AZD-7762 - CAS 860352-01-8
Catalog number:
Not Intended for Therapeutic Use. For research use only.
Checkpoint Kinase (Chk)
AZD-7762 is a synthetic small molecule inhibitor of checkpoint kinases (Chks) with potential chemosensitizing activity. AZD7762 binds to and inhibits Chks, which may prevent cell cycle arrest and subsequent nucleotide excision repair in DNA-damaged tumor cells, resulting in tumor cell apoptosis.
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white solid powder
AZD 7762; AZD7762.
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1.Aven-mediated checkpoint kinase control regulates proliferation and resistance to chemotherapy in conventional osteosarcoma.
Baranski Z1, Booij TH1, Cleton-Jansen AM2, Price LS1,3, van de Water B1, Bovée JV2, Hogendoorn PC2, Danen EH1. J Pathol. 2015 Jul;236(3):348-59. doi: 10.1002/path.4528. Epub 2015 Mar 30.
Conventional high-grade osteosarcoma is the most common primary bone sarcoma, with relatively high incidence in young people. In this study we found that expression of Aven correlates inversely with metastasis-free survival in osteosarcoma patients and is increased in metastases compared to primary tumours. Aven is an adaptor protein that has been implicated in anti-apoptotic signalling and serves as an oncoprotein in acute lymphoblastic leukaemia. In osteosarcoma cells, silencing Aven triggered G2 cell-cycle arrest; Chk1 protein levels were attenuated and ATR-Chk1 DNA damage response signalling in response to chemotherapy was abolished in Aven-depleted osteosarcoma cells, while ATM, Chk2 and p53 activation remained intact. Osteosarcoma is notoriously difficult to treat with standard chemotherapy, and we examined whether pharmacological inhibition of the Aven-controlled ATR-Chk1 response could sensitize osteosarcoma cells to genotoxic compounds.
2.Enhancement of hypoxia-activated prodrug TH-302 anti-tumor activity by Chk1 inhibition.
Meng F1, Bhupathi D2, Sun JD3, Liu Q4, Ahluwalia D5, Wang Y6, Matteucci MD7, Hart CP8. BMC Cancer. 2015 May 21;15:422. doi: 10.1186/s12885-015-1387-6.
BACKGROUND: The hypoxia-activated prodrug TH-302 is reduced at its nitroimidazole group and selectively under hypoxic conditions releases the DNA cross-linker bromo-isophosphoramide mustard (Br-IPM). Here, we have explored the effect of Chk1 inhibition on TH-302-mediated pharmacological activities.
3.Chk1 inhibition as a novel therapeutic strategy for treating triple-negative breast and ovarian cancers.
Bryant C, Rawlinson R, Massey AJ1. BMC Cancer. 2014 Aug 7;14:570. doi: 10.1186/1471-2407-14-570.
BACKGROUND: Chk1 inhibitors are currently in clinical trials as putative potentiators of cytotoxic chemotherapy drugs. Chk1 inhibitors may exhibit single agent anti-tumor activity in cancers with underlying DNA repair, DNA damage response or DNA replication defects.
4.Combined CDKN1A/TP53 mutation in bladder cancer is a therapeutic target.
Liu Y1, Kwiatkowski DJ2. Mol Cancer Ther. 2015 Jan;14(1):174-82. doi: 10.1158/1535-7163.MCT-14-0622-T. Epub 2014 Oct 27.
Invasive bladder cancer has high morbidity and nearly uniform mortality when metastatic, with no therapeutic improvement in many years. Although chemotherapy combined with Chk1 inhibition has been investigated in several cancer types in which TP53 mutation is seen, this combination treatment approach has not been studied in bladder cancer. Recently, cancer genome sequencing efforts have identified CDKN1A (p21) mutations at 14% frequency in invasive bladder cancer, co-occurring half the time with TP53 mutations. We hypothesized that combined CDKN1A-TP53 loss would make bladder cancer sensitive to combined treatment with gemcitabine and Chk1 inhibitor. Here, we show that TP53-CDKN1A double-mutant bladder cancer cell lines, 647V and RT-112, have a remarkable increase in p-Chk1 levels and G2-M arrest in response to gemcitabine treatment, with a heightened sensitivity to combination treatment with gemcitabine and either Chk1 inhibitor PF477736 or AZD7762, in comparison with other bladder cancer cell lines (either TP53 or p21 deficient).
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