E-Cadherin Upregulator ResEcad - Enhance E-cadherin Expression

REF #: 3199878
Procurenet
Short description
  • E-Cadherin Upregulator, ResEcad: A cell-permeable isoxazolocarboxamide compound that enhances the E-cadherin protein level
  • Synonyms: E-Cadherin Upregulator, ResEcad, 5-(Furan-2-yl)-N-(pyridine-4-yl)butyl)isoxazole-3-carboxamide
  • E-Cadherin Expression Restorer
  • Enhances E-cadherin protein level: Helps increase E-cadherin protein level in lung squamous cell carcinoma H520 and colorectal adenocarcinoma SW620 cells
  • Multiple applications: Suitable for diverse verticals
  • High purity and quality: Meets industry standards
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  • Procurenet Team Tshim Sha Tsui
    Hong Kong Hong Kong 3 years
Delivery options
  • 7 Days Return Back Policy
  • 2 Days Cancellation Policy
  • Ship Only
Description

E-Cadherin Upregulator, ResEcad

Product Details

Synonyms:

  • E-Cadherin Upregulator
  • ResEcad
  • 5-(Furan-2-yl)-N-(pyridine-4-yl)butyl)isoxazole-3-carboxamide

Main Features:

  • Selective and potent E-cadherin upregulator
  • Enhances the expression of E-cadherin protein
  • Potential inhibitor of epithelial-mesenchymal transition (EMT)
  • May suppress metastasis in lung squamous cell carcinoma and colorectal adenocarcinoma cells
  • Cell-permeable compound

Detailed Description:

Loss of E-cadherin expression is a common characteristic in various cancer types, including lung squamous cell carcinoma and colorectal adenocarcinoma. This loss is associated with increased invasiveness, metastasis, and poor clinical outcomes. ResEcad, also known as the E-Cadherin Upregulator, offers a potential solution to this problem.

ResEcad is a small chemical compound that specifically targets and upregulates E-cadherin protein expression in cancer cells. Its unique isoxazolocarboxamide structure enables it to penetrate cell membranes, allowing direct interaction with intracellular signaling pathways involved in E-cadherin regulation. By interacting with these pathways, ResEcad acts as an activator, effectively increasing the expression of E-cadherin at both the mRNA and protein levels.

ResEcad Mechanism of Action:

ResEcad primarily exerts its effects through the following mechanisms:

  • Activation of E-cadherin transcription: ResEcad promotes the transcription of E-cadherin gene by interacting with specific transcription factors and signaling molecules.
  • Inhibition of E-cadherin degradation: ResEcad prevents the degradation of E-cadherin protein, thereby enhancing its stability and increasing overall cellular levels.
  • Regulation of E-cadherin-related signaling pathways: ResEcad modulates various signaling pathways involved in E-cadherin expression, such as the Wnt/β-catenin and TGF-β pathways.

Applications:

ResEcad holds great promise for researchers and scientists working in the field of cancer biology, particularly those studying E-cadherin regulation and its role in tumor progression. Potential applications of ResEcad include:

  • Investigating the effects of E-cadherin upregulation on cancer cell behavior
  • Exploring the relationship between E-cadherin expression levels and tumor metastasis
  • Evaluating the potential of E-cadherin restoration as a therapeutic strategy
  • Validation of E-cadherin as a prognostic marker in lung squamous cell carcinoma and colorectal adenocarcinoma

Additional Resources:

For detailed information on ResEcad, please refer to the following resources:

  • ResEcad MSDS: This document provides important safety information, handling instructions, and precautions associated with using ResEcad.
  • Peer-reviewed papers: Access a collection of scientific articles and studies that have used ResEcad for E-cadherin upregulation research.
  • Technical documents: Find technical reports, protocols, and other supporting materials related to ResEcad and its applications.
  • Similar products: Explore related products that might be of interest to researchers working in the field of cancer biology and E-cadherin regulation.

Summary:

In summary, ResEcad is a highly effective and selective E-cadherin upregulator with the potential to inhibit epithelial-mesenchymal transition (EMT) and metastasis in lung squamous cell carcinoma and colorectal adenocarcinoma cells. Its unique composition and mechanism of action make it a valuable tool for researchers investigating the role of E-cadherin in cancer biology and exploring therapeutic interventions for EMT-related diseases.

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