| Field | Specification |
|---|---|
| Target | |
| Alternative names | LY293646 |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C17H15NO3 |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
NU 7026, also known as LY293646, is a specific DNA-PK inhibitor with an IC50 of 0.23 μM that additionally inhibits PI3K with an IC50 of 13 μM. It is supplied as an off-white to light yellow solid (C17H15NO3, MW 281.31) at 99.97% purity.
Physical & Chemical Properties
| CAS Number | 154447-35-5 |
|---|---|
| Molecular Formula | C17H15NO3 |
| Molecular Weight | 281.31 g/mol |
| Purity | 99.97% |
| Appearance | Solid |
| Color | Off-white to light yellow |
| SMILES | O=C1C2=CC=C3C=CC=CC3=C2OC(N4CCOCC4)=C1 |
| Target | DNA-PK, PI3K |
| Signaling Pathway | Cell Cycle/DNA Damage; PI3K/Akt/mTOR; Apoptosis |
| Solubility | In Vitro: DMSO: 2.5 mg/mL (8.89 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) |
| Storage | Powder: -20°C, 3 years; 4°C, 2 years. In solvent: -80°C, 1 year; -20°C, 6 months. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Biological Activity
IC50 & Target[1]
|
DNA-PK 0.23 μM (IC50) |
PI3K 13 μM (IC50) |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | 2.5 mg/mL (8.89 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 1 year) or -20°C (up to 6 months); avoid repeated freeze-thaw cycles.
Data provided by the manufacturer.
In Vitro
In exponentially growing cells that are DNA-PK proficient, but not in deficient cells, NU7026 (10 μM) enhances cytotoxicity of ionizing radiation (IR) [potentiation factor at 90% cell kill (PF90)=1.51±0.04][1]. NU7026 acts synergistically to sensitize I83 cells to Chlorambucil (CLB) 3.5-fold[2]. NU7026 is a new inhibitor of DNA-dependent protein kinase (DNA-PK), a DNA repair enzyme. At 10 μM, a dose that is nontoxic to cells per se, an NU7026 exposure of at least 4 h combined with 3 Gy radiation is needed for a significant radiosensitisation effect in CH1 human ovarian cancer cells[3]. Solutionin vitro: Dissolve NU7026 in anhydrous DMSO and add NU7026 to cells to a final concentration of 0.25% DMSO (v/v)[4].
In Vivo
NU7026 is a new inhibitor of DNA-dependent protein kinase (DNA-PK), a DNA repair enzyme. After intravenous administration to mice at 5 mg/kg, NU7026 is cleared rapidly from plasma (0.108 L/h), largely because of extensive metabolism. Bioavailability is 20 and 15% after intraperitoneal (i.p.) and p.o. administration, respectively, at 20 mg/kg[3]. Solution in vivo: For i.p. and p.o. dosing (Mice), formulate NU7026 in 10% DMSO and 5% Tween 20 in saline[3]. For i.v. dosing, formulate NU7026 in 10% ethanol, 25% PEG 200 and 5% Tween 20 in saline[3].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
Cell Assay[2]
Plate I83 cells in RPMI 1640 medium with 10% FBS (1.5×105 cells/mL) and treat with vehicle (DMSO), 5 μM CLB, CLB IC50, 10 μM NU7026, or both drugs together, for 0, 6, 24, and 48 h. Determine cell cycle distribution, apoptosis, DNA-PK phosphorylation, and γH2AX, and express results as a percentage of cells in each phase of the cycle. Analyze DNA content on a FACSCalibur flow cytometer with CellQuest software[2].
Animal Administration[3]
Mice[3] Use female BALB/c mice. For i.p. and perorally (p.o.) administration at 20 and 50 mg/kg, respectively, formulate NU7026 in 10% DMSO and 5% Tween 20 in saline. For i.v. dosing at 5 mg/kg, use a formulation of NU7026 in 10% ethanol, 25% PEG 200 and 5% Tween 20 in saline. Give control animals the vehicle alone. Inject groups of three mice per time point. Collect blood by cardiac puncture under transient anaesthesia with halothane at 0.083, 0.25, 0.5, 1, 2, 4, 6, and 24 h after administration. Centrifuge at 1500 g for 2 min to obtain plasma and store the samples at −20°C until analysis. For urinary excretion studies, administer NU7026 at 5 mg/kg i.v. and collect urine over 24 h in metabolic cages, then store at −20°C until required.
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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DNA-PK deficiency potentiates cGAS-mediated antiviral innate immunity. Nat Commun 2020 Dec 3;11(1):6182. PMID: 33273464
Cytoplasmic PARP1 links the genome instability to the inhibition of antiviral immunity through PARylating cGAS. Mol Cell 2022 Jun 2;82(11):2032-2049.e7. PMID: 35460603
Phosphorylation of TRF2 promotes its interaction with TIN2 and regulates DNA damage response at telomeres. Nucleic Acids Res 2023 Feb 22;51(3):1154-1172. PMID: 36651296
PRKDC promotes hepatitis B virus transcription through enhancing the binding of RNA Pol II to cccDNA. Cell Death Dis 2022 Apr 25;13(4):404. PMID: 35468873
Torin2 Exploits Replication and Checkpoint Vulnerabilities to Cause Death of PI3K-Activated Triple-Negative Breast Cancer Cells. Cell Syst 2020 Jan 22;10(1):66-81.e11. PMID: 31812693
LIG1 Loss in TP53-mutant Triple Negative Breast Cancer Rewires DNA Repair and Confers Sensitivity to PARP-ATR Inhibitor Combinations. Mol Cancer Ther 2026 Jul 15:10.1158/1535-7163.MCT-26-0182. PMID: 42456172
DNA damage induced by HIV-1 Vpr triggers epigenetic remodeling and transcriptional programs to enhance virus transcription and latency reactivation. PLoS Biol 2026 Feb 2;24(2):e3003621. PMID: 41628238
IGFBP-3 interacts with NONO and SFPQ in PARP-dependent DNA damage repair in triple-negative breast cancer. Cell Mol Life Sci 2019 May;76(10):2015-2030.
Enhancing CRISPR deletion via pharmacological delay of DNA-PKcs. Genome Res 2021 Mar;31(3):461-471. PMID: 33574136
Chloroquine-Induced DNA Damage Synergizes with Nonhomologous End Joining Inhibition to Cause Ovarian Cancer Cell Cytotoxicity. Int J Mol Sci 2022 Jul 7;23(14):7518. PMID: 35886866
