TED-347
目录号 : GC39540
TED-347 is a potent, irreversible, covalent and allosteric inhibitor of the TEAD?Yap protein-protein interaction. TED-347 inhibits TEAD4?Yap1 protein-protein interaction with an apparent EC50 of 5.9 μM.
Cas No.:2378626-29-8
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
TED-347 is a potent, irreversible, covalent and allosteric inhibitor of the TEAD?Yap protein-protein interaction. TED-347 inhibits TEAD4?Yap1 protein-protein interaction with an apparent EC50 of 5.9 μM.
TED-347 is found to inhibit the protein-protein interaction in a time-dependent manner. TED-347 is shown to functionally disrupt the TEAD·Yap1 interaction in cells and to reduce the viability of patient-derived glioblastoma cell lines.[1]
[1] Khuchtumur Bum-Erdene, et al. Cell Chem Biol. 2019 Mar 21;26(3):378-389.e13.
| Cas No. | 2378626-29-8 | SDF | |
| Canonical SMILES | O=C(C1=CC=CC=C1NC2=CC=CC(C(F)(F)F)=C2)CCl | ||
| 分子式 | C15H11ClF3NO | 分子量 | 313.7 |
| 溶解度 | DMSO: 250 mg/mL (796.94 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 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。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 3.1878 mL | 15.9388 mL | 31.8776 mL |
| 5 mM | 0.6376 mL | 3.1878 mL | 6.3755 mL |
| 10 mM | 0.3188 mL | 1.5939 mL | 3.1878 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Overexpressed WDR3 induces the activation of Hippo pathway by interacting with GATA4 in pancreatic cancer
J Exp Clin Cancer Res 2021 Mar 1;40(1):88.PMID:33648545DOI:10.1186/s13046-021-01879-w.
Background: WD repeat domain 3 (WDR3) is involved in a variety of cellular processes including gene regulation, cell cycle progression, signal transduction and apoptosis. However, the biological role of WDR3 in pancreatic cancer and the associated mechanism remains unclear. We seek to explore the immune-independent functions and relevant mechanism for WDR3 in pancreatic cancer. Methods: The GEPIA web tool was searched, and IHC assays were conducted to determine the mRNA and protein expression levels of WDR3 in pancreatic cancer patients. MTS, colony formation, and transwell assays were conducted to determine the biological role of WDR3 in human cancer. Western blot analysis, RT-qPCR, and immunohistochemistry were used to detect the expression of specific genes. An immunoprecipitation assay was used to explore protein-protein interactions. Results: Our study proved that overexpressed WDR3 was correlated with poor survival in pancreatic cancer and that WDR3 silencing significantly inhibited the proliferation, invasion, and tumor growth of pancreatic cancer. Furthermore, WDR3 activated the Hippo signaling pathway by inducing yes association protein 1 (YAP1) expression, and the combination of WDR3 silencing and administration of the YAP1 inhibitor TED-347 had a synergistic inhibitory effect on the progression of pancreatic cancer. Finally, the upregulation of YAP1 expression induced by WDR3 was dependent on an interaction with GATA binding protein 4 (GATA4), the transcription factor of YAP1, which interaction induced the nuclear translocation of GATA4 in pancreatic cancer cells. Conclusions: We identified a novel mechanism by which WDR3 plays a critical role in promoting pancreatic cancer progression by activating the Hippo signaling pathway through the interaction with GATA4. Therefore, WDR3 is potentially a therapeutic target for pancreatic cancer treatment.
The interaction of TEA domain transcription factor 4 (TEAD4) and Yes-associated protein 1 (YAP1) promoted the malignant process mediated by serum/glucocorticoid regulated kinase 1 (SGK1)
Bioengineered 2021 Dec;12(1):601-614.PMID:33517828DOI:10.1080/21655979.2021.1882142.
TEA domain transcription factor 4 (TEAD4) has been investigated to be implicated in the progression of various cancers, and it plays a role in the esophageal squamous cell carcinoma (ESCC). The study was designed to investigate how TEAD4 affected the progression of ESCC through Hippo signaling pathway in vitro and in vivo. The interaction of TEAD4 and Yes-associated protein (YAP) was detected though immunoprecipitation assay (IP). Following the treatment of TED-347, which was able to suppress the interaction of TEAD4 and YAP1, the malignant behaviors of cells including proliferation, invasion, and migration were assessed by EDU staining, wound healing, and transwell assay in vitro, while tumor growth was measured. Luciferase reporter plasmids containing the enhancer and promoter region of serum/glucocorticoid regulated kinase 1 (SGK1) were constructed to analyze how TEAD4 affected the transcription of SGK1. The above cell behaviors were further analyzed after the silencing of SGK1. Results showed that TED-347 hindered the promoting effect of TEAD4 overexpression on the malignant behaviors of ESCC cells, and this effect was related to the suppression of the TEAD4/YAP1 complex. Moreover, the promoter activity of SGK1 was obviously inhibited by TED-347. Decreased expression of SGK1 suppressed the above behaviors of cells and destroyed the effects of increased expression of TEAD4. Collectively, TEAD4/YAP promotes the malignant process of ESCC cells, which was inhibited by the interference of SGK1. Targeting TEAD4/YAP1 complex or SGK1 could find application in the treatment of esophageal squamous cell carcinoma.