From 11:00 pm to 12:00 pm EST ( 8:00 pm to 9:00 pm PST ) on January 6th, the website will be under maintenance. We are sorry for the inconvenience. Please arrange your schedule properly.
T2AA is a monoubiquitinated proliferating cell nuclear antigen (PCNA) inhibitor that prevents DNA repair, increases double-strandbreak (DSB) formation and promotes necroptosis and cell cycle arrest in G1 phase .
M3541 is a potent, ATP-competitive and selective ATM inhibitor with an IC50 of 0.25 nM. M3541 shows remarkable selectivity against other protein kinases. M3541 suppresses double-strandbreaks (DSB) repair and has antitumor activities .
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-strandbreaks (DSB) .
DEANO sodium is notric oxide donor. DEANO sodium potentiates the abilitv of hypoxanthine/xanthine oxidase to induce lipid peroxidation as well as DNA single- and double-strandbreaks .
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-strandbreaks .
Nimustine hydrochloride (ACNU) is a DNA cross-linking and DNA alkylating agent, which induces DNA replication blocking lesions and DNA double-strandbreaks and inhibits DNA synthesis, commonly used in chemotherapy for glioblastomas .
PFM01, N-alkylated Mirin derivative, is a MRE11 endonuclease inhibitor. PFM01 can regulate double-strandbreak repair (DSBR) by nonhomologous end-joining (NHEJ) versus homologous recombination (HR) .
p53 Activator 2 (compound 10ah) intercalats into DNA and results in significant DNA double-strandbreak.p53 Activator 2 increases the expression of p53, p-p53, CDK4, p21 to cause cell cycle arrest at G2/M phase.p53 Activator 2 induce apoptosis and significantly down-regulates the anti-apoptosis proteins Bcl-2, Bcl-xL and the levels of cyclin B1.p53 Activator 2 has anti-proliferation activity against MGC-803 cells, with an IC50 of 1.73 µM. p53 Activator 2 displays potent anticancer efficiency against MGC-803 xenograft tumors models .
NK 314 is an inhibitor for topoisomerase IIα, which generates the break of DNA double-strand. NK 314 arrests the cell cycle at G2 phase in human acute myeloid leukemia cells, inhibits the proliferation of CEM with IC90 of 55 nM .
Calicheamicin, an antitumor antibiotic, is a cytotoxic agent that causes double-strand DNA breaks. Calicheamicin is a DNA synthesis inhibitor . Calicheamicin is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
DiPT-4 is a dual TOP1/PARP1 inhibitor that induces massive DNA double-strandbreaks (DSBs), cell cycle arrest, and apoptosis in cancer cells. DiPT-4 has the potential to overcome cancer drug resistance .
N,N-Dimethyl-idarubicin, an Idarubicin (HY-17381) derivative, is a potent histone evictor which does not induce DNA double-strandbreaks. N,N-Dimethyl-idarubicin, an anthracycline, is an effective cytotoxic agent for ABCB1-overexpressing, Doxorubicin-resistant cells .
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-strandbreaks (DSB) and chromosomal abnormalities. NSC 617145 shows selective for WRN over BLM, FANCJ, ChlR1, RecQ, and UvrD helicases .
IBR2 is a potent and specific RAD51 inhibitor and inhibits RAD51-mediated DNA double-strandbreak repair. IBR2 disrupts RAD51 multimerization, accelerates proteasome-mediated RAD51 protein degradation, inhibits cancer cell growth and induces apoptosis .
GSK_WRN4 is a WRN helicase inhibitor (pIC50=7.6) with anticancer activity. GSK_WRN4 selectively inhibits the growth of MSI tumor cells in vitro and in vivo by inducing DNA double-strandbreaks, particularly at expanded TA repeats and DNA damage regions .
Tirapazamine (SR259075) is an anticancer agent that shows selective cytotoxicity for hypoxic cells in solid tumors, thereby inducing single-and double-strandbreaks in DNA, base damage, and cell death. Tirapazamine is an anticancer and bioreductive agent.Tirapazamine (SR259075) can enhance the cytotoxic effects of ionizing radiation in hypoxic cells .
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-strandbreak (DSB) repair; TI17 inhibits Trip13 function and increases DNA damage .
XSJ05 is a camptothecin (CPT) derivative that can inhibit topoisomerase I (Topo I) to exert anti-cancer activity. XSJ05 can trigger DNA double-strandbreaks, leading to DNA damage. XSJ05 can inhibit the growth of colorectal cancer (CRC), arrest the cell cycle in G2/M phase, and induce apoptosis .
