| Description |
GNE-900 is a an ATP-competitive, selective, and orally active ChK1 inhibitor with IC50s of 0.0011, 1.5 µM for ChKl, ChK2, respectively. GNE-900 abrogates the G2-M checkpoint, enhances DNA damage, and induces Apoptosis. gemcitabine (HY-17026) and GNE-900 administration shows anti-tumor activity[1].
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| Related Catalog |
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| Target |
Chk1:0.0011 μM (IC50)
Chk2:1.5 μM (IC50)
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| In Vitro |
GNE-900 (1 µM; 1-48 h) 在 HT-29 细胞中与吉西他滨 (50 nM) 联合使用时，可诱导细胞凋亡并增加裂解的 PARP 的表达[1]。 Apoptosis Analysis[1] Cell Line: HT-29 cells Concentration: 1 µM Incubation Time: 1-48 h Result: Inducesd apoptosis with increased the expression of cleaved PARP when combination with gemcitabine (50 nM).
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| In Vivo |
GNE-900 (2.5-40 mg/kg; p.o.; once) 与gemcitabine (HY-17026) 联用能降低肿瘤体积并增加 DNA 损伤和 γ-H2AX 的表达水平在大鼠中[1]。 Animal Model: Sprague-Dawley rats (HT-29 tumor xenografts)[1] Dosage: 2.5-40 mg/kg (received a dose of gemcitabine 120 mg/kg) Administration: P.o.; once Result: Decreased the tumor volume and resulted in significant enhancement of DNA damage, increased γ-H2AX levels.
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| References |
[1]. Blackwood E, et al. Combination drug scheduling defines a "window of opportunity" for chemopotentiation of gemcitabine by an orally bioavailable, selective ChK1 inhibitor, GNE-900. Mol Cancer Ther. 2013 Oct;12(10):1968-80.
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