double-strand dna breaks

Irinotecan (CPT-11), a derivative of camptothecin, is an inhibitor of DNA topoisomerase I (Topo I). Irinotecan has antitumor activity by preventing DNA strand reattachment through binding to the Topo I complex, resulting in double-stranded DNA breaks and cell death.

COH29 (RNR Inhibitor COH29) is an orally available, aromatically substituted thiazole and human ribonucleotide reductase (RNR) inhibitor with potential antineoplastic activity. COH29 binds to the ligand-binding pocket of the RNR M2 subunit (hRRM2) near the C-terminal tail, decreasing the pool of deoxyribonucleotide triphosphates needed for DNA synthesis, leading to cell cycle arrest and growth inhibition. It may also inhibit the nuclear enzyme poly (ADP-ribose) polymerase (PARP) 1, preventing DNA repair, causing accumulation of DNA breaks, and inducing apoptosis.

UNC-2170 (UNC2170 Maleate) is the methyl-lysine binding protein, 53BP1 ligand.

Calicheamicin (Calicheamicin γ1) is an antitumor antibiotic and is a DNA synthesis inhibitor. It also is a cytotoxic agent that causes double-strand DNA breaks.

Calicheamicin (GMP) refers to the GMP grade reagents of Calicheamicin. Calicheamicin (Calicheamicin γ1) is an antitumor antibiotic and is a DNA synthesis inhibitor. It also is a cytotoxic agent that causes double-strand DNA breaks.

Neocarzinostatin is an effective DNA-damaging, anti-tumor antibiotic. It recognizes double-stranded DNA bulge and induces DNA double strand breaks (DSBs). Neocarzinostatin leads to apoptosis. Neocarzinostatin has potential for EpCAM-positive cancer treatment.

5-BrdUTP sodium salt is a TdT substrate used for labeling DNA double-strand breaks.

XSJ05, a derivative of camptothecin (CPT), exhibits anti-cancer activity by inhibiting topoisomerase I (Topo I). This compound induces DNA double-strand breaks, leading to DNA damage. Furthermore, XSJ05 stifles the growth of colorectal cancer (CRC), halts the cell cycle in the G2 M phase, and induces apoptosis.

PARP1-IN-27 (Compound 9B) serves as an inhibitor of both PARP1 and PARP2, exhibiting IC 50 values of 2.53 nM and 6.45 nM, respectively, in SUM149PT cells. This compound effectively suppresses the proliferation of BRCA-mutated cancer cell lines such as SUM149PT, HCC1937, and Capan-1, with respective IC 50 values of 0.62, 1.91, and 4.26 μM. Additionally, PARP1-IN-27 exacerbates DNA double-strand breaks, enhances ROS production, causes G2 M phase cell cycle arrest, and triggers apoptosis in SUM149PT cells.

GSK_WRN4 is a WRN helicase inhibitor with anticancer activity. It induces DNA double-strand breaks and inhibits MSI tumor cell growth, making it useful in cancer research.

AcBut-N-Ac-γ-Calicheamicin serves as a toxic molecule for ADCs, inducing cell cycle arrest and apoptosis (Apoptosis) by causing DNA double-strand breaks. Primarily utilized in the synthesis of antibody-drug conjugates (ADC), it holds promise for cancer research, particularly in studies related to acute lymphoblastic leukemia (ALL) and other hematological malignancies.

Tilatamig samrotecan (AZD9592) is an antibody-drug conjugate (ADC) designed to deliver a topoisomerase I inhibitor (TOP1i). It targets epidermal growth factor receptor (EGFR) and c-MET and demonstrates antitumor activity. The compound induces DNA double-strand breaks, elevates pRAD50 and γH2AX expression, and inhibits the growth of non-small cell lung cancer.

HDAC-IN-85 (Compound 1) is an HDAC inhibitor capable of crossing the blood-brain barrier. It exhibits inhibitory effects on brain tumor cell lines and can induce acetylation, resulting in DNA double-strand breaks and promoting RAD51 ubiquitination, which disrupts the DNA repair process. HDAC-IN-85 is applicable in studies of glioblastoma.

