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Cat. No. M1801
KU-55933 Structure


Size Price Availability Quantity
Free Sample (0.5-1 mg)  USD 0 In stock
10mM*1mL in DMSO USD 58  USD58 In stock
5mg USD 48  USD48 In stock
10mg USD 68  USD68 In stock
50mg USD 196  USD196 In stock
100mg USD 328  USD328 In stock
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Quality Control & Documentation
Biological Activity

KU-55933 is a cell-permeable, potent, selective and ATP-competitive inhibitor of ATM (Ataxia telangiectasia mutated), a serine/threonine protein kinase, that exhibits an IC50 of 13 nmol/L and a Ki of 2.2 nmol/L. KU-55933 shows specificity with respect to inhibition of other phosphatidylinositol 3'-kinase-like kinases. Cellular inhibition of ATM by KU-55933 was demonstrated by the ablation of ionizing radiation-dependent phosphorylation of a range of ATM targets, including p53, gammaH2AX, NBS1, and SMC1. KU-55933 did not show inhibition of UV light DNA damage induced cellular phosphorylation events. Exposure of cells to KU-55933 resulted in a significant sensitization to the cytotoxic effects of ionizing radiation and to the DNA double-strand break-inducing chemotherapeutic agents, etoposide, doxorubicin, and camptothecin. Inhibition of ATM by KU-55933 also caused a loss of ionizing radiation-induced cell cycle arrest. By contrast, KU-55933 did not potentiate the cytotoxic effects of ionizing radiation on ataxia-telangiectasia cells, nor did it affect their cell cycle profile after DNA damage. We conclude that KU-55933 is a novel, specific, and potent inhibitor of the ATM kinase.

Customer Product Validations & Biological Datas
Source J Neurooncol (2012). Figure 2. KU-55933
Method clonogenic assay
Cell Lines U251 and U87 malignant glioma cell lines
Concentrations 10 microM
Incubation Time 24 hours or 72 hours
Results U87 cells also were sensitized by KU-55933 treatment, although the extent of sensitization was less profound
Protocol (for reference only)
Cell Experiment
Cell lines LU1205 and WM35 cells
Preparation method Apoptosis studies. Cells were exposed to soluble TRAIL (50 ng/mL) alone or in combination with cycloheximide (2 μg/mL). Different variants of combined treatment were used, including γ-irradiation (5 Gy), in the presence or absence of specific inhibitors of signaling pathways followed by TRAIL treatment. Apoptosis was then assessed by quantifying the percentage of hypodiploid nuclei using fluorescence-activated cell sorting analysis.
Concentrations 10 μM
Incubation time 48 h
Animal Experiment
Animal models LU1205 cells Human melanoma transplant in nude mice.
Formulation DMSO
Dosages 10 μM
Chemical Information
Molecular Weight 395.49
Formula C21H17NO3S2
CAS Number 587871-26-9
Solubility (25°C) DMSO 39 mg/mL
Storage Powder          -20°C   3 years ;  4°C   2 years
In solvent       -80°C   6 months ;  -20°C   1 month
Conversion of different model animals based on BSA (PMID: 27057123)
Species Mouse Rat Rabbit Guinea pig Hamster Dog
Weight (kg) 0.02 0.15 1.8 0.4 0.08 10
Body Surface Area (m2) 0.007 0.025 0.15 0.05 0.02 0.5
Km factor 3 6 12 8 5 20
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of Compound A used for a mouse (20 mg/kg) to a dose based on the BSA for a rat, multiply 20 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for Compound A of 10 mg/kg.


[1] Ivanov VN, et al. Cancer Res. Inhibition of ataxia telangiectasia mutated kinase activity enhances TRAIL-mediated apoptosis in human melanoma cells.

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Abmole Inhibitor Catalog

Keywords: KU-55933, KU55933 supplier, ATM/ATR, inhibitors, activators

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