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Fig. 1 · Structure
Cat. No.
A12752
CAS No.
154447-35-5
Formula
C17H15NO3
Mol. Weight
281.31

Documents & Downloads

NU7026

Cat. No. A12752 CAS 154447-35-5

DNA-PK inhibitor

NU7026 is a novel DNA-dependent protein kinase inhibitor that potentiates the cytotoxicity of topoisomerase II poisons used in the treatment of leukemia.

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Publications for NU7026

2 publications citing this product

  1. Bopei Cui, .et al. , Signal Transduct Target Ther, 2023, Sep 25;8(1):366 PMID: 37743418
  2. Velichko AK, .et al. , Nucleic Acids Res, 2019, May 22. pii: gkz436 PMID: 31114877
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Biological Activity

Target & Activity

Target Activity Value
DNA-PK (Cell-free assay) 0.23 μM
PI3K (Cell-free assay) 13 μM
ATM (Cell-free assay) >100 μM
ATR (Cell-free assay) >100 μM

Cellular Effect

Cell Line Activity Value Description Reference
HeLa IC50 230 nM Inhibition of DNA-PK isolated from human HeLa cell extract assessed as reduction in p53 Ser15 phosphorylation by chemiluminescence assay [PMID: 21080722]

In Vitro Studies

In CH1 ovarian carcinoma cells, 10 μM NU7026 enhanced the clonogenic effect of 3 Gy irradiation in the reported 4–24 h washout groups, while the 2 h group did not differ significantly from radiation alone. The methods also describe 24 h pretreatment, so these intervals should not be interpreted as established minimum total exposure times. [1]

NU7026 responses depend on the endpoint and cellular context. In hypoosmotically stressed HeLa cells, 50 μM NU7026 did not significantly rescue nucleolar transcriptional silencing, unlike the separately tested ATM and ATR inhibitors. [2]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Exposure dependence of CH1 radiosensitization

Cell-based study · CH1 human ovarian carcinoma cells [1]

With 10 μM NU7026 and 3 Gy irradiation, the reported 2 h washout group did not differ significantly from radiation alone; the 4, 6 and 24 h groups showed radiosensitization. NU7026 alone had little effect under the reported condition. This is a clonogenic survival experiment, not a kinase IC50 assay.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Colony formation relative to irradiated controlsrelative survival and reported t-test 2 h: no significant difference (P > 0.1); 4, 6 and 24 h: 61, 47 and 13% of radiation control, respectively (P < 0.01).[1]
Clonogenic survival with NU7026 alonesurviving fraction 91±13% of control after 10 μM for 24 h[1]

Literature-Reported Treatment Conditions

Treatment concentration
10 μM
Exposure duration
Methods specify NU7026/solvent addition for 24 h before irradiation, followed by washout at 2, 4, 6 or 24 h after exposure; colonies counted after 9 days.
Method
Clonogenic assay; triplicate flasks per group, including drug-alone, irradiation-alone and untreated controls.
Vehicle
DMSO, final 0.5%
Co-treatment
3 Gy irradiation for the adopted time-course comparison.
Reported limits
The paper calls the washout intervals drug exposure times despite its stated 24 h preincubation; minimum total exposure cannot be resolved from these descriptions. Error-bar semantics and number of independent repeats are not specified in the adopted caption.
Methods and source locations

Compound reported in the paper: NU7026

Evidence concerns the named experimental material and model; it does not establish equivalence of a current Adooq lot.

Materials and Methods: Radiosensitisation experiments and clonogenic assays / Clonogenic survival assay; Results first paragraph; Figure 2B and caption

Colony formation relative to irradiated controls: Values transcribed from Results; Figure 2B visually checked without estimating additional decimals. — Materials and Methods: Radiosensitisation experiments and clonogenic assays / Clonogenic survival assay; Results first paragraph; Figure 2B and caption

Clonogenic survival with NU7026 alone: Results narrative; ± term not identified as SD or SEM there. — Results first paragraph; Clonogenic survival assay methods

NU7026 negative control in stress-induced nucleolar transcription silencing

Cell-based study · HeLa cells under hypoosmotic stress [2]

