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Results for "

end-joining

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Apoptosis (8) Caspase (2) Cytochrome P450 (2) DNA Alkylator/Crosslinker (1) DNA-PK (2) DNA/RNA Synthesis (11) Drug Intermediate (1) Endogenous Metabolite (1) Endonuclease (2) HDAC (2) mRNA (1) NF-κB (1) RAD51 (2) Reference Standards (1)
By Research Areas:	Cancer (16) Neurological Disease (1)
Oligonucleotides:	mRNA (1) Gene Editing (1)

Inhibitors & Agonists

Screening Libraries

Isotope-Labeled Compounds

Antibodies

Oligonucleotides

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-107845

SCR7 pyrazine Maximum Cited Publications 20 Publications Verification	DNA/RNA Synthesis Apoptosis	Cancer
SCR7 pyrazine is a DNA ligase IV inhibitor that blocks *nonhomologous end-joining* (NHEJ) in a ligase IV-dependent manner. SCR7 pyrazine increases the efficiency of Cas9-mediated homology-directed repair (HDR). SCR7 pyrazine induces cell apoptosis** and has anticancer activity .

HY-150279

PolQi2 3 Publications Verification	DNA/RNA Synthesis	Others
PolQi2 is a PolΘ inhibitor that targets and inhibits alt-EJ (alternative end-joining) repair by inhibiting the helicase domain at the N-terminus of PolΘ. PolQi2 enhances the precision and integration efficiency of gene editing at different loci and in various cell lines. Furthermore, the combined use of PolQi2 with DNA-PK inhibitors reduces the off-target effects of Cas9. PolQi2 can be used in gene editing research .

HY-130603

DCZ0415 5 Publications Verification	NF-κB Apoptosis	Cancer
DCZ0415, a potent TRIP13 inhibitor, impairs nonhomologous end joining repair and inhibits NF-κB activity. DCZ0415 induces anti-myeloma activity in vitro, in vivo, and in primary cells derived from drug-resistant myeloma patients .

HY-19939S

VX-984 4 Publications Verification M9831	DNA-PK	Cancer
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-strand breaks). VX-984 can be used for glioblastomas (GBM) and non-small cell lung cancer (NSCLC) research. VX-984 is a de novo deuterium .

HY-116770

PFM01 5 Publications Verification	Endonuclease	Cancer
PFM01, N-alkylated Mirin derivative, is a MRE11 endonuclease inhibitor. PFM01 can regulate double-strand break repair (DSBR) by nonhomologous end-joining (NHEJ) versus homologous recombination (HR) .

HY-139289

ART812 3 Publications Verification	DNA/RNA Synthesis	Cancer
ART812 is an orally active DNA polymerase Polθ inhibitor with an IC₅₀ value of 7.6 nM. ART812 has an IC₅₀ value of 240 nM for cell based microhomology-mediated end joining (MMEJ) .

HY-159078

PolQi1	DNA/RNA Synthesis	Cancer
PolQi1 is a selective inhibitor targeting the Polθ domain of DNA polymerase. PolQi1 inhibits the Polθ-mediated microhomology end joining (TMEJ/alt-EJ) pathway, reducing insertion/deletion (Indels) and imprecise editing events during DNA repair. PolQi1 can enhance the efficiency and accuracy of homology-directed repair (HDR) or Prime editing, and reduce off-target effects; and in combination with DNA-PK inhibitor AZD-7648 (HY-111783), exert efficient genome editing capabilities with dual pathway regulation. PolQi1 can be mainly used in gene editing research (such as CRISPR-Cas9 or Prime editing system optimization) to improve the precision editing efficiency of difficult-to-edit cells (such as primary hepatocytes and mouse embryos) .

HY-139297

SCR130 1 Publications Verification	DNA/RNA Synthesis Apoptosis	Cancer
SCR130 is a SCR7-based *DNA nonhomologous end-joining* (NHEJ)** inhibitor. SCR130 inhibits the end-joining of DNA in a Ligase IV-dependent manner. SCR130 is specific to Ligase IV, and shows minimal or no effect on Ligase III and Ligase I mediated joining. SCR130 induces cell apoptosis and has anticancer activity .

HY-148078

PFM03 3 Publications Verification	Endonuclease	Others
PFM03 is a MRE11 Endonuclease inhibitor. PFM03 regulates DNA double-strand break repair (DSBR) by nonhomologous end-joining (NHEJ) .

