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nu7441  (MedChemExpress)


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    Structured Review

    MedChemExpress nu7441
    Nu7441, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 69 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/nu7441/KU-57788/pm42809925-51-17-18
    Average 95 stars, based on 69 article reviews
    nu7441 - by Bioz Stars, 2026-10
    95/100 stars

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    Related Articles

    Inhibition:

    Article Title: Oxidative DNA lesions destabilize centromeres and drive chromosome instability
    Article Snippet: .. For Rad51 and DNA-PKcs inhibition, the drug B02 (MCE #HY-101462) and nu7441 (MCE #HY-11006) were used at 2uM and 5uM final concentrations. ..

    Transfection:

    Article Title: DNA-PK interacts with cyclic dinucleotides and inhibits type I interferon responses
    Article Snippet: .. 18 h later, cells were pretreated with 2 μM NU7441 (#3712; Bio-Techne/Tocris) for 1 h in DMEM or RPMI prior to transfection with 2′3′-cGAMP (10 μg/ml, InvivoGen) using Lipofectamine 2000 (Thermo Fischer Scientific), following the manufacturer’s instructions. ..

    Article Title: Ultra-sensitive profiling of CRISPR-Cas off-target effects with Tracking-seq2
    Article Snippet: .. To expose cells to DNA repair inhibitors, they were added to the culture media before transfection at a final concentration of 1.25 μM KU-60648 (Yeasen, 53429ES08), 25 μM DIDS sodium salt (MCE, HY-D0086), 7.5 μM RI-1 (MCE, HY-15317), 10 μM IBR2 (MCE, HY-103710), 0.25 μM NU7441 (MCE, HY-11006), 0.5 μM STL127705 (MCE, HY-122727), 0.25 μM Olaparib (MCE, HY-10162). ..

    other:

    Article Title: GPI inactivation mediates pentose phosphate pathway flux switch-on inducing temozolomide resistance in glioma stem cell.
    Article Snippet: Temozolomide (TMZ) resistance in glioblastoma (GBM) remains a substantial clinical challenge.. Targeting glioma stem cells (GSCs) represents a promising strategy to overcome chemoresistance and tumor recurrence.. In this study, we found that GSCs maintain chemoresistance by increasing pentose phosphate pathway (PPP) flux compared with differentiated tumor cells.

    Article Title: DNA-PK interacts with cyclic dinucleotides and inhibits type I interferon responses.
    Article Snippet: Gibson cloning was performed in two steps, with amplified and purified intermediate constructs, using NEBuilder HiFi DNA Assembly Master Mix and NEB Stable Competent Escherichia coli grown at 30°C.

    Concentration Assay:

    Article Title: Ultra-sensitive profiling of CRISPR-Cas off-target effects with Tracking-seq2
    Article Snippet: .. To expose cells to DNA repair inhibitors, they were added to the culture media before transfection at a final concentration of 1.25 μM KU-60648 (Yeasen, 53429ES08), 25 μM DIDS sodium salt (MCE, HY-D0086), 7.5 μM RI-1 (MCE, HY-15317), 10 μM IBR2 (MCE, HY-103710), 0.25 μM NU7441 (MCE, HY-11006), 0.5 μM STL127705 (MCE, HY-122727), 0.25 μM Olaparib (MCE, HY-10162). ..



