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Cat. No. M1665
AZD7762 Structure
Size Price Availability Quantity
Free Sample 0.5 mg  USD 0 In stock
10mM*1mL in DMSO USD 85  USD85 In stock
2mg USD 50  USD50 In stock
5mg USD 80  USD80 In stock
10mg USD 125  USD125 In stock
50mg USD 340  USD340 In stock
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Quality Control & Documentation
Biological Activity

AZD7762 is a potent ATP-competitive checkpoint kinase inhibitor with an IC50 of 5 and <10 nM for CHK1 and CHK2 respectively.AZD7762 has been profiled extensively in vitro andin vivo in combination with DNA-damaging agents and has been shown to potentiate response in several different settings where inhibition of checkpoint kinase results in the abrogation of DNA damage-induced cell cycle arrest.

Product Citations
Customer Product Validations & Biological Datas
Source Int J Gynecol Cancer (2014). Figure 3. AZD7762
Method analysis of cell cycle distribution
Cell Lines Ovarian clear cell carcinoma cells
Concentrations 50- or 150-nmol/L
Incubation Time 48 and 72 h
Results However, after treatment with cisplatin and AZD7762, the proportion of the cells in the G0/G1 and S phases decreased dramatically
Source Int J Gynecol Cancer (2014). Figure 2. AZD7762
Method Immunofluorescence Studies
Cell Lines Ovarian clear cell carcinoma cells
Concentrations 50- or 150-nmol/L
Incubation Time 24 h
Results AZD7762 inhibited phosphorylation of Chk1 and Chk2 effectively and stabilized Cdc25A in response to cisplatin.
Protocol (for reference only)
Cell Experiment
Cell lines H29 cells
Preparation method Checkpoint Abrogation Assay
HT29 cells (3 × 105) were seeded in 96-well plates and incubated overnight. Cells were treated for 2 h with camptothecin (topoisomerase I inhibitor; 0.07 μg/mL) to induce the G2 checkpoint. Cells were then treated for 20 h with vehicle (0.5% DMSO) or caffeine (4 mmol/L; positive control) plus nocodazole (1 μg/mL) or a 12-point titration of AZD7762 (12.5 μmol/L to 6 nmol/L) plus nocodazole. Nocodazole alone-treated cells with no camptothecin pretreatment were used to determine the maximum mitotic index. Cells were fixed with 3.7% formaldehyde for 1 h, permeabilized with PBS containing 0.05% Triton X, and incubated with anti-phH3 antibody for 1 h followed by Alexa Fluor 488 anti-rabbit (Molecular Probes) and Hoechst stain for 1 h. Mitotic index was determined on the ArrayScan and expressed as the percentage of cells undergoing mitosis. The EC50 was calculated by concentration-response curve fitting using three-variable logistical equations within XLfit (model 205) with the curve bottom constrained to 0 and the top constrained to 100 by nocodazole alone treatment.
Concentrations 6nM~12.5μM
Incubation time 20 h
Animal Experiment
Animal models athymic mice bearing established H460-DNp53 or SW620 tumors and rnu rats bearing established H460-DNp53 tumors
Formulation formulated in 11.3% hydroxyproplyl-β-cyclodextrin
Dosages 25mg/kg(mouse) and 10 or 20mg/kg (rat)
Administration i.v. injection via the tail vein
Chemical Information
Molecular Weight 362.42
Formula C17H19FN4O2S
CAS Number 860352-01-8
Solubility (25°C) DMSO 50 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] Ma et al. Mol Med Report. The Chk1 inhibitor AZD7762 sensitises p53 mutant breast cancer cells to radiation in vitro and in vivo.

[2] Landau et al. Mol Cancer Ther. The Checkpoint Kinase Inhibitor AZD7762 Potentiates Chemotherapy-Induced Apoptosis of p53-Mutated Multiple Myeloma Cells.

[3] Oza et al. J Med Chem. Discovery of checkpoint kinase inhibitor (S)-5-(3-fluorophenyl)-N-(piperidin-3-yl)-3-ureidothiophene-2-carboxamide (AZD7762) by structure-based design and optimization of thiophenecarboxamide ureas.

[4] Aris et al. Cancer Res. Potentiation of the novel topoisomerase I inhibitor indenoisoquinoline LMP-400 by the cell checkpoint and Chk1-Chk2 inhibitor AZD7762.

[5] Zabludoff SD, et al. Mol Cancer Ther. AZD7762, a novel checkpoint kinase inhibitor, drives checkpoint abrogation and potentiates DNA-targeted therapies.

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Keywords: AZD7762 supplier, Checkpoint, inhibitors, activators

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