNK-3). This agent exhibits greater than 300-fold selectivity for JNK against related MAP kinases ERK1 and p38–2, and the serine threonine kinase PKA. [1] SP600125 is a reversible ATP-competitive inhibitor. In cells, SP600125 dose dependently inhibited the phosphorylation of c-Jun, the expression of inflammatory genes COX-2, IL-2, IFN-γ, TNF-α, and prevented the activation and differentiation of primary human CD4 cell cultures. [1] References on SP600125: [1] Brydon L. Bennett et al. Proc Natl Acad Sci U S A. 2001;98(24):13681-6

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    Product Information Novel Kinase Inhibitors

    for cell signaling & oncology research

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    M.Wt: 220.23
    N NH +1-713-922-4115
    Formula: C14H8N2O enquiry@selleckchem.com
    Solubility: DMSO
    Purity: 99% Tech Support
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    Storage: at -20℃ 2 years O (chemistry support)
    CAS No.: 129-56-6 techbio@selleckchem.com
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    www.selleckchem.com
    SP600125 is a JNK inhibitor (IC50=40 nM for JNK-1 and JNK-2 and 90 nM for JNK-3). This
    agent exhibits greater than 300-fold selectivity for JNK against related MAP kinases ERK1 and
    p38–2, and the serine threonine kinase PKA.[1] SP600125 is a reversible ATP-competitive inhibitor.
    In cells, SP600125 dose dependently inhibited the phosphorylation of c-Jun, the expression of
    inflammatory genes COX-2, IL-2, IFN-γ, TNF-α, and prevented the activation and differentiation
    of primary human CD4 cell cultures. [1]
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    References
    [1] Brydon L. Bennett et al. Proc Natl Acad Sci U S A. 2001;98(24):13681-6
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