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    a, BRIP1 R162Q cells show increased sensitivity to ATR inhibition. Representative colony formation assays and quantification of HCT116 cells expressing BRIP1 WT, BRIP1 R162Q, or BRIP1 knockout (KO) treated with increasing doses of the ATR inhibitor VE-822. Cells were treated overnight and colonies were allowed to form for 10 days prior to crystal violet staining. b, Quantification of survival fraction following ATR inhibition by VE-822. c, BRIP1 R162Q expressing cells show increased sensitivity to DNA-PK inhibition. Representative colony formation assays and quantification following overnight treatment with increasing doses of the DNA-PK inhibitor <t>NU7441.</t> d, Quantification of survival fraction following DNA-PK inhibition using NU7441 e, BRIP1 R162Q cells show increased sensitivity to treatment with G4-stabilizer Pyridostatin. Representative colony formation assays following overnight treatment with increasing concentrations of Pyridostatin (PDS) are shown. After drug removal, cells were cultured for 10 days before fixation and staining. f, Quantification of surviving fraction following Pyridostatin treatment b,d,f , Quantification was performed using EagleEye analysis software. Data represent the mean ± SD of three independent biological replicates. g, Schematic representation of the workflow used to perform colony formation assays in BRIP1R162Q cells upon R-loop removal by ectopic RNaseH1 expression. BRIP1 R162Q cells were transfected with RNase H1 WT or catalytically inactive RNaseH1 D145N, re-seeded, and treated the next day with the drugs indicated. Colonies were stained with crystal violet after 10 days . h-k, RNaseH1 expression decreases sensitivity to ATR VE-822 ( h,i, ) and DNA-PK NU7441 ( j,k, ) inhibition in BRIP1 R162Q expressing cells. h,j, Show representative colony formation plates and i, k, show quantifications of clonogenic survival. Data represent mean values ± SEM from three biologically independent experiments. Colony formation was quantified using EagleEye analysis software.
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    a, BRIP1 R162Q cells show increased sensitivity to ATR inhibition. Representative colony formation assays and quantification of HCT116 cells expressing BRIP1 WT, BRIP1 R162Q, or BRIP1 knockout (KO) treated with increasing doses of the ATR inhibitor VE-822. Cells were treated overnight and colonies were allowed to form for 10 days prior to crystal violet staining. b, Quantification of survival fraction following ATR inhibition by VE-822. c, BRIP1 R162Q expressing cells show increased sensitivity to DNA-PK inhibition. Representative colony formation assays and quantification following overnight treatment with increasing doses of the DNA-PK inhibitor <t>NU7441.</t> d, Quantification of survival fraction following DNA-PK inhibition using NU7441 e, BRIP1 R162Q cells show increased sensitivity to treatment with G4-stabilizer Pyridostatin. Representative colony formation assays following overnight treatment with increasing concentrations of Pyridostatin (PDS) are shown. After drug removal, cells were cultured for 10 days before fixation and staining. f, Quantification of surviving fraction following Pyridostatin treatment b,d,f , Quantification was performed using EagleEye analysis software. Data represent the mean ± SD of three independent biological replicates. g, Schematic representation of the workflow used to perform colony formation assays in BRIP1R162Q cells upon R-loop removal by ectopic RNaseH1 expression. BRIP1 R162Q cells were transfected with RNase H1 WT or catalytically inactive RNaseH1 D145N, re-seeded, and treated the next day with the drugs indicated. Colonies were stained with crystal violet after 10 days . h-k, RNaseH1 expression decreases sensitivity to ATR VE-822 ( h,i, ) and DNA-PK NU7441 ( j,k, ) inhibition in BRIP1 R162Q expressing cells. h,j, Show representative colony formation plates and i, k, show quantifications of clonogenic survival. Data represent mean values ± SEM from three biologically independent experiments. Colony formation was quantified using EagleEye analysis software.
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    a, BRIP1 R162Q cells show increased sensitivity to ATR inhibition. Representative colony formation assays and quantification of HCT116 cells expressing BRIP1 WT, BRIP1 R162Q, or BRIP1 knockout (KO) treated with increasing doses of the ATR inhibitor VE-822. Cells were treated overnight and colonies were allowed to form for 10 days prior to crystal violet staining. b, Quantification of survival fraction following ATR inhibition by VE-822. c, BRIP1 R162Q expressing cells show increased sensitivity to DNA-PK inhibition. Representative colony formation assays and quantification following overnight treatment with increasing doses of the DNA-PK inhibitor <t>NU7441.</t> d, Quantification of survival fraction following DNA-PK inhibition using NU7441 e, BRIP1 R162Q cells show increased sensitivity to treatment with G4-stabilizer Pyridostatin. Representative colony formation assays following overnight treatment with increasing concentrations of Pyridostatin (PDS) are shown. After drug removal, cells were cultured for 10 days before fixation and staining. f, Quantification of surviving fraction following Pyridostatin treatment b,d,f , Quantification was performed using EagleEye analysis software. Data represent the mean ± SD of three independent biological replicates. g, Schematic representation of the workflow used to perform colony formation assays in BRIP1R162Q cells upon R-loop removal by ectopic RNaseH1 expression. BRIP1 R162Q cells were transfected with RNase H1 WT or catalytically inactive RNaseH1 D145N, re-seeded, and treated the next day with the drugs indicated. Colonies were stained with crystal violet after 10 days . h-k, RNaseH1 expression decreases sensitivity to ATR VE-822 ( h,i, ) and DNA-PK NU7441 ( j,k, ) inhibition in BRIP1 R162Q expressing cells. h,j, Show representative colony formation plates and i, k, show quantifications of clonogenic survival. Data represent mean values ± SEM from three biologically independent experiments. Colony formation was quantified using EagleEye analysis software.
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    Image Search Results


