產(chǎn)品屬性：
產(chǎn)品名稱(chēng) | SCR130 |
規(guī)格 | 5 mg、10 mg |
貨號(hào) | EY-01Y10474 |
Cas No.: 2377858-38-1
別名: N/A
化學(xué)名: N/A
分子式: C19H13Cl2N3O2S
分子量: 418.3
溶解度: N/A
儲(chǔ)存條件: Store at -20°C
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
產(chǎn)品描述：
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.
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