Barasertib-HQPA (AZD2811)

N° de catalogueS1147 Lot :S114705

Imprimer

Données techniques

Formule

C26H30FN7O3
Poids moléculaire 507.56 Numéro CAS 722544-51-6
Solubilité (25°C)* In vitro DMSO 100 mg/mL (197.02 mM)
Water Insoluble
Ethanol Insoluble
In vivo (Ajouter les solvants au produit individuellement et dans lordre.)
Homogeneous suspension
CMC-NA
≥5mg/ml Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
* <1 mg/ml signifie légèrement soluble ou insoluble.
* Veuillez noter que Selleck teste la solubilité de tous les composés en interne, et la solubilité réelle peut différer légèrement des valeurs publiées. Ceci est normal et est dû à de légères variations dun lot à lautre.
* Expédition à température ambiante (les tests de stabilité montrent que ce produit peut être expédié sans aucune mesure de refroidissement.)

Préparation des solutions mères

Activité biologique

Description Le Defosbarasertib (AZD1152-HQPA, AZD2811, INH-34, Barasertib-HQPA) est un inhibiteur hautement sélectif d'Aurora B avec une IC50 de 0,37 nM dans un essai acellulaire, ~3700 fois plus sélectif pour Aurora B que pour Aurora A. Phase 1.
Cibles
Aurora B
(Cell-free assay)
0.37 nM
In vitro

Barasertib (AZD1152-HQPA), un inhibiteur hautement sélectif d'Aurora B, provoque la polyploïdie et l'apoptose dans de nombreuses lignées de cellules cancéreuses.
In vivo

Barasertib (AZD1152-HQPA) est un inhibiteur de la kinase aurora B et présente une efficacité contre les xénogreffes de lignées cellulaires RB1 / SCLC, les PDX RB1 / SCLC et les tumeurs neuroendocrines / Rb1 autochtones.

Protocole (de référence)

Test cellulaire :

[1]
  • Lignées cellulaires

    NCI-H82 cells, SCLC and NSCLC cell lines

  • Concentrations

    --

  • Temps dincubation

    --

  • Méthode

    --

Références

  • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6368871/
  • https://pubmed.ncbi.nlm.nih.gov/17495131/

Validation du produit par le client

Targeting PI3K, a common downstream effector of RTKs, with a selective inhibitor (GDC0941) sensitizes SOX10 knockdown cells to vemurafenib. shRNAs targeting SOX10 were introduced into A375 cells by lentiviral transduction. pLKO.1 empty vector served as a control vector (Ctrl). Cells were seeded in 6-well plates at the same density in the presence or absence of drug(s) at the indicated concentration. Cells were cultured for 2 weeks in the absence of vemurafenib or 4 weeks in the presence of vemurafenib before fixing and staining.

Données de [ Nature , 2014 , 508(7494), 118-22 ]

Primary MKPs were treated with the Aurora B inhibitor AZD-1152, and then stimulated with 20 ng/ml TPO for 5 d. Cell morphology was analyzed by Giemsa staining (Bar, 20 祄; red arrows denote mature MKs; n = 6).

Données de [ J Exp Med , 2014 , 10.1084/jem.20141123 ]

<p>: Barasertib inhibits AURKB specifically and triggers mitotic slippage. (a) Barasertib inhibits AURKB without affecting AURKA. Mitotic HeLa cells were obtained by exposure to nocodazole for 16 h followed by mechanical shake off. The cells were incubated with the indicated concentrations of Barasertib for 2 h. Nocodazole and MG132 were included to prevent mitotic exit. Lysates were prepared and analyzed with immunoblotting. Uniform loading was confirmed by immunoblotting for actin. (b) Barasertib induces mitotic slippage. HeLa cells expressing histone H2B-GFP were exposed to buffer or the indicated concentrations of Barasertib. Individual cells were then tracked for 24 h with time- lapse microscopy. Each horizontal bar represents one cell (n ¼ 50). The key is the same as in Figure 1b. (c) Summary of Barasertib-mediated mitotic slippage. Live-cell imaging after Barasertib treatment was described in panel (b). The duration of mitosis (mean±90% confidence interval) and the percentage of cells that underwent mitotic slippage during the imaging period were quantified. (d) Genome reduplication after Barasertib-mediated mitotic slippage. HeLa cells were treated with the indicated concentrations of Barasertib for 36 h. DNA contents were analyzed with flow cytometry. (e) Barasertib induces mitotic slippage and genome reduplication in HCT116. Cells were treated with the indicated concentrations of Barasertib for 24 h. DNA contents were analyzed with flow cytometry. (f) Cytotoxicity induced by Barasertib. HeLa and HCT116 cells were cultured in the presence of the indicated concentrations of Barasertib for 48 h. Proliferation was assayed with WST-1 assay. (g) Barasertib induces genome reduplication and apoptosis. HeLa cells were incubated with 50 n M of Barasertib either in the presence or absence of the caspase inhibitor Z-VAD(OMe)-FMK. The cells were harvested at the indicated time points and analyzed with flow cytometry.</p>

Données de [ Oncogene , 2014 , 33, 3550-60 ]

<p> </p><p>Dual inhibition of Aurora and SRC kinases specifically eliminates hyperploid cells. Experiment shown is same as a, b, but performed following treatment of OVCAR10 cells with MLN8237 (targeting AURKA) or AZD1152 (targeting AURKB);</p>

Données de [ Oncogene , 2012 , 31, 1217–1227 ]

Sellecks Barasertib-HQPA (AZD2811) A été cité par 171 Publications

High-throughput screening identifies Aurora kinase B as a critical therapeutic target for Merkel cell carcinoma [ Nat Commun, 2025, 16(1):1583] PubMed: 39939315
Unraveling AURKB as a potential therapeutic target in pulmonary hypertension using integrated transcriptomic analysis and pre-clinical studies [ Cell Rep Med, 2025, 6(2):101964] PubMed: 39933527
Aurora B controls microtubule stability to regulate abscission dynamics in stem cells [ Cell Rep, 2025, 44(2):115238] PubMed: 39854207
Identification of chemical inhibitors targeting long noncoding RNA through gene signature-based high throughput screening [ Int J Biol Macromol, 2025, 292:139119] PubMed: 39722392
Oversized cells activate global proteasome-mediated protein degradation to maintain cell size homeostasis [ Elife, 2025, 14e75393] PubMed: 39791360
The mechanoresponsive chromosomal passenger complex sustains furrow ingression under confinement [ J Mol Cell Biol, 2025, mjaf019] PubMed: 40693957
Overcoming MET-targeted drug resistance in MET-amplified lung cancer by aurora kinase B inhibition [ Biochim Biophys Acta Mol Cell Res, 2025, 1872(7):120001] PubMed: 40499687
Proteomic profiling identifies upregulation of aurora kinases causing resistance to taxane-type chemotherapy in triple negative breast cancer [ Sci Rep, 2025, 15(1):3211] PubMed: 39863788
Nucleosome stability safeguards cell identity, stress resilience and healthy aging [ bioRxiv, 2025, 2025.09.17.676776] PubMed: 41000743
Proteogenomic characterization of small cell lung cancer identifies biological insights and subtype-specific therapeutic strategies [ Cell, 2024, 187(1):184-203.e28] PubMed: 38181741

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