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Fig. 1 · Structure
Cat. No.
A11086
CAS No.
1080622-86-1
Formula
C17H15N7O2
Mol. Weight
349.4

Documents & Downloads

CP-466722

Cat. No. A11086 CAS 1080622-86-1

ATM inhibitor

CP-466722 is a specific ATM inhibitor that inhibits cellular ATM-dependent phosphorylation events and disruption of ATM function resulted in characteristic cell cycle checkpoint defects.

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Biological Activity

Target & Activity

Target Activity Value
ATM 410 nM

Cellular Effect

Cell Line Activity Value Description Reference
BJ EC50 > 50 μM Cytotoxicity against human BJ cells after 72 hrs by Cell Titer Glo assay [PMID: 26632965]
HT-29 IC50 > 30 μM Inhibition of ATR in human HT-29 cells assessed as reduction in Chk1 phosphorylation at Ser-345 residue after 60 mins in presence of 4-nitroquinoline-1-oxide by Hoechst 33258 staining based plate reader analysis [PMID: 27259031]
HT-29 IC50 3.42 μM Inhibition of ATM phosphorylation at Ser-1981 residue in human HT-29 cells incubated for 1 hr followed by X-ray irradiation by Hoechst staining based fluorescence plate reader analysis [PMID: 27259031]
MCF7 IC50 0.4 μM Inhibition of ATM kinase in human MCF7 cells after 1 hr by immunofluorescence assay [PMID: 26632965]

In Vitro Studies

In SKBr-3 cells, CP-466722 exposure did not increase site-specific phosphorylation of 53BP1 and MRE11 proteins. In HCT116 cells expressing the DDR-Act reporter, adding increasing concentrations of CP-466722 to etoposide treatment produced dose-dependent inhibition of the increase in p53 protein levels compared with etoposide alone. In MCF-7 cells, CP-466722 at 50 μM reduced viability by 80% after 48 hours and 90% after 72 hours. [1,2]

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

Phosphorylation response in breast cancer cells

Cell-based study · SKBr-3 cells [1]

In SKBr-3 cells, exposure to CP-466722 did not produce the increase in site-specific phosphorylation of 53BP1 and MRE11 proteins observed with AZD2461.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
site-specific phosphorylation of 53BP1 and MRE11 proteinsReported result An increase in the site-specific phosphorylation of 53BP1 and MRE11 proteins was observed after treatment for 24 hours with AZD2461 but not after exposure to CP466722[1]

Literature-Reported Treatment Conditions

Exposure duration
24 hours
Method
exposure to CP466722
Vehicle
DMSO
Reported limits
Not stated in the sentences used: dose.
Methods and source locations

Compound reported in the paper: CP-466722

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

MATERIALS AND METHODS > Drugs and chemicals (S1); RESULTS > Poly(ADP-ribose) polymerase-1 inhibition by AZD2461 induces DNA damage response in breast cancer cells (S54, S55); Figure 6. legend (S101)

site-specific phosphorylation of 53BP1 and MRE11 proteins: site-specific phosphorylation of 53BP1 and MRE11 proteins; comparator: untreated control SKBr-3 cells — RESULTS > Poly(ADP-ribose) polymerase-1 inhibition by AZD2461 induces DNA damage response in breast cancer cells (S55)

Protein response to combined treatment in reporter cells

Cell-based study · HCT116 cells expressing the DDR-Act reporter [2]

HCT116 cells expressing the DDR-Act reporter received etoposide together with increasing concentrations of CP-466722 for 24 hours. Adding CP-466722 produced dose-dependent inhibition of the increase in p53 protein levels compared with etoposide alone.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Western blot analysis of p53 and actin as controlReported result Etoposide 20 μM (E20) for 24 hours, together with increasing concentrations of CP-466722: a dose-dependent inhibition of the increase in p53 protein levels as compared to the control induction observed in the presence of Etoposide alone.[2]

Literature-Reported Treatment Conditions

Exposure duration
for 24 hours
Co-treatment
Other interventions in this design: Etoposide 20 μM. Compound effect isolated by the comparison: Etoposide alone.
Reported limits
Not stated in the sentences used: dose, route, vehicle.
Methods and source locations

Compound reported in the paper: CP-466722

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > DDR-Act-FP: A sensor for pharmacological manipulation of the DDR pathway (S54, S55); Fig 3 legend (S95, S96)

Western blot analysis of p53 and actin as control: Western blot analysis of p53 and actin as control; comparator: Etoposide alone — Results > DDR-Act-FP: A sensor for pharmacological manipulation of the DDR pathway (S54, S55); Fig 3 legend (S95, S96)