HY-100705

DMNB 6-Nitroveratraldehyde	Drug Intermediate	Neurological Disease
DMNB (6-Nitroveratraldehyde) is a photolabile proton donor that releases acidic substances when excited at a wavelength of 405 nM. DMNB can be used for the synthesis of no-carrier-added 6-[18F]fluoro-L-DOPA (6-FDOPA). DMNB is also applicable to the preparation of o-nitroaryl-bis (5-methylfur-2-yl) methanes and the synthesis of alpha-asarone (HY-N0700). DMNB is an enzyme involved in the non-homologous end joining (NHEJ) pathway responsible for DNA double-strand break (DSB) repair. DMNB can be used in PET studies of the dopaminergic system .

HY-178021

HDAC1-IN-11	HDAC DNA/RNA Synthesis Apoptosis RAD51 Caspase	Cancer
HDAC1-IN-11 (Compound 6) is a HDAC1 inhibitor with an IC₅₀ of 106.6  nM. HDAC1-IN-11 inhibits the expression of Sp1 and RAD51, thereby inducing Caspase-dependent apoptosis. HDAC1-IN-11 has antitumor activity and sensitizes Etoposide (HY-13629) and Gemcitabine (HY-17026), promoting synergistic death of NSCLC cells through the inhibition of homologous recombination and non-homologous end joining (NHEJ) pathways involved in DNA DSB repair. HDAC1-IN-11 can be used for chemotherapy of cancers like NSCLC research .

HY-178022

HDAC6-IN-63	HDAC Apoptosis Caspase RAD51 DNA/RNA Synthesis	Cancer
HDAC6-IN-63 (Compound 7) is an orally active HDAC6 inhibitor with an IC₅₀ of 145  nM. HDAC6-IN-63 inhibits the expression of Sp1 and RAD51, thereby inducing Caspase-dependent apoptosis. HDAC6-IN-63 has antitumor activity and sensitizes Etoposide (HY-13629) and Gemcitabine (HY-17026), promoting synergistic death of NSCLC cells through the inhibition of homologous recombination and non-homologous end joining (NHEJ) pathways involved in DNA DSB repair. HDAC6-IN-63 can be used for chemotherapy of cancers like NSCLC research .

HY-174499

Cas9 Nickase D10A mRNA (5moU)	mRNA	Others
Cas9 Nickase D10A mRNA expresses a version of the Streptococcus pyogenes SF370 Cas9 protein (CRISPR Associated Protein 9) that contains a D10A amino acid substitution. This mRNA also contains a C-terminal nuclear localization signal followed by a HA tag.Cas9 functions as part of the CRISPR (clustered regularly interspaced short palindromic repeats) genome editing system. In the CRISPR system, an RNA guide sequence targets the site of interest and the Cas9 protein is employed to perform the DNA cleavage. While wild-type Cas9 creates a double-stranded break at the target site, Cas9 nickase creates a single-stranded break. This favors homology-directed repair and decreases the occurrence of non-homologous end joining.

HY-123401

DDRI-18	DNA/RNA Synthesis	Cancer
DDRI-18 is a DNA damage response inhibitor that inhibits the non-homologous end-joining (NHEJ) DNA repair process. DDRI-18 is an effective chemosensitizing agent .

HY-120750

A 62176 hydrochloride	Endogenous Metabolite	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-163816

Antiproliferative agent-53-d3	Cytochrome P450	Cancer
Antiproliferative agent-53-d3 (Compound C1) is an inhibitor for theta-mediated end joining (TMEJ) in HEK293 cell with an IC₅₀ of 0.14 µM. Antiproliferative agent-53-d3 is the inhibitor for CYP2C19 and CYP2C9 with IC₅₀ of 0.77 and 3.1 µM. Antiproliferative agent-53-d3 inhibits the proliferation of DNA repair-compromised cells, with IC₅₀ of 8.1 µM for BRCA2 ^-/- DLD-1. Antiproliferative agent-53-d3 exhibits good pharmacokinetic characteristics in CD-1 mice .

HY-107845R

SCR7 pyrazine (Standard)	Reference Standards DNA/RNA Synthesis Apoptosis	Cancer
SCR7 pyrazine (Standard) is the analytical standard of SCR7 pyrazine (HY-107845). This product is intended for research and analytical applications. SCR7 pyrazine is a DNA ligase IV inhibitor that blocks nonhomologous end-joining (NHEJ) in a ligase IV-dependent manner. SCR7 pyrazine increases the efficiency of Cas9-mediated homology-directed repair (HDR). SCR7 pyrazine induces cell apoptosis and has anticancer activity .

