| Field | Specification |
|---|---|
| Target | |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C21H17NO3S2 |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
KU-55933 is a potent ATM inhibitor with an IC50 of 12.9 nM and a Ki of 2.2 nM, and it is highly selective for ATM relative to DNA-PK, PI3K/PI4K, ATR and mTOR. It is supplied as a white to khaki solid (C21H17NO3S2, MW 395.49) at 99.92% purity.
Physical & Chemical Properties
| CAS Number | 587871-26-9 |
|---|---|
| Molecular Formula | C21H17NO3S2 |
| Molecular Weight | 395.49 g/mol |
| Purity | 99.92% |
| Appearance | Solid |
| Color | White to khaki |
| SMILES | O=C1C=C(OC(C2=C3SC4=C(SC3=CC=C2)C=CC=C4)=C1)N5CCOCC5 |
| Target | ATM, DNA-PK, mTOR, PI3K |
| Signaling Pathway | Cell Cycle/DNA Damage; PI3K/Akt/mTOR; Autophagy |
| Solubility | In Vitro: DMSO: 50 mg/mL (126.43 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]
|
ATM 12.9 nM (IC50) |
DNA-PK 2500 nM (IC50) |
mTOR 9300 nM (IC50) |
PI3K 16600 nM (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 | 50 mg/mL (126.43 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.
In Vivo
Choose the formulation that suits the animal model and route of administration; percentages are volume ratios of the final working solution. Start from a clear DMSO stock (see In Vitro above), add the co-solvents one at a time in the order listed, mixing after each addition, and prepare the working solution fresh on the day of dosing. If precipitation or phase separation occurs, gentle warming or sonication can help.
Protocol 1
| Composition | 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% saline |
|---|---|
| Result | ≥ 2.5 mg/mL (6.32 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 400 μL PEG300; then 50 μL Tween-80; then 450 μL saline to bring the volume to 1 mL. Saline: dissolve 0.9 g sodium chloride in ddH2O and make up to 100 mL. |
Protocol 2
| Composition | 10% DMSO + 90% (20% SBE-β-CD in saline) |
|---|---|
| Result | ≥ 2.5 mg/mL (6.32 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 900 μL 20% SBE-β-CD in saline. 20% SBE-β-CD in saline: dissolve 2 g SBE-β-CD powder in 10 mL saline until clear (4°C, store up to one week). |
Protocol 3
| Composition | 10% DMSO + 90% Corn Oil |
|---|---|
| Result | ≥ 2.5 mg/mL (6.32 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). Use with caution if continuous dosing will exceed two weeks. For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 900 μL corn oil. |
Data provided by the manufacturer.
In Vitro
Phosphorylation of p53 at serine 15 induced by ionizing radiation is blocked by KU-55933 (10 μM). The inhibition of this ATM-dependent phosphorylation event by KU-55933 is dose-dependent, with an estimated IC50 of 300 nM. Ionizing radiation-induced phosphorylation of these ATM substrates is ablated by KU-55933. ATM is specifically inhibited by KU-55933, whereas the remaining DNA damage-activated PIKKs, ATR and DNA-PK, are not[1]. KU-55933 induces pATM, p53, E2F1 and pATR, and at the 0.5 h time point it noticeably upregulates the nuclear fraction of E2F1[2].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
Cell Assay[1]
Seed 1BR or AT4 cells in 10-cm Petri dishes and treat on day 2 (80 to 90% confluence). Preincubate the cells for 1 hour with KU-55933 or vehicle control, then expose them to 5 Gy of ionizing radiation. Run time courses of cell cycle distribution and select the optimal time for discriminating populations, 16 hours. Perform all subsequent experiments at the 16-hour time point. Stain cells with propidium iodide following standard protocols and analyze by FACS with a FACScalibur. Expose exponentially growing (50-70% confluent) SW620 cells in 60 mm dishes to KU-55933 or DMSO for 1 h, then add etoposide (final concentration of 0.1 and 1 μM); after 16 h, harvest, stain with propidium iodide, and analyze as above.
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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Therapeutic targeting of ATR yields durable regressions in small cell lung cancers with high replication stress. Cancer Cell 2021 Apr 12;39(4):566-579.e7. PMID: 33848478
Extrachromosomal DNA replication and maintenance couple with DNA damage pathway in tumors. Cell 2025 Jun 26;188(13):3405-3421.e27. PMID: 40300601
Asymmetric division in a two-cell-like state rejuvenates embryonic stem cells. Cell Res 2026 Mar;36(3):219-232. PMID: 41634384
Chromosome mis-segregation triggers cell cycle arrest through a mechanosensitive nuclear envelope checkpoint. Nat Cell Biol 2025 Jan;27(1):73-86. PMID: 39779939
ZBP1 antagonizes MRE11-mediated DNA end resection and confers synthetic lethality to PARP inhibition in ovarian cancer. Drug Resist Updat 2026 Jan:84:101319. PMID: 41192279
Refined DNA repair manipulation enables a universal knock-in strategy in mouse embryos. Nat Commun 2025 Jul 15;16(1):6502. PMID: 40664653
Nuclear IMPDH2 controls the DNA damage response by modulating PARP1 activity. Nat Commun 2024 Nov 12;15(1):9515. PMID: 39532854
Genotoxic stress-triggered β-catenin/JDP2/PRMT5 complex facilitates reestablishing glutathione homeostasis. Nat Commun 2019 Aug 21;10(1):3761.
HSPA1A and DNAJB1 regulate NELF condensate dynamics to safeguard transcriptional recovery under heat stress. Mol Cell 2026 Feb 19;86(4):674-692.e10. PMID: 41653920
Lactylation of XLF promotes non-homologous end-joining repair and chemoresistance in cancer. Mol Cell 2025 Jul 17;85(14):2654-2672.e7. PMID: 40680721
