SML0268

AZD1152-HQPA

Name: AZD1152-HQPA
Brand: SIGMA

≥98% (HPLC), aurora-B kinase inhibitor, powder

Sinónimos:

3-[[7-[3-[Ethyl(2-hydroxyethyl)amino]propoxy]-4-quinazolinyl]amino]-N-(3-fluorophenyl)-1H-pyrazole-5-acetamide

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About This Item

Fórmula empírica (notación de Hill):

C₂₆H₃₀FN₇O₃

Número CAS:

722544-51-6

Peso molecular:

507.56

UNSPSC Code:

12352200

PubChem Substance ID:

329825276

NACRES:

NA.77

MDL number:

MFCD10687152

Nombre del producto

AZD1152-HQPA, ≥98% (HPLC)

SMILES string

CCN(CCO)CCCOc1ccc2c(Nc3cc(CC(=O)Nc4cccc(F)c4)[nH]n3)ncnc2c1

InChI

1S/C26H30FN7O3/c1-2-34(10-11-35)9-4-12-37-21-7-8-22-23(16-21)28-17-29-26(22)31-24-14-20(32-33-24)15-25(36)30-19-6-3-5-18(27)13-19/h3,5-8,13-14,16-17,35H,2,4,9-12,15H2,1H3,(H,30,36)(H2,28,29,31,32,33)

InChI key

QYZOGCMHVIGURT-UHFFFAOYSA-N

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: >15 mg/mL

storage temp.

2-8°C

Quality Level

100

Categorías relacionadas

Bioactive Small Molecule Inhibitors

Bioactive Small Molecules

Application

AZD1152-HQPA has been used as a specific inhibitor of aurora kinase B (AURKB) to examine the cell cycle stage the IRG (hit compound that induces an irregular nuclear shape)-treated cells accumulate and become senescent and also to study the roles of cyclin-dependent kinase 6 (CDK6) and AURKB in restricting enterovirus 71 (EV71) infection.

AZD1152-HQPA has been used:

for the dose dependent inhibition of aurora kinase B (AURKB)
as a component to identify that, replication timing regulatory factor 1 (RIF1) and protein phosphatase 1 (PP1) are critical for the regulation of abscission timing in human cells
as a component to study the relevance of AURKB as a cancer therapeutic target

Biochem/physiol Actions

AZD1152-HQPA is a selective aurora-B kinase inhibitor; anti-cancer agent.

AZD1152-HQPA is the active metabolite of AZD-1152, a potent selective Aurora Kinase B inhibitor. AZD1152 is 50-fold selective for Aurora kinase B over Aurora kinase C and over 1000-fold selective for Aurora kinase B over Aurora Kinase A. (IC50s: aurora-A, 1,369 nmol/L; aurora-B, 0.36 nmol/L; aurora-C, 17.0 nmol/L). It is converted in plasma to the active form AZD1152-HQPA, which has been shown to have antineoplastic activity in a variety of animal models and human cancer cell lines.

Other Notes

AZD1152-HQPA has been expertly reviewed and recommended by the Chemical Probes Portal. For more information, please visit the AZD1152-HPQA probe summary on the Chemical Probes Portal website.

wgk

WGK 3

Clase de almacenamiento

11 - Combustible Solids

flash_point_f

Not applicable

flash_point_c

Not applicable

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Preclinical evaluation of the Aurora kinase inhibitors AMG 900, AZD1152-HQPA, and MK-5108 on SW-872 and 93T449 human liposarcoma cells.

Sandhya Noronha et al.

In vitro cellular & developmental biology. Animal, 54(1), 71-84 (2017-12-03)

Liposarcoma is a malignant soft tissue tumor that originates from adipose tissue and is one of the most frequently diagnosed soft tissue sarcomas in humans. There is great interest in identifying novel chemotherapeutic options for treating liposarcoma based upon molecular

Cell-based screen for altered nuclear phenotypes reveals senescence progression in polyploid cells after Aurora kinase B inhibition

Sadaie M, et al.

Molecular Biology of the Cell, 26(17), 2971-2985 (2015)

The RIF1-PP1 Axis Controls Abscission Timing in Human Cells

Bhowmick R, et al.

Current Biology (2019)

Reactive oxygen species generation and increase in mitochondrial copy number: new insight into the potential mechanism of cytotoxicity induced by aurora kinase inhibitor, AZD1152-HQPA.

Ali Zekri et al.

Anti-cancer drugs, 28(8), 841-851 (2017-06-24)

Aurora-B kinase overexpression plays important roles in the malignant progression of prostate cancer (PCa). AZD1152-HQPA, as an inhibitor of Aurora-B, has recently emerged as a promising agent for cancer treatment. In this study, we aimed to investigate the effects of

Human genome-wide RNAi screen reveals host factors required for enterovirus 71 replication

Wu KX, et al.

Nature Communications, 7, 13150-13150 (2016)

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