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    InvivoChem Cat #: V2526
    CAS #: 925701-49-1Purity ≥98%

    Description: KU-60019 is an improved analogue of KU-55933 with 10-fold higher activity than KU-55933 at blocking radiation-induced phosphorylation of key ATM targets in human glioma cells. It has IC50 of 6.3 nM for ATM in cell-free assays, 270- and 1600-fold more selective for ATM than DNA-PK and ATR,and is a highly effective radiosensitizer. KU-60019 can reduce radiation-induced S473 AKT phosphorylation in human glioma cell lines that are p53 wild type (U87) and p53 mutant (U1242). However, the suppression of AKT does not enhance radiosensitization of KU-60019. KU-60019 has been reported to inhibit cell migration and invasion in human glioma cells U87 and U1242 in a dose-dependent manner. Besides, KU-60019, to some extent, has also been shown to suppress the growth of U1242 cells.

    References: Mol Cancer Ther. 2009 Oct;8(10):2894-902; Clin Cancer Res. 2013 Jun 15;19(12):3189-200.

    Related CAS#: 925701-46-8

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    Molecular Weight (MW)547.67
    CAS No.925701-49-1
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 18 mg/mL (32.9 mM)
    Water: <1 mg/mL
    Ethanol: <1 mg/mL
    SMILESO=C(NC1=CC(CC2=C(C(C3=CC(C=C(N4CCOCC4)O3)=O)=CC=C2)S5)=C5C=C1)CN6C[[email protected]](C)O[[email protected]](C)C6
    SynonymsKU60019; KU 60019; KU-60019

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    In Vitro

    In vitro activity: Compared to KU-55933, KU-60019 is an improved more water-soluble inhibitor of the ATM kinase, while displaying similar target selectivity. KU-60019 has little activity against DNA-PKcs and ATR with IC50 values of 1.7 μM and >10 μM, respectively, as well as 229 other protein kinases such as PI3K, mTOR and mTOR/FKBP12. KU-60019 displays 3- to 10-fold more potency than KU-55933 at blocking radiation-induced phosphorylation of key ATM protein targets such as p53, γ-H2AX, and CHK2, in human glioma U87 and U1242 cells, as 1 μM of KU-60019 significantly induces >70% decrease of p53 (S15) phosphorylation to which extent ~10 μM of KU-55933 is required to achieve. KU-60019 effectively radiosensitizes human glioma cells with dose-enhancement ratio of 1.7 and 4.4 at 1 μM and 10 μM, respectively, and also radiosensitizes the normal fibroblasts but not the A-T fibroblasts. KU-60019 treatment (3 μM) blocks basal and insulin-induced AKT S473 phosphorylation by 70% and ~50%, respectively, and completely reduces radiation-induced AKT phosphorylation below the level of control. The effect of KU-60019 on AKT S473 phosphorylation can be seen in glioma cell lines and normal fibroblasts but not in A-T (h-TERT) cells, and can be significantly blocked by phosphatase inhibitor okadaic acid, suggesting a critical role of ATM kinase in regulating AKT phosphorylation via unknown phosphatase. Consistent with the inhibition of prosurvival AKT signaling, KU-60019 at 3 μM significantly inhibits migration and invasion of human glioma U87 cells by >70% and ~60%, respectively, as well as U1242 cells by >50% and ~60% respectively.

    Kinase Assay: KU-55933 has an IC50 of 13 nM and Ki of 2.2 nM in vitro and is highly specific for the ATM kinase using a panel of 60 protein kinases. KU-60019 is an improved inhibitor of the ATM kinase with an IC50 of 6.3 nM, approximately half that of KU-55933. The IC50 values for DNA-PKcs and ATR are 1.7 and >10 μM, respectively, almost 270-and 1600-fold higher than for ATM. KU-60019 is 10-fold more effective than KU-55933 at blocking radiation-induced phosphorylation of key ATM targets in human glioma cells. In human U87 glioma cells, KU-55933 completely inhibits phosphorylation of p53 (S15) at 10 μM but not at 3 μM, whereas γ-H2AX levels are only partly reduced with 10 μM 1 h after irradiation. By comparison, 3 μM KU-60019 completely inhibits p53 phosphorylation and partial inhibits at 1 μM.

    Cell Assay: Cells (U87 and U1242) are exposed to KU-60019 for 1, 3, and 5 days. Cell growth is determined by AlamarBlue. AlamarBlue is added to the medium to the recommended final concentration. Plates are incubated for 1 hour at 37 °C, fluorescence is determined on a Fluoro-Count plate reader (excitation 530 nm, emission 590 nm), and values are taken as a measure of cell growth. Cell survival is determined by trypan blue/fluorescence activated cell sorting (FACS) assay.

    In VivoSuppression of ATM-dependent STAT3 activation by KU-55933 enhances TRAIL-mediated apoptosis through up-regulation of surface DR5 expression, whereas suppression of both STAT3 and NF-κB appeares to be involved in down-regulation of cFLIP accompanied by an additional increase in apoptotic levels. The ATM inhibitor KU-55933 affectes TRAIL-mediated apoptosis more strongly than the JAK2 inhibitor, AG490, or overexpression of STAT3β.
    Animal modelAthymic female mice harboring orthotopic glioma U1242/luc-GFP tumors or human glioma U1242/luc-GFP tumors
    Formulation & DosageDissolve in saline; KU-60019 (10 μM) is delivered at a rate of 0.5 μL/h by osmotic pump; KU-60019 (250 μM) in 12.5 μL is infused by CED; Administered intratumorally by convection-enhanced delivery or osmotic pump
    ReferencesMol Cancer Ther. 2009 Oct;8(10):2894-902; Clin Cancer Res. 2013 Jun 15;19(12):3189-200.

    These protocols are for reference only. InvivoChem does not independently validate these methods.


    KU-60019 is a more effective inhibitor of the ATM kinase than KU-55933.  2009 Oct;8(10):2894-902.


    KU-60019 radiosensitizes U87 and U1242 human glioma cells and normal but not A-T fibroblasts.  2009 Oct;8(10):2894-902.



    KU-60019 inhibits migration and invasion of human glioma U87 and U1242 cells in vitro.  2009 Oct;8(10):2894-902.


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