LJI308 is a potent pan-ribosomal S6 kinase (RSK) inhibitor, with IC50s of 6 nM, 4 nM, and 13 nM for RSK1, RSK2, and RSK3, respectively. LJI308 inhibits the phosphorylation of RSK (T359/S363) and YB-1 (S102) after irradiation, treatment with EGF, and in cells expressing a KRAS mutation .
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-strandbreak events (DSBs) due to torsional strain on DNA and chromatin structure. CM03 has selective potency for pancreatic cancer cells .
(R)-IBR2 is the isomer of IBR2 (HY-103710). IBR2 is a potent and specific RAD51 inhibitor and inhibits RAD51-mediated DNA double-strandbreak repair. IBR2 disrupts RAD51 multimerization, accelerates proteasome-mediated RAD51 protein degradation, inhibits cancer cell growth and induces apoptosis .
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-strandbreaks). VX-984 can be used for glioblastomas (GBM) and non-small cell lung cancer (NSCLC) research. VX-984 is a de novo deuterium .
GSK_WRN3 is a selective inhibitor of WRN protease (IC50 = 8.6 μM). GSK_WRN3 displays a high degree of selectivity by forming a covalent binding to the Cys727 residue of the WRN protein. GSK_WRN3 reduces growth support for MSI tumor cells by inhibiting WRN protease activity, resulting in increased DNA double-strandbreaks and cell growth inhibition .
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-strandbreak repair and increases the sensitivity of cells to radiotherapy .
Neocarzinostatin, a potent DNA-damaging, anti-tumor antibiotic, recognizes double-stranded DNA bulge and induces DNA double strandbreaks(DSBs). Neocarzinostatin induces apoptosis. Neocarzinostatin has potential for EpCAM-positive cancers treatment .
Bleomycin is a glycopeptide antibiotic. Bleomycin has potent antitumour activities against a range of lymphomas, head and neck cancers and germ-cell tumours. Bleomycin can be used for the research of cancer and chemotherapy .
7-tert-Butylfascaplysin (7-TB) is a derivative of Fascaplysin (HY-112328), that can be isolated from Fascaplysinopsis sp.. 7-tert-Butylfascaplysin induces replication stress, leads to toxic DNA double-strandbreaks and apoptosis-like cell death, and thus exhibits cytotoxicity in cancer cells in nanomolar levels. 7-tert-Butylfascaplysin exhibits DNA intercalating activity with EC50 of 3.2 μM .
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 strandbreaks, and enhances radiosensitization .
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-strandbreak (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 .
MLN8054 sodium is an Aurora A inhibitor with radiosensitivity-enhancing activity. MLN8054 sodium can activate the DNA double-strandbreak reaction of prostate cancer cells in in vitro experiments. The application of MLN8054 sodium is closely related to accumulation in the G2/M phase of the cell cycle and polyploid formation. In vivo experiments show that MLN8054 sodium can significantly delay the growth of prostate cancer tumors and promote tumor cell apoptosis when used in combination with radiotherapy .
Selenocystine is a broad-spectrum anti-cancer agent. Selenocystine induces DNA damage in HepG2 cells, particularly in the form of DNA double strandbreaks (DSBs). Selenocystine exhibits great promise as a therapeutic or adjuvant agent targeting DNA repair for cancer treatment .
Temozolomide acid is a carboxylic acid derivative of Temozolomide (HY-17364) with anticancer activity. Temozolomide is a DNA alkylating agent, methylating the guanine and adenine bases of DNA, causing breaks in DNA double strand, cell cycle arrest, and eventually cell death. Temozolomide acid is promising for research of glioblastoma and brain cancer .
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-strandbreak repair. Eurycomalactone inhibits the activation of AKT/NF-κB signaling, induces apoptosis and enhances chemosensitivity to Cisplatin (HY-17394) .
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-strandbreaks (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 .
PARP1-IN-15 (Compound 6) is a PARP1 inhibitor. PARP1-IN-15 inhibits tankyrase (TNKS) and facilitates DNA double-strandbreaks damage. PARP1-IN-15 induces tumor cell apoptosis. PARP1-IN-15 has anti-cancer activity in triple-negative breast cancer (TNBC) cells and TNBC patient-derived organoids. PARP1-IN-15 can be used for research of TNBC with or without BRCA1 mutations .
The Cas9 protein, guided by sgRNA, induces DNA double-strandbreaks (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.
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-strandbreaks (DSB) .
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-strandbreaks (DSBs) and blocks homology-directed repair (HDR) in mammalian cells .
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 strandbreaks and sensitizes different cancer cell lines .
