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Pathways Recommended:	Cell Cycle/DNA Damage

Results for "

DNA damage repair mechanism

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Endogenous Metabolite (1) PARP (1)
By Research Areas:	Cancer (2)

Inhibitors & Agonists

Screening Libraries

Targets Recommended: DNA-PK DNA Methyltransferase DNA Stain DNA Alkylator/Crosslinker DNA/RNA Synthesis

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-108708

GeA-69	PARP	Cancer
GeA-69 is a selective, allosteric inhibitor of poly-adenosine-diphosphate-ribose polymerase 14 (PARP14) targeting macrodomain 2 (MD2), with a K_d 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 .

HY-W341499

5-Formyl-2'-deoxyuridine	Endogenous Metabolite	Others
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 .

HY-120750

A 62176 hydrochloride	Others	Cancer
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 .

HY-116619

(E/Z)-Dacinostat (E/Z)-NVP-LAQ824; (E/Z)-LAQ824	Others	Others
(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.	Product Name

HY-L004

Cell Cycle/DNA Damage Compound Library	2,313 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 2,313 cell cycle/DNA damage-related compounds which can be used in the research of the same.

Cell Cycle/DNA Damage Compound Library

2,313 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 2,313 cell cycle/DNA damage-related compounds which can be used in the research of the same.

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