NU7026 did not significantly rescue the stress-associated reduction in nucleolar fluorouridine incorporation. ATM and ATR inhibitors produced rescue under the compared conditions; DNA-PKcs knockdown likewise failed to rescue in the adjacent genetic comparison. The finding limits attribution of this response to DNA-PK.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Nucleolar FU fluorescence after hypoosmotic stressnegative rescue comparison n.s. for the NU7026 comparison in Figure 5C; caption reports n > 500[2]

Literature-Reported Treatment Conditions

Treatment concentration
50 μM
Exposure duration
NU7026 pretreatment for 6 h; hypoosmotic stress for 3 h in Figure 5C.
Method
5-fluorouridine incorporation detected by immunocytochemistry; fluorescence-intensity distributions compared.
Vehicle
Not specified in the retrieved compound-treatment paragraph.
Co-treatment
Hypoosmotic stress (50% DMEM/50% water); comparator inhibitors KU55933 and VE821 tested separately.
Reported limits
NU7026 target engagement was not established for this selected condition. Figure caption reports unpaired tests whereas general Statistics describes paired two-tailed tests; exact test implementation remains uncertain. Cell counts are not biological replicate counts.
Methods and source locations

Compound reported in the paper: NU7026

Evidence concerns the named experimental material and model; it does not establish equivalence of a current Adooq lot.

Materials and Methods: Drug treatment and osmotic stress, Replication and transcription, Immunofluorescence microscopy and Statistical analysis; Results: Hypoosmotic stress-induced DDR leads to ATR/ATM-dependent silencing of rDNA transcription; Figure 5C–D and caption

Nucleolar FU fluorescence after hypoosmotic stress: Box plots with median; figure image/caption checked. No numerical intensity or exact P value inferred. Adjacent PRKDC knockdown panel read as orthogonal context. — Materials and Methods: Drug treatment and osmotic stress, Replication and transcription, Immunofluorescence microscopy and Statistical analysis; Results: Hypoosmotic stress-induced DDR leads to ATR/ATM-dependent silencing of rDNA transcription; Figure 5C–D and caption

In Vivo Studies

A single 5 mg/kg intravenous dose of NU7026 in female BALB/c mice produced rapidly declining plasma exposure, reported undetectable at 4 h. This pharmacokinetic result does not demonstrate antitumor activity or validate a repeat-dose efficacy regimen. [1]

In SiHa cervical cancer xenografts, NU7026 (25 mg/kg) combined with cisplatin (5 mg/kg), both administered intraperitoneally every 3 days, produced smaller tumors and greater apoptosis than single-agent treatment. This model-specific combination result does not establish clinical efficacy or formal synergy. [3]

Mouse plasma exposure after a single intravenous dose

Animal study · Female BALB/c mice; three mice per sampling time [1]

Following a single 5 mg/kg intravenous dose, plasma NU7026 declined rapidly and was reported undetectable at 4 h. This measured exposure study does not demonstrate antitumor efficacy or validate the paper’s simulated repeat-dose schedule.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Plasma parent NU7026qualitative concentration time course Reported undetectable at 4 h after 5 mg/kg i.v.[1]

Conditions shared by the study groups

Route
Intravenous
Frequency
Single dose
Treatment course
Blood collection at 0.083, 0.25, 0.5, 1, 2, 4, 6 and 24 h post administration
Vehicle
10% ethanol, 25% PEG 200 and 5% Tween 20 in saline
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
NU7026 intravenous exposure
5 mg/kg		Vehicle alone; analytical controls showed no interfering peaksRapid decline of plasma NU7026; reported undetectable at 4 h. No efficacy endpoint adopted.[1]
NU7026 intravenous exposure
Model: Female BALB/c mice; groups of three per time point
Reported limits: No exact clearance, Cmax, AUC or half-life adopted; internal PK parameter discrepancies remain unresolved.
Methods and source locations

Compound reported in the paper: NU7026

Evidence concerns the named experimental material and model; it does not establish equivalence of a current Adooq lot.