PARP1-IN-27 (Compound 9B) is the inhibitor for PARP1 and PARP2, with IC50 of 2.53 nM and 6.45 nM in cell SUM149PT. PARP1-IN-27 inhibits the proliferation of BRCA-mutated cancer cells SUM149PT, HCC1937 and Capan-1, with IC50 of 0.62, 1.91 and 4.26 μM respectively. PARP1-IN-27 aggravates DNA double-strandbreaks, increases ROS generation, arrests cell cycle at G2/M phase, and induces apoptosis in SUM149PT .
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 strandbreaks (DSBs) in BRCA-deficient cells .
Cu(II)-Elesclomol is a Cu 2+ complex of Elesclomol (HY-12040). Cu(II)-Elesclomol induces cuproptosis. Cu(II)-Elesclomol also inducesapoptosis, causes a G1 cell cycle block and induces DNA double strandbreaks in K562 cells. Cu(II)-Elesclomol also weakly inhibits DNA topoisomerase I. Cu(II)-Elesclomol has anticancer activity .
NHEJ inhibitor-1 (Compound C2) is a trifunctional Pt(II) complex, alleviates the non-homologous end connection (NHEJ)/homologous recombination (HR)-related double strandbreaks (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 .
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) .
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-strandbreaks .
Selenocystine is a broad-spectrum anti-cancer agent. Selenocystine induces DNA damage in HepG2 cells, particularly in the form of DNA double strandbreaks (DSBs). Selenocystine exhibits great promise as a therapeutic or adjuvant agent targeting DNA repair for cancer treatment .
DNA-PK Substrate is a biological active peptide. (A substrate for DNA-dependent protein kinase (DNA-PK), phosphorylation. DNA-PK is essential for the repair of DNA double-strandbreaks. This peptide corresponding to 11–24 amino acids of human p53 with threonine 18 and serine 20 changed to alanine is used as a substrate for the assay of DNA-PK activityPyroglutamyl (pGlu) peptides may spontaneously form when either Glutamine (Q) or Glutamic acid (E) is located at the sequence N-terminus. The conversion of Q or E to pGlu is a natural occurrence and in general it is believed that the hydrophobic γ-lactam ring of pGlu may play a role in peptide stability against gastrointestinal proteases. Pyroglutamyl peptides are therefore considered a normal subset of such peptides and are included as part of the peptide purity during HPLC analysis.)
Selenocystine is a broad-spectrum anti-cancer agent. Selenocystine induces DNA damage in HepG2 cells, particularly in the form of DNA double strandbreaks (DSBs). Selenocystine exhibits great promise as a therapeutic or adjuvant agent targeting DNA repair for cancer treatment .
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-strandbreak repair. Eurycomalactone inhibits the activation of AKT/NF-κB signaling, induces apoptosis and enhances chemosensitivity to Cisplatin (HY-17394) .
The MRE11A protein is an important component of the DNA double-strand break repair mechanism and participates in the homologous recombination (HR) pathway. It interacts with RAD50 and NBS1 to form the MRN complex, which is essential for sensing and repairing DNA damage. MRE11A Protein, Human (His, GST) is the recombinant human-derived MRE11A protein, expressed by E. coli , with N-6*His, N-GST labeled tag. The total length of MRE11A Protein, Human (His, GST) is 411 a.a., .
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-strandbreaks). VX-984 can be used for glioblastomas (GBM) and non-small cell lung cancer (NSCLC) research. VX-984 is a de novo deuterium .
RAD21; HR21; KIAA0078; NXP1; double-strand-break repair protein rad21 homolog; hHR21; Nuclear matrix protein 1; NXP-1; SCC1 homolog
WB, FC
Human, Mouse, Rat
Rad21 Antibody (YA2985) is a rabbit-derived non-conjugated IgG antibody (Clone NO.: YA2985), targeting Rad21, with a predicted molecular weight of 72 kDa (observed band size: 72,128 kDa). Rad21 Antibody (YA2985) can be used for WB, FC experiment in human, mouse, rat background.
X ray repair cross complementing protein 4; DNA repair protein XRCC4; DNA doublestrandbreak repair
WB, IHC-F, IHC-P, ICC/IF, IP
Human, Mouse, Rat
XRCC4 Antibody (YA1082) is a mouse-derived non-conjugated IgG1 antibody (Clone NO.: YA1082), targeting XRCC4, with a predicted molecular weight of 38 kDa (observed band size: 38-45 kDa). XRCC4 Antibody (YA1082) can be used for WB, IHC-F, IHC-P, ICC/IF, IP experiment in human, mouse, rat background.
The Cas9 protein, guided by sgRNA, induces DNA double-strandbreaks (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.
Inquiry Online
Your information is safe with us. * Required Fields.
