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Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
12 Results for "
DNA damage repair mechanism
" in MedChemExpress (MCE) Product Catalog:
Products (12)
12 Results for "DNA damage repair mechanism" in MCE Product Catalog:
3
3 Cited Publications
Category:
Infection Microorganisms Antibiotics Disease Research Antibacterial Anticancer Disease Research Fields Other Antibiotics
Target:
GeA-69 is a selective, allosteric inhibitor of poly-adenosine-diphosphate-ribose polymerase 14 (PARP14) targeting macrodomain 2 (MD2), with a Kd value of 2.1 μM. GeA-69 involves in DNA damage repair mechanisms and prevents recruitment of PARP14 MD2 to sites of laser-induced DNA damage .
Cat. No.: HY-139621
CAS No.: 2916559-62-9
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Colibactin 742 is a covalently binding DNA-damaging agent targeting DNA, with an IC50 of 5.2 μM against human cervical cancer cells (HeLa). Colibactin 742 covalently binds to DNA, forming interstrand crosslinks (ICLs), activating the Fanconi anemia DNA repair pathway, inducing γH2AX and FANCD2 foci formation and cell cycle arrest, while exacerbating mismatch repair deficiency (MMRd)-related mutations. Colibactin 742 can mimic the genotoxicity of natural Colibactin while avoiding its instability, and is mainly used in colorectal cancer (CRC) related research, including microbial tumorigenesis mechanisms, DNA damage repair pathways, and mutation signature analysis .
Cat. No.: HY-W341499
CAS No.: 4494-26-2
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5-Formyl-2'-deoxyuridine is a product formed when the 5-methyl group of thymine in DNA undergoes oxidation due to exposure to gamma radiation or certain chemical agents. Serving as a biomarker of oxidative DNA damage, 5-formyl-2'-deoxyuridine is employed in investigations of DNA damage and repair mechanisms. Additionally, 5-Formyl-2'-deoxyuridine can be used in studies involving chemically crosslinking with peptides derived from the RecA protein .
Cat. No.: HY-W704973
CAS No.: 95740-26-4
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F-ara-EdU is a low-toxic, highly stable probe for DNA synthesis that is used as a marker for cell proliferation and DNA replication by binding to DNA or RNA in cells. F-ara-EdU can also be used to detect the rate of DNA synthesis within cells, as well as to study the mechanisms of DNA repair and damage .
Cat. No.: HY-U00265
CAS No.: 20073-24-9
Synonyms: 3-Carbethoxypsoralen; 3-Ethoxycarbonylpsoralen
3-CPs is a monofunctional furanocoumarin and a photoprotective agent targeting Staphylococcus aureus DNA, possessesing anti-UVB lethal activity. 3-CPs competitively intercalates into DNA, forming exclusively 4',5'-furan-side mono-adducts upon UVB irradiation, and irreversibly inhibits the formation of cyclobutane pyrimidine dimers. 3-CPs prevents UVB-induced DNA damage by preferentially binding to strong (AT)n sites within the DNA, without inducing lethal interstrand DNA cross-links; the limited number of mono-adducts it induces can be efficiently repaired by bacteria. 3-CPs holds potential for use in the development of photoprotective formulations for skin diseases, as well as in studies investigating bacterial DNA photodamage repair mechanisms and the optimization of photochemotherapy safety .
Cat. No.: HY-L264
1,544 compounds
DNA damage response (DDR) is a fundamental mechanism for maintaining genomic stability. When DNA damage occurs, such as single- or double-strand breaks or replication fork stalling, cells rely on key proteins including ATM, ATR, PARP, and DNA-PK to sense the damage and transmit signals, thereby regulating DNA repair, cell-cycle arrest, and cell death. Inhibition of specific DNA repair or checkpoint pathways can prevent tumor cells from effectively repairing accumulated DNA damage, ultimately leading to tumor cell death.
MCE DNA Damage Repair Inhibitor Library contains 1,544 compounds, focusing on key nodes involved in DNA damage response and DNA repair. The library covers multiple DNA repair and cell-cycle checkpoint pathways, providing a systematic compound screening tool for research on precision oncology, synthetic lethality, drug resistance mechanisms, and chemo- or radiosensitization.
Cat. No.: HY-W588285
CAS No.: 2958-98-7
Synonyms: 3-MG
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3-Methylguanine is a DNA damage product caused by alkylation. 3-Methylguanine is cytotoxic and causes cell death by inhibiting DNA replication. 3-Methylguanine can be used to study the mechanism of DNA damage caused by alkylating agents and its repair pathways .
Cat. No.: HY-120750
CAS No.: 111783-54-1
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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 .
Cat. No.: HY-116619
CAS No.: 591207-53-3
Synonyms: (E/Z)-NVP-LAQ824; (E/Z)-LAQ824
(E/Z)-Dacinostat ((E/Z)-NVP-LAQ824) is a histone deacetylase inhibitor that has the ability to induce apoptosis and enhance the activity of fludarabine in killing leukemia cells. (E/Z)-Dacinostat can trigger the production of reactive oxygen species (ROS) and DNA damage, enhance the killing effect of fludarabine on leukemia cells, and induce apoptosis. Its mechanism is related to the regulation of DNA repair processes and intracellular signaling pathways.
Cat. No.: HY-L004
3,522 compounds
DNA is prone to numerous forms of damage that can injure cells and impair fitness. Cells have developed an array of mechanisms to repair these injuries. Proliferating cells are especially vulnerable to DNA damage due to the added demands of cellular growth and division. Cell cycle checkpoints represent integral components of DNA repair that coordinate cooperation between the machinery of the cell cycle and several biochemical pathways that respond to damage and restore DNA structure. By delaying progression through the cell cycle, checkpoints provide more time for repair before the critical phases of DNA replication, when the genome is replicated, and of mitosis, when the genome is segregated. Loss or attenuation of checkpoint function may increase spontaneous and induced gene mutations and chromosomal aberrations by reducing the efficiency of DNA repair.
MCE owns a unique collection of 3,522 cell cycle/DNA damage-related compounds which can be used in the research of the same.
Cat. No.: HY-L244
761 compounds
In this era of rapid advancement in gene-editing technology, the CRISPR-Cas system, with its powerful programmability, is leading a transformation in life sciences research. It enables efficient and precise targeted modification of an organism's genome, providing a robust tool for studying gene function, treating genetic diseases, and improving crop varieties. However, bottlenecks such as insufficient editing efficiency, low homologous directed repair efficiency, and potential off-target risks remain major challenges in achieving precise genetic modifications and developing gene therapies.
To overcome these limitations, the MCE High-Efficiency Gene Editing Compound Library systematically includes 761 small molecules that are known or have the potential to enhance gene-editing efficiency. These compounds work by targeting and modulating the DNA damage repair network, mechanistically inhibiting non-homologous end joining, promoting homologous directed repair, or regulating chromatin states and cellular responses, thereby significantly optimizing editing outcomes. This library is suitable for developing "CRISPR-small molecule" combination therapy strategies, improving gene-editing efficiency, and providing a powerful tool for in-depth research into the mechanisms of DNA damage repair in gene editing.
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Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
