| Bioactivity | 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]. | ||||||||||||
| Invitro | 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]. Apoptosis Analysis[1] Cell Line: | ||||||||||||
| Name | SCR130 | ||||||||||||
| CAS | 2377858-38-1 | ||||||||||||
| Formula | C19H13Cl2N3O2S | ||||||||||||
| Molar Mass | 418.30 | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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SCR130
CAS: 2377858-38-1 F: C19H13Cl2N3O2S W: 418.30
SCR130 is a SCR7-based DNA nonhomologous end-joining (NHEJ) inhibitor. SCR130 inhibits the end-joining of DNA in a Ligas
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