Etoposide Phosphate is a selective and orally active topoisomerase II inhibitor and anticancer chemotherapy drug that inhibits cancer cell growth and induces apoptosis through DNA damage, the p53 pathway, and G2 M phase arrest of the cell cycle.

Cylindrospermopsin, a tricyclic uracil derivative, is a cyanobacterial toxin that was first discovered in an algal bloom contaminating a local drinking supply on Palm Island in Queensland, Australia after an outbreak of a mysterious disease. Cylindrospermopsin targets protein and glutathione synthesis in hepatocytes (IC50s = 1.3 and 2.4 µM, respectively), leading to cell death. [1] It has been shown to inhibit the activity of the uridine monophosphate synthase complex with a Ki value of 10 µM.[2] Cylindrospermopsin is genotoxic, inducing DNA damage as evidenced by double strand breaks and reducing cell viability in HepG2 cells at 0.1-0.5 µg ml.[3]

Topoisomerase II inhibitor 6 (Compound 5), a tryptanthrin derivative, is a potent and selective topoisomerase II inhibitor that blocks the CCRF-CEM cell cycle in the G2 phase and induces DNA double-strand breaks (DSB). It exhibits antiproliferative activity on various tumor cell lines and has potential for cancer research [1].

p53 Activator 2 (compound 10ah) intercalates into DNA, causing significant double-strand breaks and upregulating the expression of p53, p-p53, CDK4, and p21, leading to cell cycle arrest at the G2 M phase. It induces apoptosis, reduces anti-apoptosis proteins Bcl-2, Bcl-xL, and cyclin B1 levels, and shows anti-proliferative activity against MGC-803 cells with an IC50 of 1.73 μM. Additionally, p53 Activator 2 exhibits potent anticancer effectiveness in MGC-803 xenograft tumor models [1].

Simmiparib (SMOCL-9112) is a novel and potent PARP1 and PARP2 inhibitor, a derivative of Olaparib.Simmiparib induces DNA double-strand breaks (DSBs) and cell cycle arrest in homologous recombination repair (HR)-deficient cells, thereby contributing to apoptosis.Simmiparib has been used for study Parkinson's disease, Alzheimer's disease, breast cancer, and melanoma.

Amsacrine Isothionate is an aminoacridine derivative with potential antineoplastic activity. Although its mechanism of action is incompletely defined, amsacrine may intercalate into DNA and inhibit topoisomerase II, resulting in DNA double-strand breaks, arrest of the S G2 phase of the cell cycle, and cell death.

Amsacrine lactate is an aminoacridine derivative with potential antineoplastic activity. Although its mechanism of action is incompletely defined, amsacrine may intercalate into DNA and inhibit topoisomerase II, resulting in DNA double-strand breaks, arrest of the S G2 phase of the cell cycle, and cell death.

Amsacrine gluconate is an aminoacridine derivative with potential antineoplastic activity. Although its mechanism of action is incompletely defined, amsacrine may intercalate into DNA and inhibit topoisomerase II, resulting in DNA double-strand breaks, arrest of the S G2 phase of the cell cycle, and cell death.

Amonafide L-malate is the malate salt of amonafide, an imide derivative of naphthalic acid, with potential antineoplastic activity. Amonafide intercalates into DNA and inhibits topoisomerase II, resulting in DNA double-strand breaks (DSB) and inhibition of DNA replication and RNA synthesis.

PARP1-IN-12, a potent inhibitor of PARP1, demonstrates an IC50 value of 2.99 nM. It exhibits antiproliferative effects, induces apoptosis, and causes cell cycle arrest in the G2 M phase. Additionally, PARP1-IN-12 induces DNA double-strand breaks (DSBs) in BRCA-deficient cells.

Selenocystine, a broad-spectrum anticancer agent, effectively induces DNA damage, notably DNA double-strand breaks (DSBs), in HepG2 cells, showcasing significant potential as a therapeutic or adjuvant agent in targeting DNA repair mechanisms for cancer treatment [1].