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Pathways Recommended: Cell Cycle/DNA Damage
Results for "

DNA double-strand break repair

" in MedChemExpress (MCE) Product Catalog:

31

Inhibitors & Agonists

1

Biochemical Assay Reagents

3

Peptides

3

Natural
Products

3

Antibodies

1

GMP Molecules

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-101570
    Nedisertib
    Maximum Cited Publications
    27 Publications Verification

    Peposertib; M3814

    		 DNA-PK BCRP Cancer
    Nedisertib (Peposertib) is an orally active selective DNA-dependent protein kinase (DNA-PK) inhibitor with an IC50 value of less than 3 nM. Nedisertib also acts as a modulator of ABCG2, capable of reversing ABCG2-mediated multidrug resistance (MDR), thus providing new strategies for combination therapy. By inhibiting DNA double-strand break repair, Nedisertib can enhance the efficacy of chemotherapy and radiotherapy. Nedisertib exhibits antitumor activity .
    Nedisertib
  • HY-19959
    Mirin
    5+ Cited Publications

    		 ATM/ATR Apoptosis 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-110111
    T2AA
    2 Publications Verification

    		 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-126490
    Phleomycin
    2 Publications Verification

    		 Bacterial Antibiotic DNA/RNA Synthesis Infection Cancer
    Phleomycin is a copper-dependent DNA damaging agent and antibiotic with antitumor activity. Phleomycin binds to DNA and produces ROS in the presence of reducing agents (such as dithiothreitol and glutathione), inducing single-strand and double-strand breaks in DNA. Phleomycin can induce cell apoptosis or mutation and is widely used in cancer inhibition, microbial genetic transformation (as a screening marker to improve fungal transformation efficiency) and DNA repair mechanism research .
    Phleomycin
  • HY-103710
    IBR2
    5+ Cited Publications

    		 RAD51 Apoptosis Cancer
    IBR2 is a potent and specific RAD51 inhibitor and inhibits RAD51-mediated DNA double-strand break repair. IBR2 disrupts RAD51 multimerization, accelerates proteasome-mediated RAD51 protein degradation, inhibits cancer cell growth and induces apoptosis .
    IBR2
  • HY-148078
    PFM03
    3 Publications Verification

    		 Endonuclease Others
    PFM03 is a MRE11 Endonuclease inhibitor. PFM03 regulates DNA double-strand break repair (DSBR) by nonhomologous end-joining (NHEJ) .
    PFM03
  • HY-N4327
    Eurycomalactone

    		NF-κB Apoptosis Akt Bcl-2 Family Infection Inflammation/Immunology
    Eurycomalactone is an active quassinoid could be isolated from Eurycoma longifolia Jack. Eurycomalactone is a potent NF-κB inhibitor with an IC50 value of 0.5 μM. Eurycomalactone inhibits protein synthesis and depletes cyclin D1. Eurycomalactone enhances radiosensitivity through arrest cell cycle at G2/M phase and delayed DNA double-strand break repair. Eurycomalactone inhibits the activation of AKT/NF-κB signaling, induces apoptosis and enhances chemosensitivity to Cisplatin (HY-17394) .
    Eurycomalactone
  • HY-100705
    DMNB

    6-Nitroveratraldehyde

    		 Drug Intermediate Neurological Disease
    DMNB (6-Nitroveratraldehyde) is a photolabile proton donor that releases acidic substances when excited at a wavelength of 405 nM. DMNB can be used for the synthesis of no-carrier-added 6-[18F]fluoro-L-DOPA (6-FDOPA). DMNB is also applicable to the preparation of o-nitroaryl-bis (5-methylfur-2-yl) methanes and the synthesis of alpha-asarone (HY-N0700). DMNB is an enzyme involved in the non-homologous end joining (NHEJ) pathway responsible for DNA double-strand break (DSB) repair. DMNB can be used in PET studies of the dopaminergic system .
    DMNB
  • HY-15620
    Methylproamine
    1 Publications Verification

    		 DNA/RNA Synthesis Others
    Methylproamine is a DNA-binding radioprotector, acts by repair of transient radiation-induced oxidative species on DNA. Methylproamine also protects against ionizing radiation by preventing DNA double-strand breaks .
    Methylproamine
  • HY-113064
    Selenocystine
    1 Publications Verification

    		 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-115531
    UNC-2170

    		DNA/RNA Synthesis 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-164279
    YTR107

    		DNA/RNA Synthesis Cancer
    YTR107 is a radiation sensitizer. YTR107 binds to nucleophosmin1 (NPM1) and inhibits pentamer formation. YTR107 inhibits recruitment of nucleophosmin to sites of DNA damage, suppresses repair of DNA double strand breaks, and enhances radiosensitization .
    YTR107
  • 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-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-100707
    IC 86621