Viability reduction in breast cancer cells

Cell-based study · MCF-7 cells [1]

MCF-7 cells were treated with CP-466722 at concentrations ranging from 5 μM to 50 μM. At 50 μM, viability was reduced by 80% after 48 hours and 90% after 72 hours.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
numbers of viable cellscell viability 50 μM: viability reduced by 80% after 48 hours and 90% after 72 hours[1]

Literature-Reported Treatment Conditions

Treatment concentration
5 μM to 50 μM
Exposure duration
at 24 hours after plating were treated with CP466722 at a final concentration ranging from 5 μM to 50 μM for 48 hours or 72 hours
Vehicle
DMSO
Reported limits
Not stated in the sentences used: route.
Methods and source locations

Compound reported in the paper: CP-466722

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

MATERIALS AND METHODS > Drugs and chemicals (S1); MATERIALS AND METHODS > Determination of numbers of living cells (S7); RESULTS > Pharmacological interference with ataxia telangiectasia mutated kinase activity by CPP466722 inhibits proliferation of examined cancer cells and is more effective in SKBr-3 cells (S29, S30); Figure 1. legend (S62, S63, S70)

numbers of viable cells: numbers of viable cells; comparator: the control — RESULTS > Pharmacological interference with ataxia telangiectasia mutated kinase activity by CPP466722 inhibits proliferation of examined cancer cells and is more effective in SKBr-3 cells (S29, S30); Figure 1. legend (S62, S63)

In Vivo Studies

Female nude mice received CP-466722 intraperitoneally every day. Compared with vehicle, treatment significantly reduced the number of metastatic tumors in A549cisR-injected mice. [3]

Metastatic tumor response in nude mice

Animal study · 8 weeks old female nude [3]

Female nude mice received CP-466722 intraperitoneally every day. Treatment significantly reduced the number of metastatic tumors in A549cisR-injected mice compared with vehicle.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Numbers of tumor metastasis in each groupReported result CP466722 treatment significantly reduced the number of metastatic tumor in the A549cisR-injected mice[3]

Conditions shared by the study groups

Route
intraperitoneally (i.p.)
Treatment course
every day
Vehicle
10%DMSO
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
CP-466722 10 mg/kgThe control group mice (Either A549P cells or A549cisR cells) were injected with vehicle (10%DMSO) every day.CP466722 treatment significantly reduced the number of metastatic tumor in the A549cisR-injected mice[3]
CP-466722 10 mg/kg
Model: 8 weeks old female nude
Methods and source locations

Compound reported in the paper: CP-466722

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Materials and methods > In vivo mice studies (S30, S32); Results > Inhibition of ATM suppresses tumor metastasis in orthotopic xenograft mouse models (S154, S156, S162, S168)

Numbers of tumor metastasis in each group: Numbers of tumor metastasis in each group; comparator: The control group mice (Either A549P cells or A549cisR cells) were injected with vehicle (10%DMSO) every day. — Results > Inhibition of ATM suppresses tumor metastasis in orthotopic xenograft mouse models (S162, S168)

CP-466722 10 mg/kg · Materials and methods > In vivo mice studies (S32); Results > Inhibition of ATM suppresses tumor metastasis in orthotopic xenograft mouse models (S162)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 1080622-86-1
Applications ATM inhibitor
Formula C17H15N7O2
Molecular Weight 349.4
SMILES
COC1=C(C=C2C(=C1)C(=NC=N2)N3C(=NC(=N3)C4=CC=CC=N4)N)OC

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 0.24 mg/mL (0.69 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.

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] Węsierska-Gądek J, Heinzl S. Interactions Between Ataxia Telangiectasia Mutated Kinase Inhibition, Poly(ADP-ribose) Polymerase-1 Inhibition and BRCA1 Status in Breast Cancer Cells. J Cancer Prev (2014). PMID: 25337581 DOI: 10.15430/JCP.2014.19.2.125 Source material
  2. [2] Mondesert O, Frongia C, Clayton O, et al. Monitoring the Activation of the DNA Damage Response Pathway in a 3D Spheroid Model. PLoS One (2015). PMID: 26225756 DOI: 10.1371/journal.pone.0134411 Source material
  3. [3] Shen M, Xu Z, Xu W, et al. Inhibition of ATM reverses EMT and decreases metastatic potential of cisplatin-resistant lung cancer cells through JAK/STAT3/PD-L1 pathway. J Exp Clin Cancer Res (2019). PMID: 30961670 DOI: 10.1186/s13046-019-1161-8 Source material

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