| Field | Specification |
|---|---|
| Target | |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C18H16N4O3S |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
VE-821 is a potent, ATP-competitive inhibitor of ATR, with a Ki of 13 nM and an IC50 of 26 nM. It is supplied as a light green to green solid (C18H16N4O3S, MW 368.41) at 99.67% purity.
Physical & Chemical Properties
| CAS Number | 1232410-49-9 |
|---|---|
| Molecular Formula | C18H16N4O3S |
| Molecular Weight | 368.41 g/mol |
| Purity | 99.67% |
| Appearance | Solid |
| Color | Light green to green |
| SMILES | O=C(NC1=CC=CC=C1)C2=NC(C3=CC=C(C=C3)S(=O)(C)=O)=CN=C2N |
| Target | ATR, ATM, DNA-PK, PI3Kγ |
| Signaling Pathway | Cell Cycle/DNA Damage; PI3K/Akt/mTOR |
| Solubility | In Vitro: DMSO: 50 mg/mL (135.72 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) H2O: < 0.1 mg/mL (insoluble) |
| 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]
|
ATR 13 nM (Ki) |
ATM 16 μM (Ki) |
DNA-PK 2.2 μM (Ki) |
PI3Kγ 3.9 μM (Ki) |
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 (135.72 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
| H2O | < 0.1 mg/mL | insoluble |
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 | Vehicle: 10% PEG300, 2.5% Tween-80, pH 4 |
|---|
Data provided by the manufacturer.
In Vitro
VE-821 displays excellent selectivity for ATR, with minimal cross-reactivity against a large panel of unrelated protein kinases and against the related PIKK family members ATM, DNA-PK, mTOR, and PI3Kγ (Kis of 16 μM, 2.2 μM, >1 μM, and 3.9 μM, respectively)[1]. Inhibition of ATM and DNA-PK by VE-821 is also seen, with IC50 values of >8 μM and 4.4 μM, respectively[2]. Pancreatic cancer cells (PSN-1, MiaPaCa-2, and primary PancM) become significantly more sensitive to radiation and Gemcitabine with VE-821, under both normoxic and hypoxic conditions. Radiation-induced G2/M arrest in cancer cells is blocked by VE-821-mediated ATR inhibition. At 2 h post-irradiation, 1 μM VE-821 inhibits Chk1 phosphorylation (Ser 345) in both PSN-1 and MiaPaCa-2 cells treated with Gemcitabine (100 nM), radiation (6 Gy), or both[3].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
Kinase Assay[2]
Test the ability of compounds (e.g., VE-821) to inhibit ATR, ATM, or DNAPK kinase activity with a radiometric-phosphate incorporation assay. Prepare a stock solution containing the appropriate buffer, kinase, and target peptide. Add the compound of interest at varying concentrations in DMSO, to a final DMSO concentration of 7%. Initiate the assays by adding an appropriate [g-33P]ATP solution and incubate at 25°C. Stop the assays after the desired time course by adding phosphoric acid and ATP to final concentrations of 100 mM and 0.66 μM, respectively. Capture the peptides on a phosphocellulose membrane, prepare, and wash six times with 200 μL of 100 mM phosphoric acid, then add 100 μL of scintillation cocktail and count on a 1450 Microbeta Liquid Scintillation Counter. Analyze dose−response data with GraphPad Prism software[2].
Cell Assay[3]
Plate MiaPaCa-2, PSN-1, and Panc1 cells (5×104) in 96-well plates and, after 4 h, treat with VE-821 at increasing concentrations, 1 h ahead of irradiation with a single dose of 4 Gy. Replace the medium 72 h post-irradiation and measure viability with the Alamar Blue assay. Allow cells to proliferate and analyze cell viability again at day 10 for the different treatment conditions. Normalize cell viability and surviving fraction to the untreated (control) group[3].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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Different repair pathways support intact or truncated insertions by R2 retrotransposon protein. Science 2026 Feb 26;391(6788):eadz3121. PMID: 41231928
Extrachromosomal DNA replication and maintenance couple with DNA damage pathway in tumors. Cell 2025 Jun 26;188(13):3405-3421.e27. PMID: 40300601
Deubiquitination of CDC6 by OTUD6A promotes tumour progression and chemoresistance. Mol Cancer 2024 Apr 29;23(1):86. PMID: 38685067
Asymmetric division in a two-cell-like state rejuvenates embryonic stem cells. Cell Res 2026 Mar;36(3):219-232. PMID: 41634384
Radiotherapy-resistant prostate cancer cells escape immune checkpoint blockade through the senescence-related ataxia telangiectasia and Rad3-related protein. Cancer Commun (Lond) 2025 Mar;45(3):218-244. PMID: 39698847
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
Human iPSC-based Modeling of Pulmonary Fibrosis Reveals p300/CBP Inhibition Suppresses Alveolar Transitional Cell State. Nat Commun 2026 Feb 12;17(1):1214. PMID: 41680175
ATR/Chk1 signaling induces autophagy through sumoylated RhoB-mediated lysosomal translocation of TSC2 after DNA damage. Nat Commun 2018 Oct 8;9(1):4139.
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
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
