Fig. 1 · Structure

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CCT241533

Cat. No. A11108 CAS 1262849-73-9

Chk2 inhibitor

CCT241533 is a potent and selective Inhibitor of CHK2 that potentiates the cytotoxicity of PARP inhibitors.

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Biological Activity

Target & Activity

Target Activity Value
Chk2 IC50 3 nM
Chk1 IC50 245 nM
Chk2 Ki 1.16 nM

Cellular Effect

Cell Line Activity Value Description Reference
HT-29 GI50 1.4 μM Cytotoxicity against human HT-29 cells by SRB colorimetric assay [PMID: 21186793]

In Vitro Studies

CCT241533 was reported to reduce BQ expression in LCC2 and AK-47 cells. In MCF-7 cells, the reported result for KU and CCT was no significant effect on H2AX or RPA2 phosphorylation or intracellular ERα content. In HFFF2 cells, CCT241533 suppressed TGFβ1-dependent SMA and FnEDA expression compared with TGFβ1-treated samples. [1,2,3]

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

BQ expression in LCC2 cells

Cell-based study · LCC2 [1]

LCC2 cells were treated with CCT241533 at 10 nM for 72 h. CCT241533 was reported to reduce BQ expression, assessed by Western blot.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Western blot was employed to determine BQ expression.Reported result CCT241533 could reduce BQ expression in both cell lines[1]

Literature-Reported Treatment Conditions

Treatment concentration
10 nM
Exposure duration
72 h
Vehicle
DMSO
Reported limits
Not stated in the sentences used: route, control.
Methods and source locations

Compound reported in the paper: CCT241533

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

2. Results > 2.2. Suppression of CHK2 Activity Could Reduce Expression of BQ and Thus Tamoxifen Resistance (S40); 4. Materials and Methods > 4.6. Chemicals (S120); Figure 5 legend (S209, S210)

Western blot was employed to determine BQ expression.: Western blot was employed to determine BQ expression. — 2. Results > 2.2. Suppression of CHK2 Activity Could Reduce Expression of BQ and Thus Tamoxifen Resistance (S40); Figure 5 legend (S210)

Phosphorylation and intracellular ERα content in MCF-7 cells

Cell-based study · MCF-7 [2]

In MCF-7 cells assessed after 24 h, KU and CCT did not significantly affect H2AX or RPA2 phosphorylation or intracellular ERα content.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
phosphorylated γH2AX expression levelsReported result KU and CCT did not significantly affect the phosphorylation of either H2AX or RPA2 as well as ERα intracellular content[2]

Literature-Reported Treatment Conditions

Exposure duration
24 h
Reported limits
Not stated in the sentences used: dose, route, vehicle.
Methods and source locations

Compound reported in the paper: CCT241533

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

Results > The ATR:CHK1-dependent control of ERα intracellular concentration (S211, S212, S214)

phosphorylated γH2AX expression levels: phosphorylated γH2AX expression levels; comparator: control (0) — Results > The ATR:CHK1-dependent control of ERα intracellular concentration (S211, S212)

Treatment suppresses SMA and FnEDA expression in HFFF2 cells

Cell-based study · HFFF2 [3]

In HFFF2 cells, the compound was added at 1.5 μmol/L for 72 hours. Western blotting and quantification showed suppression of TGFβ1-dependent SMA and FnEDA expression compared with TGFβ1-treated samples.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Western blotting and quantificationReported result suppresses TGFβ1-dependent SMA and FnEDA expression[3]

Literature-Reported Treatment Conditions

Treatment concentration
1.5 μmol/L
Exposure duration
for 72 hours
Method
added to the cells
Vehicle
DMSO
Co-treatment
Other interventions in this design: TGFβ1 2 ng/mL. Compound effect isolated by the comparison: TGFβ1-treated samples.
Methods and source locations

Compound reported in the paper: CCT241533

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

Materials and Methods > Cell culture (S32, S34, S35); Results > Targeting ATM inhibits myofibroblast differentiation (S146); Figure 2. legend (S230, S233)

Western blotting and quantification: Western blotting and quantification; comparator: TGFβ1-treated samples — Results > Targeting ATM inhibits myofibroblast differentiation (S146); Figure 2. legend (S230)

BQ expression in AK-47 cells

Cell-based study · AK-47 [1]

AK-47 cells were treated with CCT241533 at 10 nM for 72 h. CCT241533 was reported to reduce BQ expression, assessed by Western blot.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Western blot was employed to determine BQ expression.Reported result CCT241533 could reduce BQ expression in both cell lines[1]

Literature-Reported Treatment Conditions

Treatment concentration
10 nM
Exposure duration
72 h
Vehicle
DMSO
Reported limits
Not stated in the sentences used: route, control.
Methods and source locations

Compound reported in the paper: CCT241533

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

2. Results > 2.2. Suppression of CHK2 Activity Could Reduce Expression of BQ and Thus Tamoxifen Resistance (S40); 4. Materials and Methods > 4.6. Chemicals (S120); Figure 5 legend (S209, S210)

Western blot was employed to determine BQ expression.: Western blot was employed to determine BQ expression. — 2. Results > 2.2. Suppression of CHK2 Activity Could Reduce Expression of BQ and Thus Tamoxifen Resistance (S40); Figure 5 legend (S210)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 1262849-73-9
Applications Chk2 inhibitor
Formula C23H27FN4O4
Molecular Weight 442.2
SMILES
CC(C)([C@@H]1CNC[C@H]1NC2=N/C(=C/3\C=C(C=CC3=O)F)/NC4=CC(=C(C=C42)OC)OC)O

Storage & Solubility

In Vitro Solubility

Reported Solubility

No reported solubility data are available for this product.

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] Tsoi H, Tsang WC, Man EPS, et al. Checkpoint Kinase 2 Inhibition Can Reverse Tamoxifen Resistance in ER-Positive Breast Cancer. Int J Mol Sci (2022). PMID: 36293165 DOI: 10.3390/ijms232012290 Source material
  2. [2] Pescatori S, Leone S, Cipolletti M, et al. Clinically relevant CHK1 inhibitors abrogate wild-type and Y537S mutant ERα expression and proliferation in luminal primary and metastatic breast cancer cells. J Exp Clin Cancer Res (2022). PMID: 35418303 DOI: 10.1186/s13046-022-02360-y Source material
  3. [3] Mellone M, Piotrowska K, Venturi G, et al. ATM Regulates Differentiation of Myofibroblastic Cancer-Associated Fibroblasts and Can Be Targeted to Overcome Immunotherapy Resistance. Cancer Res (2022). PMID: 36353752 DOI: 10.1158/0008-5472.CAN-22-0435 Source material

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