1. Cell Cycle/DNA Damage
    Apoptosis
  2. DNA/RNA Synthesis
    Apoptosis
  3. SCR130

SCR130 

Cat. No.: HY-139297
Handling Instructions

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.

For research use only. We do not sell to patients.

SCR130 Chemical Structure

SCR130 Chemical Structure

CAS No. : 2377858-38-1

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5 mg USD 850 In-stock
Estimated Time of Arrival: December 31
10 mg USD 1360 In-stock
Estimated Time of Arrival: December 31
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Based on 1 publication(s) in Google Scholar

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Description

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].

In Vitro

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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Apoptosis Analysis[1]

Cell Line: Reh cells
Concentration: 7 μM, 14 μM, and 21 μM
Incubation Time: 48 hours
Result: Showed a concentration-dependent increase in the number of late and early apoptotic cells.

Western Blot Analysis[1]

Cell Line: Reh cells
Concentration: 7 μM, 14 μM, and 21 μM
Incubation Time: 48 hours
Result: Revealed a concentration-dependent increase in levels of pATM and activation of p53 through phosphorylation.
Molecular Weight

418.30

Formula

C₁₉H₁₃Cl₂N₃O₂S

CAS No.
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