    		DNA-PK Apoptosis Inflammation/Immunology Cancer
    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-101570G
    Nedisertib

    Peposertib; M3814

    		 DNA-PK BCRP Cancer
    Nedisertib (GMP) (Peposertib (GMP)) is Nedisertib (HY-101570) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Nedisertib is an orally active selective DNA-dependent protein kinase (DNA-PK) inhibitor with an IC50 value of less than 3 nM. Nedisertib also acts as a modulator of ABCG2, capable of reversing ABCG2-mediated multidrug resistance (MDR), thus providing new strategies for combination therapy. By inhibiting DNA double-strand break repair, Nedisertib can enhance the efficacy of chemotherapy and radiotherapy. Nedisertib exhibits antitumor activity .
    Nedisertib
  • HY-123232
    KU-0058684

    		PARP Cancer
    KU-0058684 is a potent PARP inhibitor, with an IC50 of 3.2 nM for PARP-1. KU-0058684 significantly reduces DNA double strand break (DSB) repair .
    KU-0058684
  • HY-170907
    HDAC-IN-85

    		HDAC DNA/RNA Synthesis RAD51 Cancer
    HDAC-IN-85 (Compound 1) is a BBB-permeable HDAC inhibitor. HDAC-IN-85 has an inhibitory effect on brain tumor cell lines. HDAC-IN-85 can induce acetylation, leading to DNA double-strand breaks, and induce the ubiquitination of RAD51, disrupting the DNA repair process. HDAC-IN-85 can be used in the research of glioblastoma .
    HDAC-IN-85
  • HY-175466
    BER-IN-1

    		PARP DNA/RNA Synthesis Apoptosis Cancer
    BER-IN-1 is a base excision repair (BER) inhibtor, targeting DNA abasic sites. BER-IN-1 cleaves abasic sites via β- and β,δ-elimination mechanisms, disrupts the base excision repair (BER) pathway and leads to DNA double-strand breaks (DSBs). BER-IN-1 can enhance the effectiveness of the PARP inhibitor Olaparib (HY-10162) in homologous recombination (HR)-proficient cancer cells (MDA-MB-231, HeLa, and SKOV3). BER-IN-1 induces an S-phase arrest and apoptosis companied with Olaparib (HY-10162). BER-IN-1 can be used for the research of cancer, such as breast, cervical and ovarian cancer .
    BER-IN-1
  • HY-118897
    UNC-2170 maleate

    		DNA/RNA Synthesis Cancer
    UNC-2170 maleate is the maleate salt form of UNC-2170 (HY-115531). UNC-2170 maleate is a selective inhibitor for the methyl-lysine binding protein 53BP1, with IC50 of 29 µM and Kd of 22 µM. UNC-2170 maleate 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 maleate
  • HY-114923
    SU-11752

    		DNA-PK PI3K Cancer
    SU-11752 is an inhibitor for DNA-dependent protein kinase (DNA-PK) with an IC50 of 0.13 μM. SU-11752 inhibits PI3K p110γ kinase with IC50 of 1.1 μM. SU-11752 binds competitively for ATP-site in DNA-PK, results in inhibition of intracellular DNA double-strand break repair and increases the sensitivity of cells to radiotherapy .
    SU-11752
  • HY-103710A
    (R)-IBR2

    		RAD51 Cancer
    (R)-IBR2 is the isomer of IBR2 (HY-103710). IBR2 is a potent and specific RAD51 inhibitor and inhibits RAD51-mediated DNA double-strand break repair. IBR2 disrupts RAD51 multimerization, accelerates proteasome-mediated RAD51 protein degradation, inhibits cancer cell growth and induces apoptosis .
    (R)-IBR2
  • HY-126972
    RI(dl)-2

    		RAD51 Cancer
    RI(dl)-2 blocks RAD51’s D-loop activity in biochemical systems with an IC50 value of 11.1 µM and inhibits homologous recombination (HR) activity with an IC50 value of 3.0 µM. RI(dl)-2 inhibits HR-mediated repair of DNA double strand breaks and sensitizes different cancer cell lines .
    RI(dl)-2
  • HY-122226
    IC-87361

    		DNA-PK Apoptosis Cancer
    IC-87361 is a DNA-dependent protein kinase (DNA-PKcs) inhibitor with an IC50 of 35 nM, and radiosensitizer. IC-87361 inhibits the catalytic activity of DNA-PKcs and blocks non-homologous end joining (NHEJ) DNA double-strand break repair. IC-87361 can be used for the research of lung cancer and melanoma .
    IC-87361
  • HY-181786
    ATM-IN-13

