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Prexasertib Mesylate Hydrate (Synonyms: LY2606368 Mesylate Hydrate; LY2940930)
Prexasertib Mesylate Hydrate (LY2606368 Mesylate Hydrate) 是一种选择性的，ATP 竞争性的第二代细胞周期检测点激酶 1 (CHK1) 抑制剂，Ki 为 0.9 nM，IC50 为 <1 nm。prexasertib mesylate hydrate 抑制 chk2 (ic50=8 nM) 和 RSK1 (IC50=9 nM)。Prexasertib Mesylate Hydrate 引起双链 DNA 断裂和复制突变，导致细胞凋亡 (apoptosis)。Prexasertib Mesylate Hydrate 显示有效的抗肿瘤活性。
Prexasertib Mesylate Hydrate Chemical Structure
CAS No. : 1234015-57-6
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是否有货 |
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| 100 mg |
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询价 |
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| 250 mg |
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询价 |
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| 500 mg |
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* Please select Quantity before adding items.
Prexasertib Mesylate Hydrate 的其他形式现货产品:
Prexasertib Prexasertib dihydrochloride Prexasertib dimesylate
| 生物活性 |
Prexasertib Mesylate Hydrate (LY2606368 Mesylate Hydrate) 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 mesylate hydrate inhibits chk2 (ic50=8 nM) and RSK1 (IC50=9 nM). Prexasertib Mesylate Hydrate causes double-stranded DNA breakage and replication catastrophe resulting in apoptosis. Prexasertib Mesylate Hydrate shows potent anti-tumor activity[1][2].
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| IC50 & Target |
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Chk1
0.9 nM (Ki)
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Chk1
<1 nM (IC50)
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Chk2
8 nM (IC50)
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体外研究
(In Vitro) |
Prexasertib Mesylate Hydrate (LY2606368 Mesylate Hydrate) inhibits MELK (IC50=38 nM), SIK (IC50=42 nM), BRSK2 (IC50=48 nM), ARK5 (IC50=64 nM). LY2606368 requires CDC25A and CDK2 to cause DNA damage[1].
Prexasertib Mesylate Hydrate (33, 100 nM; for 7 hours) results in DNA damage during S-phase in HeLa cells[1].
Prexasertib Mesylate Hydrate (8-250 nM; pre-treated for 15 minutes) inhibits CHK1 autophosphorylation (S296) and CHK2 autophosphorylation (S516) in HT-29 cells[1].
Prexasertib Mesylate Hydrate (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 Mesylate Hydrate (33 nM; for 12 hours) causes chromosomal fragmentation in HeLa cells. Prexasertib Mesylate Hydrate (100 nM; 0.5 to 9 hours) induces replication stress and depletes the pool of available RPA2 for binding to DNA[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Cycle Analysis[1]
| Cell Line: |
HeLa cells |
| Concentration: |
33, 100 nM |
| Incubation Time: |
For 7 hours |
| Result: |
Had an IC50 of 37 nM and resulted in the G2-M population received DNA damage during S-phase but continued to progress through the cell cycle into an early mitosis. |
Western Blot Analysis[1]
| Cell Line: |
HT-29 cells |
| Concentration: |
8, 16, 31, 63, 125, 250 nM |
| Incubation Time: |
Pre-treated for 15 minutes |
| Result: |
Inhibited CHK1 autophosphorylation (S296) and CHK2 autophosphorylation (S516) (IC50 of less than 31 nM) in HT-29 cells. |
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体内研究
(In Vivo) |
Prexasertib Mesylate Hydrate (LY2606368 Mesylate Hydrate; 1-10 mg/kg; SC; twice daily for 3 days, rest 4 days; for three cycles) causes growth inhibition in tumor xenografts[1].
Prexasertib Mesylate Hydrate (15 mg/kg; SC) causes CHK1 inhibition in the blood and the phosphorylation of both H2AX (S139) and RPA2 (S4/S8)[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
| Animal Model: |
Female CD-1 nu-/nu- mice (26-28 g) with Calu-6 cells[1] |
| Dosage: |
1, 3.3, or 10 mg/kg |
| Administration: |
SC; twice daily for 3 days, rest 4 days; for three cycles |
| Result: |
Caused statistically significant tumor growth inhibition (up to 72.3%). |
| Animal Model: |
Female CD-1 nu-/nu- mice (26-28 g) with Calu-6 cells[1] |
| Dosage: |
15 mg/kg (Pharmacokinetic Analysis) |
| Administration: |
SC (200 μL) |
| Result: |
CHK1 was 7 ng/mL at 12 hours and 3 ng/mL by 24 hours in plasma exposures.
Phosphorylation of both H2AX (S139) and RPA2 (S4/S8) was detectable at 4 hours, showing the rapid occurrence of DNA damage. |
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| 运输条件 |
Room temperature in continental US; may vary elsewhere.
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| 储存方式 |
Please store the product under the recommended conditions in the Certificate of Analysis.
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| 参考文献 |
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[1]. King C, et al. LY2606368 Causes Replication Catastrophe and Antitumor Effects through CHK1-Dependent Mechanisms. Mol Cancer Ther. 2015 Sep;14(9):2004-13.
[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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