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AZD7762 Catalog No.GC10546

Checkpoint kinase inhibitor,ATP competitive

Size Price Stock Qty
10mM (in 1mL DMSO)
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In stock
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Sample solution is provided at 25 µL, 10mM.

Quality Control

Quality Control & SDS

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Cell experiment: [1]

Cell lines

T47D and MCF7 cells

Preparation method

The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.

Reaction Conditions

100 nM, 24 hours


A clearly enhanced radiosensitization of AZD7762 was observed in the p53 mutant T47D cells but not in the wild-type p53 MCF7 cells. In the p53 mutant T47D cells, the cytotoxicity produced by AZD7762 in combination with radiation was significantly greater than that caused by the radiation alone. In the wild-type p53 MCF7 cells, although there was a trend for AZD7762 to sensitize cells to radiation, this difference did not reach a statistical significance.

Animal experiment: [2]

Animal models

Female athymic nude mice injected with HT-29 cells

Dosage form

Intraperitoneal injection, 25 mg/kg, given immediately after radiation treatment and 8 hours later


AZD7762 treatment alone had little effect on tumor growth, whereas fractionated radiation delayed tumor growth. The time for tumors to reach thrice the initially measured tumor volume relative to the control for AZD7762 alone, fractionated radiation, and AZD7762 plus fractionated radiation was 2.3 (P < 0.53), 7.4 (P < 0.07), and 18.7 (P < 0.00014) days, respectively. Relative to fractionated radiation alone, the combination of AZD7762 and fractionated radiation was also highly significant. Thus, the combination of AZD7762 and fractionated radiation showed a greater tumor growth delay than the sum of the individual treatments alone.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.


[1] Ma Z, Yao G, Zhou B, et al. The Chk1 inhibitor AZD7762 sensitises p53 mutant breast cancer cells to radiation in vitro and in vivo. Molecular medicine reports, 2012, 6(4): 897-903.

[2] Mitchell J B, Choudhuri R, Fabre K, et al. In vitro and in vivo radiation sensitization of human tumor cells by a novel checkpoint kinase inhibitor, AZD7762. Clinical Cancer Research, 2010, 16(7): 2076-2084.

Chemical Properties

Cas No. 860352-01-8 SDF
Chemical Name 3-(carbamoylamino)-5-(3-fluorophenyl)-N-[(3S)-piperidin-3-yl]thiophene-2-carboxamide
Canonical SMILES C1CC(CNC1)NC(=O)C2=C(C=C(S2)C3=CC(=CC=C3)F)NC(=O)N
Formula C17H19FN4O2S M.Wt 362.42
Solubility ≥18.1mg/mL in DMSO, <2.89 mg/mL in EtOH, <2.37 mg/mL in H2O Storage Store at -20°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
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**When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / CoA (available online).



AZD7762 is a novel ATP competitive inhibitor of checkpoint kinases. Chk family checkpoint kinases include Chk1 and Chk2. They are activated in response to DNA damage and phosphorylate CDC25A, CDC25C protein phosphatases, which delay cell cycle progression. Therefore, Chk activation initiates cell cycle checkpoint, causes cell cycle arrest, and allows DNA repair.

AZD7762 is a potent selective inhibitor of Chk1. It binds to the ATP binding pocket and compete ATP binding in a reversible manner. AZD7762 inhibits Chk1 phosphorylation of CDC25C peptide with an IC50 of 5 nM. The Ki is 3.6 nM. It is equally potent against Chk2 but less potent against CAM, Yes, Fyn, Lyn, Hck and Lck. [1]

AZD7762 prevents cell cycle arrest and DNA repair in DNA damaged tumor cells, causing tumor cell apoptosis. Hence, it potentiates the antitumor activity of DNA damaging agents and can be used as a chemosensitizing agent. [2]

Half life of AZD7762 is 1-2 hours in mice [3]

[1]Zabludoff SD, et al. AZD7762, a novel checkpoint kinase inhibitor, drives checkpoint abrogation and potentiates DNA-targeted therapies. Mol Cancer Ther, 2008, 7(9): 2955-2966.
[2]Landau HJ, et al. The checkpoint kinase inhibitor AZD7762 potentiates chemotherapy-induced apoptosis of p53-mutated multiple myeloma cells. Mol Cancer Ther. 2012, 11(8): 1781-1788
[3]Goteti K, et al. Preclinical pharmacokinetic/pharmacodynamic models to predict synergistic effects of co-administered anti-cancer agents. Cancer Chemother Pharmacol. 2010, 66(2): 245-254.