Prexasertib dimesylate (Synonyms: LY2606368 dimesylate) |
| Catalog No.GC60301 |
프렉사서팁 디메실레이트(LY2606368 디메실레이트)는 0.9 nM의 Ki 및 1 nM 미만의 IC50을 갖는 선택적 ATP-경쟁 2세대 체크포인트 키나제 1(CHK1) 억제제입니다. 프렉사세르팁 디메실레이트는 CHK2(IC50=8 nM) 및 RSK1(IC50=9 nM)을 억제합니다. Prexasertib dimesylate는 이중 가닥 DNA 파손 및 복제 재앙을 일으켜 세포자멸사를 유발합니다. Prexasertib dimesylate는 강력한 항종양 활성을 나타냅니다.
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Cas No.: 1234015-58-7
Sample solution is provided at 25 µL, 10mM.
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Prexasertib dimesylate (LY2606368 dimesylate) is a selective, ATP-competitive second-generation checkpoint kinase 1 (CHK1) inhibitor with a Ki of 0.9 nM and an IC50 of <1 nM. Prexasertib dimesylate inhibits CHK2 (IC50=8 nM) and RSK1 (IC50=9 nM). Prexasertib dimesylate causes double-stranded DNA breakage and replication catastrophe resulting in apoptosis. Prexasertib dimesylate shows potent anti-tumor activity[1][2].
Prexasertib dimesylate (LY2606368 dimesylate) inhibits MELK (IC50=38 nM), SIK (IC50=42 nM), BRSK2 (IC50=48 nM), ARK5 (IC50=64 nM). Prexasertib dimesylate requires CDC25A and CDK2 to cause DNA damage[1]. Prexasertib dimesylate (33, 100 nM; for 7 hours) results in DNA damage during S-phase in HeLa cells[1]. Prexasertib dimesylate (8-250 nM; pre-treated for 15 minutes) inhibits CHK1 autophosphorylation (S296) and CHK2 autophosphorylation (S516) in HT-29 cells[1]. Prexasertib dimesylate (4 nM; 24 hours) results in a large shift in cell-cycle populations from G1 and G2-M to S-phase with an accompanied induction of H2AX phosphorylation in U-2 OS cells[1]. Prexasertib dimesylate (33 nM; for 12 hours) causes chromosomal fragmentation in HeLa cells. Prexasertib dimesylate (100 nM; 0.5 to 9 hours) induces replication stress and depletes the pool of available RPA2 for binding to DNA[1]. Cell Cycle Analysis[1] Cell Line: HeLa cells
Prexasertib dimesylate (LY2606368 dimesylate; 1-10 mg/kg; SC; twice daily for 3 days, rest 4 days; for three cycles) causes growth inhibition in tumor xenografts[1]. Prexasertib dimesylate (15 mg/kg; SC) causes CHK1 inhibition in the blood and the phosphorylation of both H2AX (S139) and RPA2 (S4/S8)[1]. Animal Model: Female CD-1 nu-/nu- mice (26-28 g) with Calu-6 cells[1]
[1]. King C, et al. LY2606368 Causes Replication Catastrophe and Antitumor Effects through CHK1-Dependent Mechanisms. Mol Cancer Ther. 2015 Sep;14(9):2004-1 [2]. Yin Y, et al. Chk1 inhibition potentiates the therapeutic efficacy of PARP inhibitor BMN673 in gastric cancer. Am J Cancer Res. 2017 Mar 1;7(3):473-483.
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