CAS No. : 860352-01-8

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Cat. No. : HY-10992
M.Wt: 362.42
Formula: C17H19FN4O2S
Purity: >98 %
Storage: at 20℃ 2 years
Solubility: 10 mM in DMSO
Introduction of 860352-01-8 :

AZD-7762 is a potent ATP-competitive checkpoint kinase (Chk) inhibitor in with IC50 of 5 nM for Chk1. IC50 & Target: IC50: 5 nM (ChK1), 5 nM (ChK2)[1] In Vitro: AZD-7762 (AZD7762) is an equally potent inhibitor of Chk1 and Chk2 in vitro. AZD-7762 potently inhibits Chk1 and Chk2, abrogates DNA damage-induced S and G2 checkpoints, enhances the efficacy of gemcitabine and topotecan, and modulates downstream checkpoint pathway proteins. AZD-7762 potently inhibits Chk1 phosphorylation of a cdc25C peptide with an IC50 of 5 nM as measured by a scintillation proximity assay. The Ki for AZD-7762 is determined to be 3.6 nM. Kinetic characterization suggests that AZD-7762 binds in the ATP-binding site of Chk1 and is thought to compete directly for ATP binding in a reversible manner. AZD-7762 is shown to abrogate the G2 arrest induced by Camptothecin with an average EC50 of 10 nM (n=12) and maximal abrogation in the range of 100 nM[1]. In Vivo: In the rat H460-DNp53 xenograft study, AZD-7762 (AZD7762) potentiates the antitumor activity of Gemcitabine in a dose-dependent manner by a decrease in %T/C with increasing dose (48% and 32%, 10 and 20 mg/kg AZD-7762, respectively). In the mouse xenograft study in combination with Irinotecan, SW620 established tumors are treated with vehicle, Irinotecan alone, AZD-7762 alone, or AZD-7762 in combination with Irinotecan. AZD-7762 dosed alone shows insignificant antitumor activity, whereas Irinotecan alone displays striking and significant activity (%T/C with increasing dose is 9 and 1, respectively ). In combination with AZD-7762, %T/C increases significantly to -66% and -67%, respectively[1]. AZD7762 combination with CX-5461 induces cancer cell death of Tp53-null (Tp53-/-) Eμ-Myc lymphoma cells in vitro and in vivo[2].

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