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Results for "

end-joining

" in MedChemExpress (MCE) Product Catalog:

12

Inhibitors & Agonists

2

Isotope-Labeled Compounds

1

Antibodies

1

Oligonucleotides

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-139297

    DNA/RNA Synthesis Apoptosis Cancer
    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 .
    SCR130
  • HY-107845
    SCR7 pyrazine
    Maximum Cited Publications
    11 Publications Verification

    CRISPR/Cas9 DNA/RNA Synthesis Apoptosis Cancer
    SCR7 pyrazine is a DNA ligase IV inhibitor that blocks nonhomologous end-joining (NHEJ) in a ligase IV-dependent manner. SCR7 pyrazine is also a CRISPR/Cas9 enhancer which increases the efficiency of Cas9-mediated homology-directed repair (HDR). SCR7 pyrazine induces cell apoptosis and has anticancer activity .
    SCR7 pyrazine
  • HY-148078

    Endonuclease Others
    PFM03 is a MRE11 Endonuclease inhibitor. PFM03 regulates DNA double-strand break repair (DSBR) by nonhomologous end-joining (NHEJ) .
    PFM03
  • HY-116770
    PFM01
    1 Publications Verification

    Endonuclease Cancer
    PFM01, N-alkylated Mirin derivative, is a MRE11 endonuclease inhibitor. PFM01 can regulate double-strand break repair (DSBR) by nonhomologous end-joining (NHEJ) versus homologous recombination (HR) .
    PFM01
  • HY-150279

    DNA/RNA Synthesis Others
    PolQi2 is a PolΘ inhibitor that targets and inhibits alt-EJ (alternative end-joining) repair by inhibiting the helicase domain at the N-terminus of PolΘ. PolQi2 enhances the precision and integration efficiency of gene editing at different loci and in various cell lines. Furthermore, the combined use of PolQi2 with DNA-PK inhibitors reduces the off-target effects of Cas9, significantly improving the fidelity and performance of CRISPR/Cas9 gene editing. PolQi2 can be used in gene editing research .
    PolQi2
  • HY-139289
    ART812
    1 Publications Verification

    DNA/RNA Synthesis Cancer
    ART812 is an orally active DNA polymerase Polθ inhibitor with an IC50 value of 7.6 nM. ART812 has an IC50 value of 240 nM for cell based microhomology-mediated end joining (MMEJ) .
    ART812
  • HY-130603
    DCZ0415
    4 Publications Verification

    NF-κB Apoptosis Cancer
    DCZ0415, a potent TRIP13 inhibitor, impairs nonhomologous end joining repair and inhibits NF-κB activity. DCZ0415 induces anti-myeloma activity in vitro, in vivo, and in primary cells derived from drug-resistant myeloma patients .
    DCZ0415
  • HY-19939S
    VX-984
    4 Publications Verification

    M9831

    DNA-PK Cancer
    VX-984 is an orally active, potent, selective and BBB-penetrated DNA-PK inhibitor. VX-984 efficiently inhibits NHEJ (non-homologous end joining) and increases DSBs (DNA double-strand breaks). VX-984 can be used for glioblastomas (GBM) and non-small cell lung cancer (NSCLC) research. VX-984 is a de novo deuterium .
    VX-984
  • HY-123401

    DNA/RNA Synthesis Cancer
    DDRI-18 is a DNA damage response inhibitor that inhibits the non-homologous end-joining (NHEJ) DNA repair process. DDRI-18 is an effective chemosensitizing agent .
    DDRI-18
  • HY-120750

    Others Cancer
    A 62176 hydrochloride is a compound that targets DNA topoisomerase II and has the activity of inhibiting purine synthesis in cancer cells. A 62176 hydrochloride interferes with c-MYC mRNA expression by interacting with G-quadruplex. The main mechanism of action of A 62176 hydrochloride is by displacing nucleosomes from the quadruplex of non-template strand rDNA, resulting in rapid redistribution of nucleosomes. The application potential of A 62176 hydrochloride is that it causes DNA damage and relies on BRCA1/2-mediated homologous recombination and DNA-PK-mediated non-homologous end-joining pathways to repair the damage .
    A 62176 hydrochloride
  • HY-164062

    CRISPR/Cas9 Others
    The Cas9 protein, guided by sgRNA, induces DNA double-strand breaks (DSBs) at specific genomic locations, activating the cell's endogenous DNA repair mechanisms, non-homologous end joining (NHEJ), or homology-directed repair (HDR), for repairing the targeted DSBs, enabling genome DNA target recognition and cleavage. LZCap AG(3'Acm) Cas9 mRNA can be used together with purified sgRNA for CRISPR/Cas genome editing, where the expressed Cas9 protein acts in conjunction with sgRNA to perform cleavage.
    LZCap AG(3'Acm) Cas9 mRNA
  • HY-163816

    Cytochrome P450 Cancer
    Antiproliferative agent-53-d3 (Compound C1) is an inhibitor for theta-mediated end joining (TMEJ) in HEK293 cell with an IC50 of 0.14 µM. Antiproliferative agent-53-d3 is the inhibitor for CYP2C19 and CYP2C9 with IC50 of 0.77 and 3.1 µM. Antiproliferative agent-53-d3 inhibits the proliferation of DNA repair-compromised cells, with IC50 of 8.1 µM for BRCA2 -/- DLD-1. Antiproliferative agent-53-d3 exhibits good pharmacokinetic characteristics in CD-1 mice .
    Antiproliferative agent-53-d3

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