    a, BRIP1 R162Q cells show increased sensitivity to ATR inhibition. Representative colony formation assays and quantification of HCT116 cells expressing BRIP1 WT, BRIP1 R162Q, or BRIP1 knockout (KO) treated with increasing doses of the ATR inhibitor VE-822. Cells were treated overnight and colonies were allowed to form for 10 days prior to crystal violet staining. b, Quantification of survival fraction following ATR inhibition by VE-822. c, BRIP1 R162Q expressing cells show increased sensitivity to DNA-PK inhibition. Representative colony formation assays and quantification following overnight treatment with increasing doses of the DNA-PK inhibitor NU7441. d, Quantification of survival fraction following DNA-PK inhibition using NU7441 e, BRIP1 R162Q cells show increased sensitivity to treatment with G4-stabilizer Pyridostatin. Representative colony formation assays following overnight treatment with increasing concentrations of Pyridostatin (PDS) are shown. After drug removal, cells were cultured for 10 days before fixation and staining. f, Quantification of surviving fraction following Pyridostatin treatment b,d,f , Quantification was performed using EagleEye analysis software. Data represent the mean ± SD of three independent biological replicates. g, Schematic representation of the workflow used to perform colony formation assays in BRIP1R162Q cells upon R-loop removal by ectopic RNaseH1 expression. BRIP1 R162Q cells were transfected with RNase H1 WT or catalytically inactive RNaseH1 D145N, re-seeded, and treated the next day with the drugs indicated. Colonies were stained with crystal violet after 10 days . h-k, RNaseH1 expression decreases sensitivity to ATR VE-822 ( h,i, ) and DNA-PK NU7441 ( j,k, ) inhibition in BRIP1 R162Q expressing cells. h,j, Show representative colony formation plates and i, k, show quantifications of clonogenic survival. Data represent mean values ± SEM from three biologically independent experiments. Colony formation was quantified using EagleEye analysis software.

    Journal: bioRxiv

    Article Title: Role of a childhood cancer-linked BRIP1/FANCJ germline variant in genomic instability and cancer cell vulnerability

    doi: 10.64898/2026.03.24.714005

    Figure Lengend Snippet: a, BRIP1 R162Q cells show increased sensitivity to ATR inhibition. Representative colony formation assays and quantification of HCT116 cells expressing BRIP1 WT, BRIP1 R162Q, or BRIP1 knockout (KO) treated with increasing doses of the ATR inhibitor VE-822. Cells were treated overnight and colonies were allowed to form for 10 days prior to crystal violet staining. b, Quantification of survival fraction following ATR inhibition by VE-822. c, BRIP1 R162Q expressing cells show increased sensitivity to DNA-PK inhibition. Representative colony formation assays and quantification following overnight treatment with increasing doses of the DNA-PK inhibitor NU7441. d, Quantification of survival fraction following DNA-PK inhibition using NU7441 e, BRIP1 R162Q cells show increased sensitivity to treatment with G4-stabilizer Pyridostatin. Representative colony formation assays following overnight treatment with increasing concentrations of Pyridostatin (PDS) are shown. After drug removal, cells were cultured for 10 days before fixation and staining. f, Quantification of surviving fraction following Pyridostatin treatment b,d,f , Quantification was performed using EagleEye analysis software. Data represent the mean ± SD of three independent biological replicates. g, Schematic representation of the workflow used to perform colony formation assays in BRIP1R162Q cells upon R-loop removal by ectopic RNaseH1 expression. BRIP1 R162Q cells were transfected with RNase H1 WT or catalytically inactive RNaseH1 D145N, re-seeded, and treated the next day with the drugs indicated. Colonies were stained with crystal violet after 10 days . h-k, RNaseH1 expression decreases sensitivity to ATR VE-822 ( h,i, ) and DNA-PK NU7441 ( j,k, ) inhibition in BRIP1 R162Q expressing cells. h,j, Show representative colony formation plates and i, k, show quantifications of clonogenic survival. Data represent mean values ± SEM from three biologically independent experiments. Colony formation was quantified using EagleEye analysis software.

    Article Snippet: Cells were incubated with culture medium supplemented with mitomycin C (MMC; Carl Roth, 4150.1), hydroxyurea (HU; Sigma-Aldrich, H8627), pyridostatin (PDS; MedChemExpress, HY-15176), NU7441 (KU-57788; Selleckchem, S2638), or VE-822 (berzosertib; Selleckchem, S7102) at the indicated concentrations and time points.

    Techniques: Inhibition, Expressing, Knock-Out, Staining, Cell Culture, Software, Transfection