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Cat. No. M1809

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NU7441 Structure

KU 57788

Size Price Availability Quantity
Free Sample 0.5 mg  USD 0 In stock
5mg USD 65  USD65 In stock
10mg USD 100  USD100 In stock
50mg USD 330  USD330 In stock
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Quality Control & Documentation
Biological Activity

NU7441 (KU 57788) is a potent and selective DNA-dependent protein kinase (DNA-PK) inhibitor with IC50 values of 14, 1700, 5000, >100000 and >100000 nM for DNA-PK, mTOR, PI 3-K, ATM and ATR respectively. NU7441 strongly inhibited DNA-PK in cell lines (IC(50) = 0.3 μM) but only weakly inhibited PI3 K (IC(50) = 7 μM). The only available anti-phospho-DNA-PK antibody also recognised some phosphoprotein targets of ATM. NU7441 (KU 57788) caused doxorubicin- and IR-induced DNA DSBs (measured by γ-H2AX foci) to persist and also slightly decreased homologous recombination activity, as assessed by Rad51 foci. Chemo- and radio-potentiation were induced by NU7441 in M059-Fus-1, but not in DNA-PK-deficient M059 J cells. DNA-PK was highly expressed in a chronic lymphocytic leukaemia sample but undetectable in resting normal human lymphocytes, although it could be induced by PHA-P treatment. In K652 cells, DNA-PK expression was not related to cell cycle phase. NU7441 increased etoposide-induced tumor growth delay 2-fold without exacerbating etoposide toxicity to unacceptable levels. In conclusion, NU7441 (KU 57788) shows sufficient proof of principle through in vitro and in vivo chemosensitization and radiosensitization to justify further development of DNA-PK inhibitors for clinical use.

Product Citations
Customer Product Validations & Biological Datas
Source bioRxiv (2020 Mar) Figure 6. NU7441 (Abmole Bioscience, Houston, TX, USA)
Method BLRR assay
Cell Lines BLRR cells
Concentrations 2×10^-3 M
Incubation Time 1 h
Results Following NU7441 treatment, the Gluc signal increased as the Vluc signal decreased in a dose-dependent manner.
Source Breast Cancer Res Treat (2014). Figure 2. NU7441
Method Western analysis
Cell Lines human breast cancer cells
Concentrations 1 μM
Incubation Time 1 h
Results "Repair was slower in the other two cell lines, which took approximately 18 h to repair 90 % of the breaks. NU7441 retarded the repair in all three cell lines with the greatest effect being observed in MCF-7 cells , where 20 % of DSBs persisted for at least 24 h."
Protocol (for reference only)
Cell Experiment
Cell lines SW620, LoVo, V3, and V3-YAC cells
Preparation method Cytotoxicity and growth inhibition studies.
We exposed exponentially growing cells in six-well plates or 6-cm dishes to etoposide or doxorubicin with or without NU7441 (0.5 or 1.0 μmol/L) for 16 hours. For radiosensitization studies, NU7441 was added to the cells 1 hour before irradiation. V3 and V3-YAC cells were exposed to γ-irradiation (3.1 Gy/min 137Cesium, Gammacell 1000 Elite, Nordion International Ltd., Ottawa, Ontario, Canada). SW620 and LoVo were exposed to X-irradiation (2.9 Gy/min at 230 kV, 10 mA; Gulmay Medical Ltd., Camberly, United Kingdom) due to the equipment available. After irradiation, the cells were incubated with or without NU7441 for a further 16 hours. Cells were then harvested by trypsinization, counted, and seeded into 10-cm diameter Petri dishes at densities varying from 100 to 100,000 per dish in drug-free medium for colony formation. Cell growth inhibition following 5-day continuous exposure to NU7441 was determined in LoVo and SW620 cells grown in 96-well plates as described previously.
Concentrations 0, 2, 4, 6, 8μ M
Incubation time 5 days
Animal Experiment
Animal models CD-1 nude mice bearing palpable SW620 colorectal cancer xenografts
Formulation dissolved in 40% PEG 400 in saline
Dosages 10 mg/kg
Administration i.p.
Chemical Information
Molecular Weight 413.49
Formula C25H19NO3S
CAS Number 503468-95-9
Solubility (25°C) DMSO 10 mg/mL
Storage Powder          -20°C   3 years ;  4°C   2 years
In solvent       -80°C   6 months ;  -20°C   1 month

[1] Zhao Y, et al. Cancer Res. Preclinical evaluation of a potent novel DNA-dependent protein kinase inhibitor NU7441.

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Keywords: NU7441, KU 57788 supplier, PI3K, inhibitors, activators

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