1. Cell Cycle/DNA Damage
  2. ATM/ATR
  3. CGK733


Cat. No.: HY-15520 Purity: 99.83%
Handling Instructions

CGK733 is a potent ATM/ATR inhibitor, used for the research of cancer.

For research use only. We do not sell to patients.

CGK733 Chemical Structure

CGK733 Chemical Structure

CAS No. : 905973-89-9

Size Price Stock Quantity
10 mM * 1 mL in DMSO USD 77 In-stock
Estimated Time of Arrival: December 31
10 mg USD 70 In-stock
Estimated Time of Arrival: December 31
50 mg USD 300 In-stock
Estimated Time of Arrival: December 31
100 mg USD 500 In-stock
Estimated Time of Arrival: December 31
500 mg USD 2000 In-stock
Estimated Time of Arrival: December 31
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Customer Review

Based on 4 publication(s) in Google Scholar

Top Publications Citing Use of Products

    CGK733 purchased from MCE. Usage Cited in: Biomaterials. 2019 Oct;219:119377.

    CGK-733 (1 μM) pretreatment attenuates the protein expression of p-ATM/ATR, p-H2AX, and DR5 in prostate cancer cells induced by RuSe (40 μM).

    View All ATM/ATR Isoform Specific Products:

    • Biological Activity

    • Protocol

    • Purity & Documentation

    • References

    • Customer Review


    CGK733 is a potent ATM/ATR inhibitor, used for the research of cancer.

    IC50 & Target[1]





    In Vitro

    CGK733 (4.2 ng/μL-12.5 ng/μL) enhances taxol-induced cytotoxicity in HBV-positive HCC cells. CGK733 (4.2 ng/μL) accelerates the formation of multinucleated cells and promotes the exit of mitosis in taxol-treated HBV-positive HCC cells[1]. CGK733 (10 μM) causes the loss of cyclin D1 through the ubiquitin-dependent proteasomal degradation pathway in MCF-7 and T47D breast cancer cell lines. CGK733 (0.6-40 μM) shows inhibitory activities against proliferation of LnCap prostate cancer cells, HCT116 colon cancer cells, MCF-7 and T47D estrogen receptor positive breast cancer cells, and MDA-MB436 ER negative breast cancer cells. Moreover, CGK733 inhibits proliferation of non-transformed mouse BALB/c 3T3 embryonic fibroblast cells. In addition, CGK733 (10 μM) inhibits MCF-7 proliferation, and the effect can not be suppressed by pan-caspase inhibition[2]. CGK733 (10 μM) results in 1.6-fold increase in ATM reporter activity in HEK-293 cells[3].

    In Vivo

    CGK733 (25 mg/kg, i.p.) increases the ATM reporter activity (reports inactivation of ATM kinase activity) compared to control mice, with 2.4-fold, 3.1-fold, and 1.3-fold changes at 1, 4, and 8 hours, respectively[3].

    Molecular Weight




    CAS No.





    Room temperature in continental US; may vary elsewhere.

    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Solvent & Solubility
    In Vitro: 

    DMSO : ≥ 100 mg/mL (179.91 mM)

    *"≥" means soluble, but saturation unknown.

    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 1.7991 mL 8.9954 mL 17.9908 mL
    5 mM 0.3598 mL 1.7991 mL 3.5982 mL
    10 mM 0.1799 mL 0.8995 mL 1.7991 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

      Solubility: 2.5 mg/mL (4.50 mM); Suspended solution; Need ultrasonic

    • 2.

      Add each solvent one by one:  10% DMSO    90% corn oil

      Solubility: ≥ 2.5 mg/mL (4.50 mM); Clear solution

    *All of the co-solvents are provided by MCE.
    Cell Assay

    Cells are seeded in 96-well plates at a predetermined optimal cell density to ensure exponential growth for duration of the assay. After a 24 h preincubation, growth medium is replaced with experimental medium containing the appropriate drug concentrations or 0.1% (v/v) vehicle control. After a 48 h incubation, cell proliferation is estimated using the sulforhodamine B colorimetric assay and expressed as the mean ± SE for six replicates as a percentage of vehicle control (taken as 100%). Experiments are performed independently at least three times. Statistical analyses are performed using a two-tailed Student's t test. P < 0.05 is considered to be statistically significant[2].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration

    Four to six weeks old athymic CD-1 female mice are acclimatized for at least one week before use. The mice are injected sub-cutaneously with 2×106 D54-ATMR cells in each flank. Tumors are allowed to grow to the size of 100-150 mm3. Mice are injected intraperitoneally with vehicle control (DMSO), CGK-733, KU-55933 (25 mg/kg) or irradiated with 5 Gy to each flank. Bioluminescence is acquired on Xenogen IVIS Spectrum system after injecting 400 μg/100 μL of D-luciferin at baseline (-3h) as well as 1, 4, and 8 hours after drug administration[3].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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    CGK733CGK 733CGK-733ATM/ATRAtaxia telangiectasia mutatedATM and RAD3 relatedInhibitorinhibitorinhibit

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