SCR7 pyrazine

SCR7 pyrazine 是一种 DNA 连接酶 IV 抑制剂，以连接酶 IV 依赖性方式阻断非同源末端连接 (NHEJ)。 SCR7 吡嗪也是一种 CRISPR/Cas9 增强剂，可提高 Cas9 介导的同源定向修复 (HDR) 的效率。 SCR7 pyrazine 可诱导细胞凋亡并具有抗癌活性。

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库存: 现货

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5mg

￥775.00

620.00

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10mg

￥1362.00

1090.00

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25mg

￥2350.00

1880.00

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Background

SCR7 pyrazine is an inhibitor of DNA ligase IV [1].

DNA Ligase IV is involved in sealing of double-strand breaks (DSBs) during nonhomologous end-joining (NHEJ). DSBs have been considered as one of the most lethal types of DNA damage within cells. Unrepaired DSBs may lead to chromosomal rearrangements such as translocations and deletions, resulting in oncogenic transformations or cell death. In higher eukaryotes, NHEJ is one of the primary mechanisms of DSB repair and is active throughout the cell cycle. NHEJ plays a major role in providing resistance to cancer cells to these radio- and chemotherapy agents [1].

SCR7 blocked Ligase IV-mediated joining by interfering with its DNA binding in cell-free repair system. SCR7 inhibited NHEJ in a Ligase IV-dependent manner within cells, and activated the intrinsic apoptotic pathway. SCR7 dose-dependent decreased cell proliferation in MCF7, A549, and HeLa cells with an IC50 of 40, 34, and 44 μM, respectively. In T47D, A2780, and HT1080 cells, the IC50 values were 8.5, 120, and 10 μM, respectively [1].

SCR7 treatment (10 mg/kg, six doses) significantly reduced breast adenocarcinoma-induced tumor and impeded tumor progression in mouse models in mouse models. Coadministered of SCR7 with DSB-inducing therapeutic modalities significantly enhanced their sensitivity.

Reference:
[1] Srivastava M, Nambiar M, Sharma S, et al.? An inhibitor of nonhomologous end-joining abrogates double-strand break repair and impedes cancer progression[J]. Cell, 2012, 151(7): 1474-1487.