SCR7

Catalog No.S7742 Batch:S774204

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Technical Data

Formula

C18H12N4OS
Molecular Weight 332.38 CAS No. 14892-97-8
Solubility (25°C)* In vitro DMSO 66 mg/mL (198.56 mM)
Ethanol 4 mg/mL (12.03 mM)
Water Insoluble
In vivo (Add solvents to the product individually and in order)
Clear solution
5%DMSO 40%PEG300 5%Tween80 50%ddH2O
3.3mg/ml Taking the 1 mL working solution as an example, add 50 μL of 66 mg/ml clarified DMSO stock solution to 400 μL of PEG300, mix evenly to clarify it; add 50 μL of Tween80 to the above system, mix evenly to clarify; then continue to add 500 μL of ddH2O to adjust the volume to 1 mL. The mixed solution should be used immediately for optimal results. 
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description SCR7 is a specific DNA Ligase IV inhibitor, which blocks nonhomologous end-joining (NHEJ). It increases the efficiency of HDR-mediated genome editing up to 19-fold using CRISPR/Cas9 in mammalian cells and mouse embryos.
Targets
DNA Ligase IV [1]
In vitro SCR7 effectively inhibits the formation of multimers at 200 μM and above. SCR7 successfully inhibits cell proliferation of MCF7, A549, HeLa, T47D, A2780, HT1080, and Nalm6 with IC50 of 40, 34, 44, 8.5, 120, 10, and 50 μM, respectively.[1] SCR7 suppresses the NHEJ repair of CRISPR-Cas9-induced DSBs.[2]SCR7 increases the efficiency of HDR-mediated genome editing up to 19-fold using CRISPR/Cas9 in mammalian cells and mouse embryos[3].
In vivo SCR7 treatment (10 mg/kg, i.m.) significantly reduces breast adenocarcinoma-induced tumor, and exhibits 4-fold increase in lifespan compared with control group. However, in Swiss albino mice with Dalton’s lymphoma tumor model, SCR7 (20 mg/kg, i.p.) exhibits neither tumor regression nor increase in lifespan. In BALB/c mice, SCR7 (20 mg/kg, i.p.) significantly enhances the cytotoxic effects of radiation, etoposide and 3-Aminobenzamide on tumor derived from Dalton’s lymphoma (DLA) cells.[1]

Protocol (from reference)

Kinase Assay:

[1]
  • Complementation of SCR7 Inhibition with Purified Ligase IV

    Complementation experiment is carried out by adding increasing concentrations of purified Ligase IV/XRCC4 complex (30, 60, and 120 fmol) along with the oligomeric DNA substrates (5’ compatible and 5’-5’ noncompatible ends) to the SCR7-treatedextracts. Reactions are incubated for 2 h at 25℃. The reaction products are then resolved on 8% denaturing PAGE. The gel is dried and exposed and the signal is detected with a PhosphorImager and analyzed with Multi Gauge (V3.0) software.
Cell Assay:

[1]
  • Cell lines

    MCF7, CEM, HeLa, A549, HT1080, A2780, T47D, Nalm6, N114 and K562 cells

  • Concentrations

    250 μM

  • Incubation Time

    48 h

  • Method

    Cell proliferation of cancer cells are determined by MTT and trypan blue assays. Briefly, MCF7, CEM, HeLa, A549, HT1080, A2780, T47D, Nalm6, N114 and K562 cells are grown in presence of SCR7 (10, 50, 100, and 250 μM) for 24 or 48 h, and subjected to MTT or trypan blue assays. Each experiment is repeated a minimum of three independent times.
Animal Study:

[1]
  • Animal Models

    BALB/c mice

  • Dosages

    10 mg/kg

  • Administration

    i.m.

Customer Product Validation

, , J Cell Mol Med, 2017, 21(12):3337-3346

Data from [Data independently produced by , , Cell Res, 2017, 27(6):801-814]

Data from [Data independently produced by , , Mutat Res Genet Toxicol Environ Mutagen, 2015, 793:2-8]

Selleck's SCR7 has been cited by 38 publications

The fragile X locus is prone to spontaneous DNA damage that is preferentially repaired by nonhomologous end-joining to preserve genome integrity [ iScience, 2024, 27(2):108814] PubMed: 38303711
Simultaneous inhibition of DNA-PK and Polϴ improves integration efficiency and precision of genome editing [ Nat Commun, 2023, 14(1):4761] PubMed: 37580318
MDM2 antagonists promote CRISPR/Cas9-mediated precise genome editing in sheep primary cells [ Mol Ther Nucleic Acids, 2023, 31:309-323] PubMed: 36726409
Selective utilization of non-homologous end-joining and homologous recombination for DNA repair during meiotic maturation in mouse oocytes [ Cell Prolif, 2023, 56(4):e13384] PubMed: 36564861
In situ correction of various β-thalassemia mutations in human hematopoietic stem cells [ Front Cell Dev Biol, 2023, 11:1276890] PubMed: 38333188
Increase of c-FOS promoter transcriptional activity by the dual leucine zipper kinase [ Naunyn Schmiedebergs Arch Pharmacol, 2023, none] PubMed: 36700987
Identifying key underlying regulatory networks and predicting targets of orphan C/D box SNORD116 snoRNAs in Prader-Willi syndrome [ bioRxiv, 2023, 10.1101/2023.10.03.560773] PubMed: 37873184
Disparate pathways for extrachromosomal DNA biogenesis and genomic DNA repair [ bioRxiv, 2023, 2023.10.22.563489] PubMed: 37961138
Functional editing of endogenous genes through rapid selection of cell pools (Rapid generation of endogenously tagged genes in Drosophila ovarian somatic sheath cells) [ Nucleic Acids Res, 2022, gkac448] PubMed: 35639929
Development of a Novel Reference Material for Tumor Mutational Burden Measurement Based on CRISPR/Cas9 Technology [ Front Oncol, 2022, 12:845636] PubMed: 35574377

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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

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