| Field | Specification |
|---|---|
| Target | |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C17H15N7O2 |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
CP-466722 is a rapidly reversible ATM inhibitor with an IC50 of 0.41 μM, and it has no effect on PI3K or other closely related PI3K-like protein kinase (PIKK) family members. It is supplied as a white to off-white solid (C17H15N7O2, MW 349.35) at 99.74% purity.
Physical & Chemical Properties
| CAS Number | 1080622-86-1 |
|---|---|
| Molecular Formula | C17H15N7O2 |
| Molecular Weight | 349.35 g/mol |
| Purity | 99.74% |
| Appearance | Solid |
| Color | White to off-white |
| SMILES | NC1=NC(C2=NC=CC=C2)=NN1C3=C4C=C(OC)C(OC)=CC4=NC=N3 |
| Target | ATM |
| Signaling Pathway | Cell Cycle/DNA Damage; PI3K/Akt/mTOR |
| Solubility | In Vitro: DMSO: 1 mg/mL (2.86 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, 2 years; -20°C, 1 year. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Biological Activity
IC50 & Target[2]
|
ATM 4.1 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 | 1 mg/mL (2.86 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 2 years) or -20°C (up to 1 year); avoid repeated freeze-thaw cycles.
Data provided by the manufacturer.
In Vitro
CP-466722 (CP466722, 6-10 μM) inhibits IR-induced ATM kinase activity, and this inhibition is rapidly and completely reversible. In mouse cells, CP466722 (6, 10 μM) inhibits p53 induction and ATM-dependent phosphorylation, but CP466722 fails to inhibit ATR activity, as well as the ATR-dependent phosphorylation of Chk1. In cells, CP466722 (6 μM) disrupts ATM-dependent cell cycle checkpoints[1]. In MCF7 cells, CP466722 (1 μM) completely inhibits ATM-dependent phosphorylation, and in MCF7 cells CP466722 (10 μM) reduces pKAP1 phosphorylation, with an IC50 of 0.41 μM. Both pATM and pKAP1 signals are blocked by CP466722 (10 μM)[2]. CP-466722 (CP466722, 5-50 μM) suppresses proliferation of SKBr-3 cancer cells more strongly than that of MCF-7 cancer cells. After 48 hours of treatment, CP466722 (10 μM) also slightly raises the proportions of MCF-7 and SKBr-3 cells in the G1 phase[3].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
Kinase Assay[1]
To screen for small molecule inhibitors of ATM kinase activity, carry out an in vitro kinase assay and develop an ELISA assay that measures the phosphorylation status of the ATM downstream target p53. Purify recombinant GST-p53(1-101) and full-length Flag-tagged ATM & ATR for use in the ELISA and in vitro kinase assays. Coat Nunc 96 well Maxisorp plates overnight (4°C) with 2 μg of purified, recombinant GST-p53(1-101) in PBS. Perform all subsequent incubations at room temperature. Wash the plates (0.05% v/v-Tween/PBS), then add 30-60 ng of purified recombinant full-length ATM kinase, in 80 μL final volume of reaction buffer (1 μM ATP, 1 mM DTT, 10 mM MnCl2, 10 mM MgCl2, 50 mM NaCl2, and 20 mM HEPES), with or without compound. Add compounds, including CP-466722 (10 μM), to plates in duplicate and incubate the kinase assay (90 min). Wash the plates (0.05% v/v-Tween/PBS), block (1 h, 1% w/v-BSA/PBS), and rinse, then add anti-Phospho(Ser15)-p53 antibody (1:1000/PBS) and incubate (1 h). Wash the plates (0.05% v/v-Tween/PBS) to reduce non-specific binding, then incubate (1 h) with HRP-conjugated goat anti-rabbit IgG secondary antibody (1:5000/PBS). Detect secondary antibody linked to the phosphorylated GST-p53(1-101) protein with TMB substrate reagent. Develop the plates (15-30 min) and stop the reaction (1M H2SO4 final concentration) before determining absorbance (λ450 nm). Characterize compounds that inhibit ATM kinase activity in ELISA assays for inhibition of ATM/ATR kinases using in vitro kinase assays. Use Western blotting with the anti-Phospho(Ser15)-p53 antibody as a readout of ATM/ATR inhibition[1].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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ATR/Chk1 signaling induces autophagy through sumoylated RhoB-mediated lysosomal translocation of TSC2 after DNA damage. Nat Commun 2018 Oct 8;9(1):4139.
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
Inhibition of Pim-2 kinase by LT-171-861 promotes DNA damage and exhibits enhanced lethal effects with PARP inhibitor in multiple myeloma. Biochem Pharmacol 2021 Aug:190:114648. PMID: 34111425
The Effects and Mechanism of ATM Kinase Inhibitors in Toxoplasma gondii. Int J Mol Sci 2024 Jun 25;25(13):6947. PMID: 39000057
Combination of PARP inhibitor and temozolomide to suppress chordoma progression. J Mol Med (Berl) 2019 Aug;97(8):1183-1193.
