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Pathways Recommended:	Cell Cycle/DNA Damage

Results for "

DNA damage response genes

" in MedChemExpress (MCE) Product Catalog:

By Targets:	DNA/RNA Synthesis (4) Akt (1) Apoptosis (5) ATM/ATR (1) Caspase (1) CDK (7) Cytochrome P450 (1) DYRK (1) MDM-2/p53 (1) Molecular Glues (3) PARP (3) PROTACs (2) RAD51 (1) Topoisomerase (1)
By Research Areas:	Cancer (12)
Click Chemistry:	Alkynes (1)

Inhibitors & Agonists

Screening Libraries

Click Chemistry

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

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-168162

ZLC491	PROTACs CDK	Cancer
ZLC491 is an orally active PROTAC degrader that selectively targets CDK12/CDK13 and exhibits certain oral bioavailability. ZLC491 induces cereblon- and proteasome-dependent selective degradation of CDK12 and CDK13. ZLC491 inhibits the transcription and expression of long genes, and mainly acts on a subset of DNA damage response genes. ZLC491 inhibits the proliferation of various triple-negative breast cancer cells. ZLC491 can be used in research related to triple-negative breast cancer .

HY-144981

HQ461 1 Publications Verification	CDK Molecular Glues	Cancer
HQ461 is a molecular glue that promotes CDK12-DDB1 interaction to trigger cyclin K degradation. HQ461-mediated degradation of cyclin K impairs CDK12 function, resulting in decreased CDK12 substrate phosphorylation, downregulation of DNA damage response genes, and cell death .

HY-163944

LL-K12-18	DNA/RNA Synthesis Molecular Glues CDK Apoptosis RAD51 ATM/ATR PARP	Cancer
LL-K12-18 is a CDK12 kinase inhibitor and a dual-site molecular glue. LL-K12-18 inhibits human CDK12 with an IC₅₀ value of 283.9 nM, and selectively degrades cyclin K via the ubiquitin-proteasome system by stabilizing the CDK12-DDB1 complex. LL-K12-18 downregulates DNA damage response genes, reduces the phosphorylation level of CTD Ser2 in RNA polymerase II, and modulates biomarkers such as ATM, RAD51, γ-H2AX and cleaved PARP, thereby effectively inducing apoptosis and inhibiting proliferation of breast cancer cells. LL-K12-18 exhibits high target selectivity and serves as a research tool for studies on triple-negative breast cancer .

HY-173059

CDK12/13-IN-3	CDK	Cancer
CDK12/13-IN-3 (Compound 12b) is the orally active inhibitor for CDK that inhibits CDK12 and CDK13 with IC₅₀ of 107.4 nM and 79.4 nM. CDK12/13-IN-3 inhibits the phosphorylation of Ser2 on the CTD of RNA polymerase II, induces DNA damage, and downregulates the gene expression of DNA damage response (DDR). CDK12/13-IN-3 exhibits antiproliferative activity against multiple cancer cells with IC₅₀ of nanomolar levels. CDK12/13-IN-3 exhibits antitumor effect in mouse models, exhibits good pharmacokinetic properties with an oral bioavailability of 53.6% .

HY-125209A

TH5427 hydrochloride	Apoptosis PARP DNA/RNA Synthesis	Cancer
TH5427 hydrochloride is a NUDT5 inhibitor with a human target IC₅₀ of 29 nM, ~690-fold selectivity over MTH1 in vitro, and selective functional inhibition over other NUDIX hydrolases including NUDT9 .TH5427 hydrochloride binds to the active site of NUDT5, blocking enzymatic activity related to ADP-ribose metabolism and PAR-derived ATP synthesis .TH5427 hydrochloride blocks progestin-dependent nuclear ATP synthesis, impairs progestin-induced chromatin remodeling, inhibits histone H1 displacement, disrupts progestin-dependent gene regulation, and abrogates progestin-dependent proliferation in breast cancer cells .TH5427 hydrochloride functions as a versatile probe to study nuclear ATP dynamics and ADP-ribose-related metabolism in cells .TH5427 hydrochloride engages NUDT5 at physiological temperatures, as demonstrated by Drug Affinity Responsive Target Stability (DARTS) assay .TH5427 hydrochloride stabilizes NUDT5 against thermal denaturation in cell lysates and intact cells, as shown by cellular thermal shift assay (CETSA) .TH5427 hydrochloride functionally inhibits NUDT5 activity, leading to downstream effects on oxidative DNA damage and DNA replication in triple-negative breast cancer (TNBC) cells .TH5427 hydrochloride suppresses proliferation of TNBC cells without inducing cell death or apoptosis, slows DNA replication in TNBC cells, promotes accumulation of oxidative DNA lesions, and triggers DNA damage response in TNBC cells .TH5427 hydrochloride suppresses growth of TNBC cells in vitro, inhibits growth of TNBC xenograft tumors in nude mice in vivo, and shows greater potency against TNBC cell lines compared to ER-positive and normal-like breast cell lines .TH5427 hydrochloride can be used for the research of breast cancer and triple-negative breast cancer .

HY-177780

Cyclin K degrader 2	Molecular Glues CDK Apoptosis	Cancer
Cyclin K degrader 2 is a molecular glucose degrading agent that targets the cyclin K protein. Cyclin K degrader 2 has inhibitory activity against CDK1 and CDK9. Cyclin K degrader 2 causes a decrease in RNA polymerase II Ser2 phosphorylation levels, downregulation of DNA damage response gene expression, accumulation of DNA damage, G1 phase arrest of the cell cycle, and apoptosis. Cyclin K degrader 2 can be used for cancer research .

