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Submit ReviewZLD 1039 is a potent and selective EZH2 inhibitor (IC50 = 5.6 nM). Displays selectivity for EZH2 over a panel of HMTs (inhibition less than 30% at 16 μM). Blocks H3K27 methylation in breast cancer cell lines. Induces tumor regression and metastasis in breast cancer xenograft-bearing mice. Reactivates silenced tumor suppressors in vivo. Orally bioavailable.
| 分子量 | 612.8 |
| 公式 | C36H48N6O3 |
| 储存 | Store at -20°C |
| 纯度 | ≥98% (HPLC) |
| CAS Number | 1826865-46-6 |
| PubChem ID | 132517142 |
| InChI Key | SZAYCVHJDOWSNY-UHFFFAOYSA-N |
| Smiles | CCN(C1=CC(C2=CN=C(N3CCN(CC3)C)C=C2)=CC(C(NCC4=C5CCCCC5=C(NC4=O)C)=O)=C1C)C6CCOCC6 |
上方提供的技术数据仅供参考。批次相关数据请参见分析证书。
Tocris products are intended for laboratory research use only, unless stated otherwise.
参考文献是支持产品生物活性的出版物。
Song et al (2016) Corrigendum: Selective inhibition of EZH2 by ZLD1039 blocks H3K27methylation and leads to potent anti-tumor activity in breast cancer. Sci.Rep. 29 24893 PMID: 27128979
关键词: ZLD 1039, ZLD 1039 supplier, ZLD1039, Potent, selective, EZH2, inhibitors, inhibits, orally, bioavailable, H3K27, methylation, 5847, Tocris Bioscience
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Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*请注意,Tocris 仅会向正规科研企业/机构地址发送文献。
Written by Susanne Müller-Knapp and Peter J. Brown, this review gives an overview of the development of chemical probes for epigenetic targets, as well as the impact of these tool compounds being made available to the scientific community. In addition, their biological effects are also discussed. Epigenetic compounds available from Tocris are listed.
Written by Kirsty E. Clarke, Victoria B. Christie, Andy Whiting and Stefan A. Przyborski, this review provides an overview of the use of small molecules in the control of stem cell growth and differentiation. Key signaling pathways are highlighted, and the regulation of ES cell self-renewal and somatic cell reprogramming is discussed. Compounds available from Tocris are listed.
This poster summarizes the main metabolic pathways in cancer cells and highlights potential targets for cancer therapeutics. Genetic changes and epigenetic modifications in cancer cells alter the regulation of cellular metabolic pathways providing potential cancer therapeutic targets.
This poster summarizes the main epigenetic targets in cancer. The dysregulation of epigenetic modifications has been shown to result in oncogenesis and cancer progression. Unlike genetic mutations, epigenetic alterations are considered to be reversible and thus make promising therapeutic targets.