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Nu7026

Manufactured by Cayman Chemical
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NU7026 is a small molecule compound that functions as an inhibitor of the DNA-dependent protein kinase (DNA-PK) enzyme. DNA-PK plays a critical role in the non-homologous end joining (NHEJ) pathway of DNA double-strand break repair. NU7026 can be used in research applications to study the effects of DNA-PK inhibition.

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Lab products found in correlation

Nu7441, by Bio-Techne (2 mentions) Nu7026, by Bio-Techne (1 mentions) Dimethyl sulfoxide (dmso), by Merck Group (1 mentions) Ve822, by Cayman Chemical (1 mentions) Mirin, by Cayman Chemical (1 mentions) Trichostatin a tsa, by Cayman Chemical (1 mentions) Azd7762, by Cayman Chemical (1 mentions) Celltiter blue cell viability assay, by Promega (1 mentions) Everolimus, by Selleck Chemicals (1 mentions) Ku 57788 nu 7441, by Selleck Chemicals (1 mentions) Crt0066101, by Selleck Chemicals (1 mentions) Cc 115, by Selleck Chemicals (1 mentions) Osi 906, by Selleck Chemicals (1 mentions) Ku 0063794, by Selleck Chemicals (1 mentions) Ldn193189, by Axon Medchem (1 mentions)

3 protocols using nu7026

1

DNA-PKcs Inhibition in MEFs

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When indicated, MEFs were pre-treated for 30 min or 1 h with the indicated concentration of the DNA-PKcs inhibitors NU7026 (Cayman Chemical) or NU7441 (Tocris), or cultured with a single dose of NU7026 for proliferation assays.
Wilson J.E., Petrucelli A.S., Chen L., Koblansky A.A., Truax A.D., Oyama Y., Rogers A.B., Brickey W.J., Wang Y., Schneider M., Mühlbauer M., Chou W.C., Barker B.R., Jobin C., Allbritton N.L., Ramsden D.A., Davis B.K, & Ting J.P. (2015). Inflammasome-independent role of AIM2 in suppressing colon tumorigenesis by interfering with DNA-PK–dependent Akt activation. Nature medicine, 21(8), 906-913.
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2

Comprehensive Small Molecule Library for DNA Repair

Cited 1 time
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Commercially available small molecules used in this study were SCR7 (Tocris; 5342), Azidothymidine (AZT; Tocris), B02 (Sigma; SML0364), 6-Hydroxy-DL-DOPA (DOPA; Tocris), Cyclosporin H (CsH) (Sigma; SML 1575), Mirin (Cayman; 13208), Olaparib (LC Labs; O-9201), AZD7762 (Cayman; 11491), VE822 (Cayman; 24198), RS1 (Calbiochem; 553510), NU7026 (Cayman; 13308), NU7441 (Tocris; 3712), Trichostatin A (TSA) (Cayman; 89730), Pevonedistat (MLN4924) (Selleckchem; S7109), and M3814 (MedKoo; 206478). As a control, this study included the CRISPY Mix (51 (link)), which is the combination of 20 μM NU7026 (NHEJ inhibitor), 0.01 μM TSA (HDAC inhibitor) and 0.5 μM MLN4924 (improves CtIP) (NSC 15520 was not available). Stock solutions were prepared in dimethylsulfoxide (DMSO) (Sigma) and diluted to working concentrations before use. The medium was changed 24 h after the addition of small molecules. We listed the detailed information and working concentrations of small molecules in Supplementary Table S2.
Fu Y.W., Dai X.Y., Wang W.T., Yang Z.X., Zhao J.J., Zhang J.P., Wen W., Zhang F., Oberg K.C., Zhang L., Cheng T, & Zhang X.B. (2021). Dynamics and competition of CRISPR–Cas9 ribonucleoproteins and AAV donor-mediated NHEJ, MMEJ and HDR editing. Nucleic Acids Research, 49(2), 969-985.
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3

Cell Viability Assay for Drug Synergy

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The cells were seeded in triplicate in clear, flat-bottomed 96-well plates in appropriate concentrations (MP46 and MM66: 4000 cells/well, MP38: 6000 cells/well, OMM2.3 and OMM2.5: 2000 cells/well, OMM1: 1500 cells/well). The next day, the medium was supplemented either with a single compound or a combination of the drugs. Five days later, the number of viable cells was determined using a CellTiter-Blue cell viability assay (Promega, Fitchburg, WI, USA). Everolimus, KU-0063794, OSI-906, CC-115, CRT0066101, and KU-57788 (NU7441) were purchased from Selleck Chemicals (Houston, TX, USA), LDN-193189 was obtained from Axon Medchem (Groningen, The Netherlands), and NU7026 was obtained from Cayman Chemical (Ann Arbor, MI, USA).
The synergistic score was calculated according to the Excess over Bliss model [42 (link)] using the formula:
where Fa is the fractional activity.
Glinkina K., Groenewoud A., Teunisse A.F., Snaar-Jagalska B.E, & Jochemsen A.G. (2022). Novel Treatments of Uveal Melanoma Identified with a Synthetic Lethal CRISPR/Cas9 Screen. Cancers, 14(13), 3186.
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