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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
45 Results for "
joining
" in MedChemExpress (MCE) Product Catalog:
Products (45)
45 Results for "joining" in MCE Product Catalog:
21
21 Publications Verification
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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 .
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6 Cited Publications
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 .
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5 Cited Publications
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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) .
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4 Cited Publications
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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) .
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4 Cited Publications
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PFM03 is a MRE11 Endonuclease inhibitor. PFM03 regulates DNA double-strand break repair (DSBR) by nonhomologous end-joining (NHEJ) .
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3 Cited Publications
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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 .
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1
1 Cited Publications
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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 .
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1 Cited Publications
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UNC9512 is a selective 53BP1 inhibitor with an IC50 of 0.46 μM, and a Kd values of 0.17 μM. UNC9512 binds 53BP1 and its tandem Tudor domain, disrupts histone H4 interaction, and inhibits 53BP1 activity. UNC9512 can be used as a probe for DNA damage repair and Gene editing .
Cat. No.: HY-P99829
CAS No.: 1869937-48-3
Synonyms: PF-06647020; ABBV-647; h6M24-vc0101
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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) .
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T4 DNA ligase is the product of gene 30 of phage T4. T4 DNA ligase catalyzes the repair of single-stranded nicks in duplex DNA and joins duplex DNA restriction fragments having either blunt or cohesive ends. T4 DNA ligase catalyze the sealing of adjacent 5′-phosphate and 3′-hydroxyl termini at single-stranded breaks in double-stranded DNA.T4 DNA ligase is an ATP-dependent ligase enzyme. T4 DNA ligase can be used in various biotechnological applications. T4 DNA ligase can join the ends of single-stranded DNA in the absence of any duplex DNA structure at the ligation site .
Cat. No.: HY-P3752
CAS No.: 92327-84-9
Synonyms: H-Gly-Ala-Tyr-OH
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Synonyms: 6-Nitroveratraldehyde
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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 .
Cat. No.: HY-158346
CAS No.: 2922287-81-6
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RP-2119 is an orally bioactive Polymerase Theta (Polθ) inhibitor, with an IC50 of 0.7 nM against human Polθ ATPase. RP-2119 reduces Polθ activity and exerts antiproliferative effects in BRCA2-deficient cancer cells. RP-2119 exhibits antitumor activity in BRCA2-deficient cancer cell xenograft mouse models . RP-2119 can be used for the research of cancer and homologous recombination-deficient cancers, including brca1/brca2-mutant cancers and shld2-mutant cancers .
Cat. No.: HY-P4383
CAS No.: 20274-80-0
Cat. No.: HY-P3605
CAS No.: 106061-19-2
Synonyms: GAP (25-53), human
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Cat. No.: HY-P5229A
Cat. No.: HY-E70576
CAS No.: 2747966-35-2
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TelN Protelomerase is a prokaryotic telomerase of bacteriophage N15. TelN Protelomerase is an enzyme with cleaving-joining activity, which is required for the formation of linear prophage DNA with closed ends in lysogenic bacteria. TelN Protelomerase cleaves both DNA strands and joins the resulting ends to form covalently closed hairpin structures .
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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
