SCR130 是一种基于 SCR7 的 DNA 非同源末端连接 (NHEJ) 抑制剂。 SCR130 以依赖连接酶 IV 的方式抑制 DNA 的末端连接。SCR130 对连接酶 IV 具有特异性，对连接酶 III 和连接酶 I 介导的连接的影响很小或没有影响。SCR130 诱导细胞凋亡 (apoptosis) 并具有抗癌活性。
货号:ajcx34230
CAS:2377858-38-1
分子式:C19H13Cl2N3O2S
分子量：418.3
溶解度:N/A
纯度：98%
存储：Store at -20°C
库存：现货

Background:

SCR130 is a SCR7-based DNA nonhomologous end-joining (NHEJ) inhibitor. SCR130 inhibits the end-joining of DNA in a Ligase IV-dependent manner. SCR130 is specific to Ligase IV, and shows minimal or no effect on Ligase III and Ligase I mediated joining. SCR130 induces cell apoptosis and has anticancer activity[1].

SCR130 (7-21 μM; 48 hours) increase in the number of late and early apoptotic cells. SCR130 induces apoptosis by both intrinsic and extrinsic pathways. SCR130 increases the expression of p-p53, BCL2 and MCL1, and CYTOCHROME C, BAX, and BAK also increaseed. The activation of caspase 8, increase in expression of FAS and SMAC-DIABLO proteins are also observed[1].SCR130 (48 hours) exhibits cytotoxicity in Reh, HeLa, CEM, Nalm6, and N114 cells with IC50 values of 14.1 μM, 5.9 μM, 6.5 μM, 2.2 μM, and 11 μM, respectively[1].SCR130 can potentiate the effect of radiation (0.5 and 1 Gy) by inducing enhanced cell death upon coadministration in Reh and Nalm6 cell lines[1].SCR130 blocks the endogenous NHEJ leading to accumulation of unrepaired DNA breaks. Treatment with SCR130 leads to inhibition of endogenous NHEJ, resulting in the accumulation of DNA double-strand breaks (DSBs) and cell death by activating apoptotic pathways[1].

[1]. Ujjayinee Ray, et al. Identification and characterization of novel SCR7-based small-molecule inhibitor of DNA end-joining, SCR130 and its relevance in cancer therapeutics. Mol Carcinog. 2020 Jun;59(6):618-628.