HY-181611

Polθ-IN-10	DNA/RNA Synthesis Apoptosis Cytochrome P450	Cancer
Polθ-IN-10 is an orally active Polθ-pol inhibitor (with a human IC₅₀ of 1.3 nM) that exhibits oral bioavailability in mice and rats. Polθ-IN-10 binds to the allosteric site of Polθ-pol, disrupts the microhomology-mediated end-joining DNA repair pathway, and inhibits CYP2C9 (IC₅₀=1.63 μM). Polθ-IN-10 selectively inhibits the proliferation of HR-deficient cancer cells and induces apoptosis. Polθ-IN-10 is applicable to the research of HR-deficient cancers .

HY-122226

IC-87361	DNA-PK	Cancer
IC-87361 is a DNA-dependent protein kinase (DNA-PKcs) inhibitor and radiosensitizer. IC-87361 inhibits the catalytic activity of DNA-PKcs and blocks non-homologous end joining (NHEJ) DNA double-strand break repair. IC-87361 can be used for the research of lung cancer and melanoma .

HY-181557

SY-589	DNA Alkylator/Crosslinker DNA/RNA Synthesis Apoptosis	Cancer
SY-589 is an orally active DNA polymerase Polθ helicase domain inhibitor (IC₅₀=2.29 nM) and DNA damage inducer. SY-589 inhibits the ATPase activity of the Polθ helicase domain and blocks the Polθ-mediated microhomology-mediated end joining (MMEJ) DNA repair pathway (IC₅₀=0.85 nM). SY-589 also induces the accumulation of DNA double-strand breaks by increasing γ-H2AX levels. SY-589 exerts antiproliferative effects on BRCA2-deficient cells and is used in the research of HR-deficient tumors .

Cat. No.	Product Name

HY-L244

High-Efficiency Gene Editing Compound Library	724 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 724 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

724 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 724 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	Chemical Structure

HY-19939S

VX-984 4 Publications Verification
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-strand breaks). VX-984 can be used for glioblastomas (GBM) and non-small cell lung cancer (NSCLC) research. VX-984 is a de novo deuterium .

HY-163816

Antiproliferative agent-53-d3
Antiproliferative agent-53-d3 (Compound C1) is an inhibitor for theta-mediated end joining (TMEJ) in HEK293 cell with an IC₅₀ of 0.14 µM. Antiproliferative agent-53-d3 is the inhibitor for CYP2C19 and CYP2C9 with IC₅₀ of 0.77 and 3.1 µM. Antiproliferative agent-53-d3 inhibits the proliferation of DNA repair-compromised cells, with IC₅₀ of 8.1 µM for BRCA2 ^-/- DLD-1. Antiproliferative agent-53-d3 exhibits good pharmacokinetic characteristics in CD-1 mice .

Antiproliferative agent-53-d3

Antiproliferative agent-53-d3 (Compound C1) is an inhibitor for theta-mediated end joining (TMEJ) in HEK293 cell with an IC₅₀ of 0.14 µM. Antiproliferative agent-53-d3 is the inhibitor for CYP2C19 and CYP2C9 with IC₅₀ of 0.77 and 3.1 µM. Antiproliferative agent-53-d3 inhibits the proliferation of DNA repair-compromised cells, with IC₅₀ of 8.1 µM for BRCA2 ^-/- DLD-1. Antiproliferative agent-53-d3 exhibits good pharmacokinetic characteristics in CD-1 mice .

Cat. No.	Compare	Product Name	Application	Reactivity	Image

HY-P82555

	XLF Antibody (YA2300) Cernunno; Nhej1; Non homologous end joining factor 1; Protein cernunnos; XLF; XRCC4 like factor	WB, IHC-P, ICC/IF, FC	Human, Mouse, Rat
	XLF Antibody (YA2300) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to XLF.

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Cat. No.	Product Name		Classification

HY-174499

Cas9 Nickase D10A mRNA (5moU)		mRNA Gene Editing
Cas9 Nickase D10A mRNA expresses a version of the Streptococcus pyogenes SF370 Cas9 protein (CRISPR Associated Protein 9) that contains a D10A amino acid substitution. This mRNA also contains a C-terminal nuclear localization signal followed by a HA tag.Cas9 functions as part of the CRISPR (clustered regularly interspaced short palindromic repeats) genome editing system. In the CRISPR system, an RNA guide sequence targets the site of interest and the Cas9 protein is employed to perform the DNA cleavage. While wild-type Cas9 creates a double-stranded break at the target site, Cas9 nickase creates a single-stranded break. This favors homology-directed repair and decreases the occurrence of non-homologous end joining.

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