Molecular Weight(MW): 419.91
CHIR-124 is a novel and potent Chk1 inhibitor with IC50 of 0.3 nM in a cell-free assay. It shows 2,000-fold selectivity against Chk2, 500- to 5,000-fold less activity against CDK2/4 and Cdc2.
Cited by 10 Publications
4 Customer Reviews
Cell proliferation of IGR-CaP1-R100 cells. Cells were treated with 100nM CHIR-124 in the presence or absence of 100nM Docetaxel or with Docetaxel alone during 4 days. Proliferation was assessed using WST1.
Oncotarget 2014 5(3), 667-78. CHIR-124 purchased from Selleck.
Treatment with a selective Chk1 inhibitor impairs nuclear localization of apoptin in a dose-dependent manner. (A) H1299 cells were infected with Ad-Apwt and treated with DMSO or the indicated concentrations of CHIR-124 (Chk1-i). At 24 h postinfection, the cells were processed for Flag immunofluorescence.
J Virol, 2016, 90(20):9433-45. CHIR-124 purchased from Selleck.
(A) Chemical structure of CHEK1 inhibitor CHIR-241. (B) In vitro cell viability assay for CHIR-241 with U87 GBM cells and NHA. (C) In vitro cell growth assay showed that CHIR-241 decreased cell proliferation of U87 when combined with radiation (P < .01, with t tests). (D) Kaplan-Meier analysis was performed for the comparison of survival in U87-implanted mice treated with or without CHIR-241 (P = .0072, with log-rank test).
Transl Oncol, 2018, 11(1):140-146. CHIR-124 purchased from Selleck.
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|Description||CHIR-124 is a novel and potent Chk1 inhibitor with IC50 of 0.3 nM in a cell-free assay. It shows 2,000-fold selectivity against Chk2, 500- to 5,000-fold less activity against CDK2/4 and Cdc2.|
CHIR-124 is a quinolone-based small molecule that is structurally unrelated to other known inhibitors of Chk1. CHIR-124 interacts synergistically with topoisomerase poisons (e.g., Camptothecin or SN-38) in causing growth inhibition in a variety of cancer cell lines, including breast carcinoma (MDA-MB-231 and MDA-MB-435) and colon carcinoma (SW-620 and Colo205), all of which contains the mutant p53 gene. CHIR-124 abrogates the SN-38-induced S and G2-M checkpoints and potentiates apoptosis in MDA-MD-435 breast cancer cells. The abrogation of the G2-Mcheckpoint and induction of apoptosis by CHIR-124 are enhanced by the loss of p53.  CHIR-124 also potently targets other kinases such as PDGFR and Flt3 with IC50 of 6.6 nM and 5.8 nM, respectively. 
|In vivo||CHIR-124 potentiates the growth inhibitory effects of Irinotecan by abrogating the G2-M checkpoint and increasing tumor apoptosis in an orthotopic breast cancer xenograft model.|
Chk1 Assay:For the Chk1 assay, the kinase domain is expressed in Sf9 insect cells, and a biotinylated cdc25c peptide containing the consensus Chk1/Chk2 phosphorylation site (*)(biotin-[AHX]SGSGS*GLYRSPSMP-ENLNRPR[CONH2]) is used as the substrate. A dilution series of CHIR-124 is mixed with a kinase reaction buffer containing a final concentration of 30 mM Tris-HCl (pH 7.5), 10 mM MgCl2, 2 mM DTT, 4 mM EDTA, 25 mMβ-glycerophosphate, 5 mM MnCl2, 0.01% bovine serum albumin, 1.35 nM CHK1 kinase domain, 0.5 μM peptide substrate, and 1 AM unlabeled ATP, plus 5 nM 33Pγ-labeled ATP (specific activity = 2,000 Ci/mmol). Reactions and detection of the phosphate transfer are carried out by a radioactive method. Reactions are incubated at room temperature for 1 to 4 hours and the phosphorylated peptide captured on streptavidin-coated microtiter plates containing stop reaction buffer (25 mM EDTA [ethylenediaminetetraacetic acid], 50 mMHEPES, pH 7.5). Phosphorylated peptide is measured with the DELFIA TRF system using a Europium-labeled anti-phosphotyrosine antibody PT66. The concentration of CHIR-124 for IC50 is calculated using nonlinear regression with XL-Fit data analysis software.
|In vitro||DMSO||7 mg/mL (16.67 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
1% DMSO+30% polyethylene glycol+1% Tween 80
For best results, use promptly after mixing.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
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