    		ATM/ATR Cancer
    ATM-IN-13 (A36) is an orally active, selective ATM kinase inhibitor with a human IC50 of 0.3 nM. ATM-IN-13 blocks the ATM-mediated DNA double-strand break repair signaling pathway, reduces the phosphorylation levels of ATM and p53, and inhibits ATM-dependent DNA damage response. ATM-IN-13 can be used in the research of colorectal cancer .
    ATM-IN-13
  • HY-181254
    PARP1/NAMPT-IN-1

    		PARP NAMPT DNA/RNA Synthesis Apoptosis Cancer
    PARP1/NAMPT-IN-1 is a potent and dual PARP1 and NAMPT inhibitor with IC50 values of 1.2 nM and 6.7 nM, respectively. PARP1/NAMPT-IN-1 can disrupt the homologous recombination repair (HRR) pathway, leading to the accumulation of DNA double-strand breaks (DSBs), inducing cell cycle arrest and apoptosis, and also has antimigratory effects. PARP1/NAMPT-IN-1 exhibits excellent antitumor effects in a breast cancer xenograft model. PARP1/NAMPT-IN-1 can be used for the study of triple-negative breast cancer (TNBC) .
    PARP1/NAMPT-IN-1
  • HY-103710R
    IBR2 (Standard)

    		Reference Standards RAD51 Apoptosis Cancer
    IBR2 (Standard) is the analytical standard of IBR2 (HY-103710). This product is intended for research and analytical applications. IBR2 is a potent and specific RAD51 inhibitor and inhibits RAD51-mediated DNA double-strand break repair. IBR2 disrupts RAD51 multimerization, accelerates proteasome-mediated RAD51 protein degradation, inhibits cancer cell growth and induces apoptosis .
    IBR2 (Standard)
  • HY-101570R
    Nedisertib (Standard)

    Peposertib (Standard); M3814 (Standard)

    		 DNA-PK Reference Standards BCRP Cancer
    Nedisertib (Standard) is the analytical standard of Nedisertib (HY-101570). This product is intended for research and analytical applications. Nedisertib (Peposertib) is an orally active selective DNA-dependent protein kinase (DNA-PK) inhibitor with an IC50 value of less than 3 nM. Nedisertib also acts as a modulator of ABCG2, capable of reversing ABCG2-mediated multidrug resistance (MDR), thus providing new strategies for combination therapy. By inhibiting DNA double-strand break repair, Nedisertib can enhance the efficacy of chemotherapy and radiotherapy. Nedisertib exhibits antitumor activity .
    Nedisertib (Standard)
  • HY-181557
    SY-589

    		DNA Alkylator/Crosslinker DNA/RNA Synthesis Apoptosis Cancer
    SY-589 is an orally active DNA polymerase Polθ helicase domain inhibitor (IC50=2.29 nM) and DNA damage inducer. SY-589 inhibits the ATPase activity of the Polθ helicase domain and blocks the Polθ-mediated microhomology-mediated end joining (MMEJ) DNA repair pathway (IC50=0.85 nM). SY-589 also induces the accumulation of DNA double-strand breaks by increasing γ-H2AX levels. SY-589 exerts antiproliferative effects on BRCA2-deficient cells and is used in the research of HR-deficient tumors .
    SY-589
  • HY-183488
    R9-caPep

    RRRRRRRRRCCLGIPEQEY

    		 Apoptosis PARP Cancer
    R9-caPep (RRRRRRRRRCCLGIPEQEY) is a cell-penetrating peptide derived from proliferating cell nuclear antigen (PCNA). R9-caPep selectively blocks the interactions between PCNA and FEN1, as well as between PCNA and LIGI, while preserving the binding of POLD3 to PCNA. R9-caPep interferes with DNA synthesis and homologous recombination-mediated double-strand DNA break repair, inducing S-phase arrest, DNA damage accumulation, and apoptosis. R9-caPep inhibits the growth of tumor volume and weight of neuroblastoma in nude mice . R9-caPep can be used in research related to neuroblastoma and triple-negative breast cancer .
    R9-caPep
  • HY-183630
    AZD4956

    		DNA/RNA Synthesis Cancer
    AZD4956 is a potent and selective DNA polymerase theta (POLQ) inhibitor. AZD4956 exhibits an IC50 value of less than 3 μmol/L against POLQ and 3.4 μmol/L against MMEJ. AZD4956 suppresses the MMEJ pathway and enhances the activity of DNA-damaging agents in HRR-deficient cellular contexts. AZD4956 shows antitumor activity in BRCA1/2-mutated triple-negative breast cancer and prostate cancer models. AZD4956 can be used for the study of homologous recombination-deficient tumors .
    AZD4956

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