Catalog No.S2893 Synonyms: LY293646
Molecular Weight(MW): 281.31
NU7026 is a potent DNA-PK inhibitor with IC50 of 0.23 μM in cell-free assays, 60-fold selective for DNA-PK than PI3K and inactive against both ATM and ATR.
Cited by 14 Publications
5 Customer Reviews
M059K cells were transfected with Scrambled, ERCC1, EGFR, or EGFR–ERCC1 siRNA. Following 48 hours of siRNA transfection, Scrambled siRNA and ERCC1 siRNA-transfected cells were treated with 1 µmol/L gefitinib or 125 nMol/L NU7026, or both, while EGFR siRNA and EGFR–ERCC1 siRNA-transfected cells were treated with 125 nMol/L of NU7026 1 hour prior 4 Gy IR treatment. Survival of these cells was then assessed 72 hours following IR treatment via MTT assay.
Clin Cancer Res, 2014, 20(13): 3496-50. NU7026 purchased from Selleck.
DNA damage-induced inhibition of rRNA synthesis is dependent on DNA-PK and PARP-1 activity. Representative nuclei stained by EU are shown 22 h after 2 h treatment with 25 µg/ml cisplatin. Cells were treated with cisplatin under the following conditions: pretreatment with Nu7026 (Nu7026, 26) or Nu7441 (Nu7441, 41)
Nucleic Acids Res 2013 41(15), 7378-86. NU7026 purchased from Selleck.
(B) Effect of DNA-PK inhibition on N-OH-PhIP-induced DDR. Cells were treated with N-OH-PhIP (10 μM) with or without DNA-PK inhibitor (DNA-PKi) NU7026 for 14 h. Samples were then subjected to SDS-PAGE and western blot analysis was performed as indicated. Hsp90 was used as loading control.
Nucleic Acids Res, 2016, 44(21):10259-10276. NU7026 purchased from Selleck.
(B) CLL cells were subjected to UV-C light (30 J/m2) (left panel) or IR at a dose of 5 Gy (right panel) and immediately incubated in the absence or presence of 3 μM APC or 10 μM NU7026. γH2AX was analyzed by flow cytometry at the indicated times and expressed as fold change (UV) or as % of the value at time 0 (IR). In all panels, results are means ± SEM of 3–5 independent experiments. Significance relative to the absence of APC (shown at the last incubation time) was analyzed by two-way Anova followed by Bonferroni post-test: **P < 0.01; ****P < 0.0001.
Oncotarget, 2016, 7(25):38367-38379. NU7026 purchased from Selleck.
In vitro selectivity study of [18F]FMTA-2. ZSTK474 (ATP-competitive PI3K inhibitor), GDC-0941 (ATP-competitive PI3K inhibitor), Akt 1/2 inhibitor, PIK-75 (allosteric PI3K inhibitor), NU7441 (DNA-PK inhibitor), NU7026 (DNA-PK inhibitor), KU-55933 (ATM kinase inhibitor), AZ20 (ATR kinase inhibitor), ETP-46464 (ATR kinase inhibitor) and KU0063794 (mTOR inhibitor), respectively (n = 3–6, *P b 0.05, **P < 0.01 vs. control, Mann-Whitney U test). Kinase inhibitors (0.5 μM) were co-incubated with [18F]FMTA-2 (0.15 MBq/mL).
Nucl Med Biol, 2016, 43(1):101-7. NU7026 purchased from Selleck.
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Choose Selective DNA-PK Inhibitors
|Description||NU7026 is a potent DNA-PK inhibitor with IC50 of 0.23 μM in cell-free assays, 60-fold selective for DNA-PK than PI3K and inactive against both ATM and ATR.|
NU7026 potentiates ionizing radiation induced cytotoxicity in a concentration-dependent manner in V3YAC and PARP-1+/+ cells. NU7026 completely abolishes potentially lethal damage recovery in growth-arrested cells. NU7026 inhibits DNA DSB repair by 56% in the V3YAC cell line.  NU7026 (10 μM) potentiates the growth inhibitory effects of idarubicin, daunorubicin, doxorubicin, etoposide, mAMSA, and mitoxantrone with PF50 values ranging from approximately 19 for mAMSA to approximately 2 for idarubicin in K562 cells. NU7026 (10 μM) also potentiates the growth inhibitory effect of etoposide in this leukemia cell line with a PF50 value of 10.53. NU7026 (10 μM) enhances the etoposide-induced cell cycle G2 blockade in K562 cells. NU7026 potentiates topo II poisons involves inhibition of nonhomologous end joining and a G2/M checkpoint arrest.  NU7026 (10 μM) exposure of 4 h in combination with 3 Gy radiation is required for a significant radiosensitisation effect in CH1 human ovarian cancer cells.  NU7026 (< 10 μM) plus chlorambucil has synergistic cytotoxic activity at nontoxic doses of NU7026 in a CLL cell line (I83) and in primary CLL-lymphocytes. NU7026 (10 μM) increases chlorambucil-induced G(2)/M arrest in I83 cells. NU7026 (10 μM) enhances chlorambucil -induced γH2AX throughout the cell cycle in the I83 cell line. NU7026 (10 μM) Increases chlorambucil-Induced apoptosis in the I83 cell line.  NU7026 (55 μM) results in a dramatic induction of telomere fusion in p53 null MEFs and significantly fewer telomere fusions in p53 and ligase IV double null MEFs. 
|In vivo||NU7026 (20mg/kg, i.v.) undergoes rapid plasma clearance (0.108/hour) in mice and this is largely attributed to extensive metabolism. Bioavailability following interperitoneal (i.p.) and p.o. administration of NU7026 at dose of 20 mg/kg is 20 and 15%, respectively. |
-  Veuger SJ, et al. Cancer Res, 2003, 63(18), 6008-6015.
-  Willmore E, et al. Blood, 2004, 103(12), 4659-4665.
-  Nutley BP, et al. Br J Cancer, 2005, 93(9), 1011-1018.
|In vitro||DMSO||1 mg/mL (3.55 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
1% DMSO+30% polyethylene glycol+1% Tween 80
For best results, use promptly after mixing.
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