Barasertib-HQPA (AZD2811)

카탈로그 번호S1147 배치:S114706

인쇄

기술 자료

화학식

C26H30FN7O3
분자량 507.56 CAS 번호 722544-51-6
용해도 (25°C)* 시험관 내(In vitro) DMSO 100 mg/mL (197.02 mM)
Water Insoluble
Ethanol Insoluble
생체 내(In Vivo) (개별적으로 순서대로 용매를 제품에 첨가하십시오.)
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/ml은 약간 용해되거나 불용해됨을 의미합니다.
* Selleck은 모든 화합물의 용해도를 자체적으로 테스트하며, 실제 용해도는 게시된 값과 약간 다를 수 있습니다. 이는 정상적인 현상이며, 약간의 배치 간 변동으로 인해 발생합니다.
* 실온 배송 (안정성 테스트 결과 이 제품은 냉각 조치 없이 배송될 수 있음을 보여줍니다.)

원액 준비

생물학적 활성

설명 Defosbarasertib (AZD1152-HQPA, AZD2811, INH-34, Barasertib-HQPA)는 무세포 분석에서 IC50이 0.37 nM인 고도로 선택적인 Aurora B 억제제이며, Aurora A보다 Aurora B에 대해 ~3700배 더 선택적입니다. 1상.
표적
Aurora B
(Cell-free assay)
0.37 nM
시험관 내(In vitro)

Barasertib (AZD1152-HQPA)는 고도로 선택적인 Aurora B 억제제로, 많은 암세포주에서 배수성 및 세포자멸사를 유발합니다.
생체 내(In Vivo)

Barasertib (AZD1152-HQPA)는 aurora B 키나아제 억제제이며, RB1 / SCLC 세포주 이종이식, RB1 / SCLC PDX 및 자가 Rb1 / 신경내분비 종양에 대해 효능이 있습니다.

프로토콜 (참조)

세포 분석:

[1]
  • 세포주

    NCI-H82 cells, SCLC and NSCLC cell lines

  • 농도

    --

  • 배양 시간

    --

  • 방법

    --

참조

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

고객 제품 검증

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.

데이터 출처 [ 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).

데이터 출처 [ 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>

데이터 출처 [ 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>

데이터 출처 [ Oncogene , 2012 , 31, 1217–1227 ]

Sellecks Barasertib-HQPA (AZD2811) 인용됨 171 출판물

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

반품 정책
Selleck Chemical의 무조건 반품 정책은 고객에게 원활한 온라인 쇼핑 경험을 보장합니다. 구매에 어떤 식으로든 불만족하시면, 수령일로부터 7일 이내에 모든 품목을 반품하실 수 있습니다. 제품 품질 문제(프로토콜 관련 문제 또는 제품 관련 문제)가 발생하는 경우, 원래 구매일로부터 365일 이내에 모든 품목을 반품하실 수 있습니다. 제품 반품 시 아래 지침을 따르십시오.

배송 및 보관
Selleck 제품은 실온에서 운송됩니다. 실온에서 제품을 받으셨더라도 안심하십시오. Selleck 품질 검사 부서에서 한 달간의 상온 보관이 분말 제품의 생물학적 활성에 영향을 미치지 않음을 확인하는 실험을 수행했습니다. 수령 후, 데이터시트에 설명된 요구 사항에 따라 제품을 보관하십시오. 대부분의 Selleck 제품은 권장 조건에서 안정적입니다.

인간, 수의학 진단 또는 치료 용도로 사용하지 마십시오.