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Results for "

double-strand breaks (DSB)

" in MedChemExpress (MCE) Product Catalog:

15

Inhibitors & Agonists

1

Peptides

1

Natural
Products

1

Isotope-Labeled Compounds

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-110111
    T2AA

    		DNA/RNA Synthesis Cancer
    T2AA is a monoubiquitinated proliferating cell nuclear antigen (PCNA) inhibitor that prevents DNA repair, increases double-strand break (DSB) formation and promotes necroptosis and cell cycle arrest in G1 phase .
    T2AA
  • HY-110185
    NSC 617145

    		DNA/RNA Synthesis Cancer
    NSC 617145 is a selective werner syndrome helicase (WRN) helicase inhibitor with an IC50 value of 230 nM. NSC 617145 inhibits WRN ATPase, and induces double-strand breaks (DSB) and chromosomal abnormalities. NSC 617145 shows selective for WRN over BLM, FANCJ, ChlR1, RecQ, and UvrD helicases .
    NSC 617145
  • HY-111183
    Neocarzinostatin

    Zinostatin; Vinostatin

    		 DNA/RNA Synthesis Bacterial Apoptosis Antibiotic Infection Cancer
    Neocarzinostatin, a potent DNA-damaging, anti-tumor antibiotic, recognizes double-stranded DNA bulge and induces DNA double strand breaks (DSBs). Neocarzinostatin induces apoptosis. Neocarzinostatin has potential for EpCAM-positive cancers treatment .
    Neocarzinostatin
  • HY-149348
    DiPT-4

    		Topoisomerase PARP Apoptosis Cancer
    DiPT-4 is a dual TOP1/PARP1 inhibitor that induces massive DNA double-strand breaks (DSBs), cell cycle arrest, and apoptosis in cancer cells. DiPT-4 has the potential to overcome cancer drug resistance .
    DiPT-4
  • HY-100707
    IC 86621

    IC 86621 is a potent DNA-dependent protein kinase (DNA-PK) inhibitor, with an IC50 of 120 nM. IC 86621 also acts as a selective and reversible ATP-competitive inhibitor.IC 86621 inhibits DNA-PK mediated cellular DNA double-strand break (DSB) repair (EC50=68 µM). IC 86621 increases DSB-induced antitumor activity without cytotoxic effects. IC 86621 can protects rheumatoid arthritis (RA) T cells from apoptosis .
    IC 86621
  • HY-Q04764
    TI17

    		Thyroid Hormone Receptor Apoptosis Cancer
    TI17 is an inhibitor of the thyroid hormone receptor-interacting protein Trip13 and has anticancer activity. TI17 effectively inhibits multiple myeloma (MM) cell proliferation and induces cell cycle arrest and apoptosis. Trip13 is an AAA-ATPase that mediates double-strand break (DSB) repair; TI17 inhibits Trip13 function and increases DNA damage .
    TI17
  • HY-113064
    Selenocystine

    		Endogenous Metabolite Cancer
    Selenocystine is a broad-spectrum anti-cancer agent. Selenocystine induces DNA damage in HepG2 cells, particularly in the form of DNA double strand breaks (DSBs). Selenocystine exhibits great promise as a therapeutic or adjuvant agent targeting DNA repair for cancer treatment .
    Selenocystine
  • HY-121862
    CM03

    		DNA/RNA Synthesis Cancer
    CM03 is a potent DNA G-quadruplexes (G4s) ligand. CM03 can stabilise G4s, downregulating more G4-containing genes as well as increasing incidence of double-strand break events (DSBs) due to torsional strain on DNA and chromatin structure. CM03 has selective potency for pancreatic cancer cells .
    CM03
  • 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-115531
    UNC-2170

    		Others Cancer
    UNC-2170 is a functionally active, fragment-like ligand for 53BP1 (IC50=29 µM; Kd=22 µM). UNC-2170 shows at least 17-fold selectivity for 53BP1 as compared to nine other methyl-lysine (Kme) reader proteins. 53BP1 is a Kme binding protein that plays a central role in DNA Damage Repair (DDR) pathways and is recruited to sites of double-strand breaks (DSB) .
    UNC-2170
  • HY-115552
    Simmiparib

    		PARP Cancer
    Simmiparib is a highly potent and orally active PARP1 and PARP2 inhibitor with IC50 values of 1.75 nM and 0.22 nM, respectively. Simmiparib has more potent PARP1/2 inhibition than its parent Olaparib (HY-10162). Simmiparib induces DNA double-strand breaks (DSB) accumulation and G2/M arrest in homologous recombination repair (HR)-deficient cells, thereby inducing apoptosis. Simmiparib exhibits remarkable anticancer activities in cells and nude mice bearing xenografts .
    Simmiparib
  • HY-150765
    PARP1-IN-12

    		PARP Apoptosis Cancer
    PARP1-IN-12 is a potent PARP1 inhibitor with an IC50 of 2.99 nM. PARP1-IN-12 exhibits antiproliferative activity, can induce cell apoptosis and cause cycle arrest at G2/M phase. PARP1-IN-12 also can induce DNA double strand breaks (DSBs) in BRCA-deficient cells .
    PARP1-IN-12
  • HY-117693
    Mirin
    1 Publications Verification

    		 ATM/ATR Cancer
    Mirin is a potent Mre11-Rad50-Nbs1 (MRN) complex inhibitor. Mirin prevents MRN-dependent activation of ATM (IC50=12 μM) without affecting ATM protein kinase activity, and it inhibits Mre11-associated exonuclease activity. Mirin abolishes the G2/M checkpoint and homology-dependent repair in mammalian cells. Mirin prevents ATM activation in response to DNA double-strand breaks (DSBs) and blocks homology-directed repair (HDR) in mammalian cells .
    Mirin
  • HY-146194
    NHEJ inhibitor-1

    		Reactive Oxygen Species Cancer
    NHEJ inhibitor-1 (Compound C2) is a trifunctional Pt(II) complex, alleviates the  non-homologous end connection (NHEJ)/homologous recombination (HR)-related double strand breaks (DSBs) repairs to evade Cisplatin-resistance in non-small cell lung cancer (NSCLC). NHEJ inhibitor-1 inhibits the damage repair proteins Ku70 and Rad51 to make tumors re-sensitive to Cisplatin。NHEJ inhibitor-1 also induces ROS generation and MMP deduction .
    NHEJ inhibitor-1
  • HY-151939
    BLM-IN-2

    		DNA/RNA Synthesis Apoptosis Cancer
    BLM-IN-2 is a Bloom's Syndrome Protein (BLM) inhibitor with an IC50 value of 0.8 μM. BLM-IN-2 effectively suppresses the proliferation, invasion, cell cycle arrest and apoptosis of CRC cells. BLM-IN-2 can be used for the reserarch of colorectal cancer (CRC) .
    BLM-IN-2

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