Materials and Methods: Animals, Test compounds, In vivo experiments, Analytical method; Results paragraph beginning The plasma clearance; Figure 3 and caption

Plasma parent NU7026: LC/MS/MS; analytical limit of quantitation reported as 20 nM. Undetectable is the authors’ wording, not an independently calculated threshold. — Materials and Methods: Animals, Test compounds, In vivo experiments, Analytical method; Results paragraph beginning The plasma clearance; Figure 3 and caption

NU7026 intravenous exposure · Materials and Methods: Animals, Test compounds, In vivo experiments, Analytical method; Results paragraph beginning The plasma clearance; Figure 3 and caption

NU7026 and cisplatin in SiHa xenografts

Animal study · SiHa cervical cancer xenografts in 5-week-old female nude mice; n = 5 per group [3]

The NU7026–cisplatin combination produced smaller tumors and greater TUNEL staining than single-agent treatment in the reported xenograft comparison. NU7026 alone also increased apoptosis relative to control. These are combination results in this model, without a quantitative synergy analysis.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Xenograft tumor volume, terminal tumor weight and TUNEL positivitydirection of combination effect Combination: smaller tumors and increased apoptosis versus the single agents, as reported; n = 5 per group.[3]

Conditions shared by the study groups

Route
Intraperitoneal (combination Results explicitly states both compounds injected intraperitoneally)
Frequency
Every 3 days
Treatment course
From tumor volume approximately 100 mm³; monitored to 6 weeks, collection at day 42
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
NU7026 plus cisplatin
NU7026 25 mg/kg; cisplatin 5 mg/kg		Concurrent saline, NU7026-alone and cisplatin-alone groups; shared control groups across the paper’s mouse xenograft experimentsSmaller tumor volumes/weights and greater TUNEL positivity with combination than the single-agent groups, as reported and visually checked in Fig. 2E–G.[3]
NU7026 plus cisplatin
Model: SiHa xenografts in female nude mice; five mice per group
Reported limits: NU7026 vehicle and exact number of administrations not specified in the retrieved main text. No numerical effect sizes estimated from plotted points.
Methods and source locations

Compound reported in the paper: NU7026

Evidence concerns the named experimental material and model; it does not establish equivalence of a current Adooq lot.

Results: NU7026 improves CDDP sensitivity via enhancing DNA damage in vitro and in vivo; Figure 2E–G and caption; Methods: Mouse xenograft model and Statistical analyses

Xenograft tumor volume, terminal tumor weight and TUNEL positivity: Fig. 2E reports mean ± SEM for volume; 2F–G report mean ± SD for weight/TUNEL. Caption indicates Student’s t test; no exact effect sizes extracted. — Results: NU7026 improves CDDP sensitivity via enhancing DNA damage in vitro and in vivo; Figure 2E–G and caption; Methods: Mouse xenograft model and Statistical analyses

NU7026 plus cisplatin · Results: NU7026 improves CDDP sensitivity via enhancing DNA damage in vitro and in vivo; Figure 2E–G and caption; Methods: Mouse xenograft model and Statistical analyses

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 154447-35-5
Applications DNA-PK inhibitor
Formula C17H15NO3
Molecular Weight 281.31
SMILES
C1COCCN1C2=CC(=O)C3=C(O2)C4=CC=CC=C4C=C3

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 1 mg/mL (3.55 mM)
Water Insoluble
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
28 mg/mL
Vehicle
1% DMSO+30% polyethylene glycol+1% Tween 80

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Nutley BP, Smith NF, Hayes A, et al. Preclinical pharmacokinetics and metabolism of a novel prototype DNA-PK inhibitor NU7026 British journal of cancer (2005). PMID: 16249792 DOI: 10.1038/sj.bjc.6602823 Source material
  2. [2] Velichko AK, Petrova NV, Luzhin AV, et al. Hypoosmotic stress induces R loop formation in nucleoli and ATR/ATM-dependent silencing of nucleolar transcription Nucleic acids research (2019). PMID: 31114877 DOI: 10.1093/nar/gkz436 Source material
  3. [3] Zhou Y, Liu F, Xu Q, et al. Inhibiting Importin 4-mediated nuclear import of CEBPD enhances chemosensitivity by repression of PRKDC-driven DNA damage repair in cervical cancer Oncogene (2020). PMID: 32661323 DOI: 10.1038/s41388-020-1384-3 Source material

Publications

2 publications citing this product

  1. Bopei Cui, .et al. , Signal Transduct Target Ther, 2023, Sep 25;8(1):366 PMID: 37743418
  2. Velichko AK, .et al. , Nucleic Acids Res, 2019, May 22. pii: gkz436 PMID: 31114877

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