Home Cell Cycle CDK inhibitor NU6027

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NU6027 CDK inhibitor

Cat.No.S7114

NU6027 is a potent ATR/CDK inhibitor, inhibits CDK1/2, ATR and DNA-PK with Ki of 2.5 μM/1.3 μM, 0.4 μM and 2.2 μM, and this compound enters cells more readily than the 6-aminopurine-based inhibitors.
NU6027 CDK inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 251.28

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Quality Control

Batch: S711401 DMSO]50 mg/mL]false]Ethanol]3 mg/mL]false]Water]Insoluble]false Purity: 99.89%
99.89

Chemical Information, Storage & Stability

Molecular Weight 251.28 Formula

C11H17N5O2

 Storage (From the date of receipt)
CAS No. 220036-08-8 Download SDF Storage of Stock Solutions

Synonyms N/A Smiles C1CCC(CC1)COC2=NC(=NC(=C2N=O)N)N

Solubility

In vitro
Batch:

DMSO : 50 mg/mL ( (198.98 mM) Moisture-absorbing DMSO reduces solubility. Please use fresh DMSO.)

Ethanol : 3 mg/mL

Water : Insoluble

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo
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Mechanism of Action

Features
A more potent inhibitor of cdk1 and cdk2 than NU2058.
Targets/IC50/Ki
ATR [2]
0.4 μM(Ki)
CDK2 [1]
1.3 μM(Ki)
DNA-PK [2]
2.2 μM(Ki)
CDK1 [1]
2.5 μM(Ki)
In vitro
NU6027 is soaked into crystals of monomeric CDK2 and the structure refined to a resolution of 1.85 Å. This compound (100μM) inhibits growth of human tumor cells with mean GI50 of 10 μM. It causes a reduction in the number of cells in S-phase but not G1 or G2/M in MCF7 cells. [1] This chemical is a potent inhibitor of cellular ATR activity with IC50 of 6.7 μM in MCF7 cells and 2.8 μM in GM847KD cells, and enhances hydroxyurea and cisplatin cytotoxicity in an ATR-dependent manner. This inhibitor (10 μM) inhibits CDK2-mediated pRbT821 by 42% and pCHK1S345 by 70%. It significantly potentiates sensitivity of cisplatin (1.4-fold at 4 μM and 8.7-fold at 10 μM), doxorubicin (1.3-fold at 4 μM and 2.5-fold at 10 μM), camptothecin (1.4-fold at 4 μM and 2-fold at 10 μM) and hydroxyurea (1.8-fold at 4 μM) aganist MCF7 cells. It also potentiates 2Gy IR in a concentration-dependent manner and the cytotoxicity of camptothecin and temozolomide (a DNA methylating agent) at concentrations above and below their LC50. This compound (10 μM) attenuates G2/M arrest following DNA damage, inhibits RAD51 focus formation and increases the cytotoxicity of the major classes of DNA-damaging anticancer cytotoxic therapy but not the antimitotic, paclitaxel in MCF7 cells. It (4 μM) is synthetically lethal when DNA single-strand break repair is impaired either through poly(ADP-ribose) polymerase (PARP) inhibition or defects in XRCC1 in MCF7 cells. [3] This chemical (4 μM) increases the proportion of cell in early apoptosis to 7.5% after 48 hours treatment in EM-C11 cells compared to 1.73% in untreated cells. This treatment (10 μM) reduces survival in XRCC1 deficient OVCAR-4 cells compared to proficient cells. It enhances cytotoxicity of cisplatin in XRCC1 deficient OVCAR-3 cells compared to XRCC1 proficient cells. This compound enhances Cisplatin induced DSB accumulation in XRCC1 deficient OVCAR-3 cells. [4]
Kinase Assay
Enzyme Inhibition Studies
Inhibition of cyclin B1/CDK1 is assayed using enzyme prepared from starfish oocytes. Inhibition of cyclinA3/CDK2 is determined using a similar assay and an assay buffer comprised of 50 mM Tris-HCl pH 7.5 containing 5 mM MgCl2. The final ATP concentration in both CDK assays is 12.5 μM, and the IC50 concentration for this compound is the concentration required to inhibit enzyme activity by 50% under the assay conditions used. To determine the Km for ATP for cyclin B1/CDK1 and cyclin A3/CDK2, and Ki values for this chemical, assays are performed in the absence of this chemical and at two fixed concentrations of this compound (5 μM and 10 μM), with ATP concentrations ranging from 6.25 μM to 800 μM. Data are fitted to the Michaelis−Menten equation using unweighted nonlinear least squares regression.
References

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