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(rac)-BAY1238097 Sale

目录号 : GC34446

(rac)-BAY1238097是一种BET抑制剂,对BRD4的IC50值为1.02μM。用于癌症研究。

(rac)-BAY1238097 Chemical Structure

Cas No.:1564268-19-4

规格 价格 库存 购买数量
10mM (in 1mL DMSO)
¥1,881.00
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5mg
¥1,710.00
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10mg
¥2,610.00
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50mg
¥9,900.00
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100mg
¥17,550.00
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Sample solution is provided at 25 µL, 10mM.

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产品描述

(rac)-BAY1238097 is a BET inhibitor, with an IC50 of 1.02 μM for BRD4. Used in cancer research[1]. IC50: 1.02 μM (BRD4)[1]

[1]. Stephan Siegel, et al. 2,3-benzodiazepines. WO2014026997A1.

Chemical Properties

Cas No. 1564268-19-4 SDF
Canonical SMILES CC1N(C(NC)=O)N=C(C2=CC=C(N3CCN(C)CC3)C=C2)C4=CC(OC)=C(OC)C=C4C1
分子式 C25H33N5O3 分子量 451.56
溶解度 DMSO : 150 mg/mL (332.18 mM) 储存条件 Store at -20°C
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储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 2.2145 mL 11.0727 mL 22.1455 mL
5 mM 0.4429 mL 2.2145 mL 4.4291 mL
10 mM 0.2215 mL 1.1073 mL 2.2145 mL
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Research Update

Targeting rac and Cdc42 GTPases in Cancer

Cancer Res 2018 Jun 15;78(12):3101-3111.PMID:29858187DOI:10.1158/0008-5472.CAN-18-0619.

rac and Cdc42 are small GTPases that have been linked to multiple human cancers and are implicated in epithelial to mesenchymal transition, cell-cycle progression, migration/invasion, tumor growth, angiogenesis, and oncogenic transformation. With the exception of the P29S driver mutation in melanoma, rac and Cdc42 are not generally mutated in cancer, but are overexpressed (gene amplification and mRNA upregulation) or hyperactivated. rac and Cdc42 are hyperactivated via signaling through oncogenic cell surface receptors, such as growth factor receptors, which converge on the guanine nucleotide exchange factors that regulate their GDP/GTP exchange. Hence, targeting rac and Cdc42 represents a promising strategy for precise cancer therapy, as well as for inhibition of bypass signaling that promotes resistance to cell surface receptor-targeted therapies. Therefore, an understanding of the regulatory mechanisms of these pivotal signaling intermediates is key for the development of effective inhibitors. In this review, we focus on the role of rac and Cdc42 in cancer and summarize the regulatory mechanisms, inhibitory efficacy, and the anticancer potential of Rac- and Cdc42-targeting agents. Cancer Res; 78(12); 3101-11. ©2018 AACR.

Targeting rac and Cdc42 GEFs in Metastatic Cancer

Front Cell Dev Biol 2020 Apr 8;8:201.PMID:32322580DOI:10.3389/fcell.2020.00201.

The Rho family GTPases Rho, rac, and Cdc42 have emerged as key players in cancer metastasis, due to their essential roles in regulating cell division and actin cytoskeletal rearrangements; and thus, cell growth, migration/invasion, polarity, and adhesion. This review will focus on the close homologs rac and Cdc42, which have been established as drivers of metastasis and therapy resistance in multiple cancer types. rac and Cdc42 are often dysregulated in cancer due to hyperactivation by guanine nucleotide exchange factors (GEFs), belonging to both the diffuse B-cell lymphoma (Dbl) and dedicator of cytokinesis (DOCK) families. rac/Cdc42 GEFs are activated by a myriad of oncogenic cell surface receptors, such as growth factor receptors, G-protein coupled receptors, cytokine receptors, and integrins; consequently, a number of rac/Cdc42 GEFs have been implicated in metastatic cancer. Hence, inhibiting GEF-mediated rac/Cdc42 activation represents a promising strategy for targeted metastatic cancer therapy. Herein, we focus on the role of oncogenic rac/Cdc42 GEFs and discuss the recent advancements in the development of rac and Cdc42 GEF-interacting inhibitors as targeted therapy for metastatic cancer, as well as their potential for overcoming cancer therapy resistance.

Crossroads of PI3K and rac pathways

Small GTPases 2015;6(2):71-80.PMID:25942647DOI:10.4161/21541248.2014.989789.

rac and PI3Ks are intracellular signal transducers able to regulate multiple signaling pathways fundamental for cell behavior. PI3Ks are lipid kinases that produce phosphorylated lipids which, in turn, transduce extracellular cues within the cell, while rac is a small G protein that impacts on actin organization. Compelling evidence indicates that in multiple circumstances the 2 signaling pathways appear intermingled. For instance, phosphorylated lipids produced by PI3Ks recruit and activate GEF and GAP proteins, key modulators of rac function. Conversely, PI3Ks interact with activated rac, leading to rac signaling amplification. This review summarizes the molecular mechanisms underlying the cross-talk between rac and PI3K signaling in 2 different processes, cell migration and ROS production.

Aberrant rac pathway signalling in glioblastoma

Small GTPases 2021 Mar;12(2):81-95.PMID:31032735DOI:10.1080/21541248.2019.1612694.

Glioblastoma is an aggressive and incurable form of brain cancer. Both mutation analysis in human glioblastoma and mouse modelling studies have shown that aberrant activation of the PI 3-kinase pathway is a central driver of glioblastoma malignancy. The small GTPase rac is activated downstream of this pathway, mediating a subset of the effects of aberrant PI 3-kinase pathway activation. Here I discuss the current state of our knowledge on rac activation mechanisms in glioblastoma. Current knowledge on roles for specific PI 3-kinase pathway responsive rac guanine nucleotide exchange factors in glioblastoma is reviewed. rac is best known for its role in promoting cell motility and invasion, but there is also evidence for roles in multiple other cellular processes with cancer relevance, including proliferation, differentiation, apoptosis, DNA damage responses, metabolism, angiogenesis and immunosuppression. I review what is known about the role of rac in these processes in glioblastoma. Finally, I assess possible strategies to inhibit this pathway in glioblastoma through either direct inhibition of rac or inhibition of upstream activators or downstream mediators of rac signalling.

The diverse roles of rac signaling in tumorigenesis

Cell Cycle 2011 May 15;10(10):1571-81.PMID:21478669DOI:10.4161/cc.10.10.15612.

rac is a member of the Rho family of small GTPases, which act as molecular switches to control a wide array of cellular functions. In particular, rac signaling has been implicated in the control of cell-cell adhesions, cell-matrix adhesions, cell migration, cell cycle progression and cellular transformation. As a result of its functional diversity, rac signaling can influence several aspects of tumorigenesis. Consistent with this, in vivo evidence that rac signaling contributes to tumorigenesis is continuously emerging. Additionally, our understanding of the mechanisms by which rac signaling is regulated is rapidly expanding and consequently adds to the complexity of how rac signaling could be modulated during tumorigenesis. Here we review the numerous biological functions and regulatory mechanisms of rac signaling and discuss how they could influence the different stages of tumorigenesis.