HY-173273

YJZ5118	CDK Apoptosis DNA/RNA Synthesis Akt	Cancer
YJZ5118 is a selective CDK12/CDK13 inhibitor with IC₅₀ values of 39.5 nM and 26.4 nM. YJZ5118 suppresses transcription of DNA damage response genes and induces DNA damage in tumor cells. YJZ5118 inhibits proliferation and triggers apoptosis. YJZ5118 inhibits RNA polymerase II Ser2 phosphorylation and increases Akt pathway activity. YJZ5118 exhibits synergistic effects with Akt inhibitors. YJZ5118 can be used for the research of cancer, such as prostate cancer .

HY-E70830

HIPK2 Recombinant Human Active Protein Kinase	DYRK	Cancer
Homeodomain interacting protein kinase 2 (HIPK2) is an evolutionary conserved serine/threonine kinase that regulates gene expression by phosphorylation of transcription factors and accessory components of the transcription machinery. HIPK2 is activated in response to DNA-damaging agents or morphogenic signals. HIPK2 Recombinant Human Active Protein Kinase is a recombinant HIPK2 protein that can be used to study HIPK2-related functions .

HY-182926

Topoisomerase I/II-IN-9	DNA/RNA Synthesis Topoisomerase	Cancer
Topoisomerase I/II-IN-9 is a topoisomerase I/II inhibitor (IC₅₀<10 μM) and a DNA damage inducer. Topoisomerase I/II-IN-9 blocks the interaction between the enzyme and DNA by binding to the DNA-binding pocket of the enzyme. Topoisomerase I/II-IN-9 activates the cGAS-STING pathway and promotes the accumulation of cytoplasmic double-stranded DNA. This further drives the production of type I interferons, CCL5, CXCL10 and interferon-stimulated genes, and induces anti-tumor immune responses in vivo. Topoisomerase I/II-IN-9 can be applied to the research of related diseases such as triple-negative breast cancer, colorectal cancer and gastric cancer .

HY-119578

Imiprothrin	Cytochrome P450	Cancer
Imiprothrin is an inducer that induces CYP1A2 and metallothionein 1a, with significant genotoxicity and cytotoxicity. In rat hepatocytes, Imiprothrin initiates detoxification responses by triggering the overexpression of these two genes. Imiprothrin induces chromosomal aberrations and micronucleus formation in rat bone marrow cells, and causes DNA damage in hepatocytes. Imiprothrin triggers oxidative stress in rats, leading to lipid peroxidation, excessive reactive oxygen species production and redox imbalance, which in turn impairs liver and kidney functions and causes tissue damage. Imiprothrin inhibits weight gain in mice, and even causes high mortality in female mice at high doses. However, it shows no carcinogenicity in rat experiments; among relevant indicators, aspartate aminotransferase and total protein are identified as sensitive toxicity biomarkers .

HY-181035

DN1679	PROTACs CDK	Cancer
DN1679 is a potent, selective and orally active CRBN-dependent CDK12/13 PROTAC dual degrader. DN1679 shows DC₅₀ of 8.8/9.8 nM (MDA-MB-231), 5.1/6.4 nM (MDA-MB-157) and 17.2/15.8 nM (MDA-MB-468) for CDK12/13. DN1679 can downregulate DNA damage response gene mRNA levels, such as ATM, ATR, BRCA1 and RAD51. DN1679 demonstrates a potent synergistic anti-tumor effect companied with Olaparib (HY-10162). DN1679 can be used for research of triple-negative breast cance .

HY-183831

GPS167	MDM-2/p53 PARP Caspase Apoptosis	Cancer
GPS167 is a CLK kinase inhibitor that potently and selectively inhibits recombinant human CLK1, CLK2 and CLK4. By inhibiting CLK-mediated phosphorylation of SRSF10, GPS167 upregulates the protein-binding ability of CLK1 and CLK4 with SRSF10, downregulates oncogenic BCLAF1-L and upregulates tumor-suppressive BCLAF1-S, regulates alternative splicing of genes such as MDM2 and MDM4, stabilizes p53 protein and induces DNA damage, ultimately triggering tumor cell apoptosis. GPS167 can block the epithelial-mesenchymal transition process of tumors, activate intracellular double-stranded RNA-mediated antiviral immune responses, and produce synergistic cytotoxicity when combined with microtubule-targeting drugs. GPS167 can be used in research related to various cancers including colorectal cancer .

Cat. No.	Product Name

HY-L244

High-Efficiency Gene Editing Compound Library	730 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 730 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.

High-Efficiency Gene Editing Compound Library

730 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 730 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.

Cat. No.	Product Name		Classification

HY-119578

Imiprothrin		Alkynes
Imiprothrin is an inducer that induces CYP1A2 and metallothionein 1a, with significant genotoxicity and cytotoxicity. In rat hepatocytes, Imiprothrin initiates detoxification responses by triggering the overexpression of these two genes. Imiprothrin induces chromosomal aberrations and micronucleus formation in rat bone marrow cells, and causes DNA damage in hepatocytes. Imiprothrin triggers oxidative stress in rats, leading to lipid peroxidation, excessive reactive oxygen species production and redox imbalance, which in turn impairs liver and kidney functions and causes tissue damage. Imiprothrin inhibits weight gain in mice, and even causes high mortality in female mice at high doses. However, it shows no carcinogenicity in rat experiments; among relevant indicators, aspartate aminotransferase and total protein are identified as sensitive toxicity biomarkers .

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