AdB-2/3 Fiber Multimers Open Epithelial Junctions
Find Innovative SolutionsGenerate Solutions
Solution Overview
Problem
Current methods for treating disorders associated with epithelial tissue, such as solid tumors and inflammatory bowel diseases, face challenges in accessing therapeutic agents due to the trapping of these agents in intercellular junctions, limiting their efficacy.
Innovation Solution
Administration of AdB-2/3 fiber multimers or their functional equivalents, which bind to desmoglein-2 (DSG2) receptors, triggering the transient opening of intercellular junctions, thereby enhancing the delivery and efficacy of therapeutic, diagnostic, and imaging agents to epithelial tissues.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If therapeutic agents are administered to treat disorders of epithelial tissue, then treatment efficacy is limited, but this is because the agents are trapped in intercellular junctions and cannot access the target tissue effectively
Solution Approach 1:
The patent applies preliminary action by first administering AdB-2/3 fiber multimers to open intercellular junctions before administering the therapeutic agent. This preliminary opening of junctions creates access pathways that enable subsequent therapeutic agents to reach their targets effectively, resolving the contradiction between limited efficacy and poor tissue access
Solution Approach 2:
The AdB-2/3 fiber multimers act as an intermediary substance that mediates between the therapeutic agent and the epithelial tissue. The fiber multimers bind to DSG2 receptors and trigger junction opening, serving as a bridge that enables the therapeutic agent to overcome the barrier of tight intercellular junctions and access the target tissue
2Productivity
If CAR or CD46 receptors are used for adenovirus attachment, then virus entry is efficient, but these receptors are trapped in tight adherence junctions and are not accessible to ads
Solution Approach 1:
The patent uses AdB-2/3 fiber multimers to preliminarily open intercellular junctions before the adenovirus can attempt attachment. This preliminary action exposes the CAR and CD46 receptors that were previously trapped in tight junctions, enabling efficient virus attachment and entry while resolving the accessibility problem
Solution Approach 2:
The invention effectively extracts or releases the CAR and CD46 receptors from their trapped state in tight adherence junctions. By triggering junction opening through DSG2 binding, the receptors are taken out of the inaccessible junctional complex and made available on the cell surface for adenovirus attachment
Applied Scientific Principles
This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.
Function Achieved in This Case
Improves the access and penetration of therapeutic agents across epithelial tissues, increasing their therapeutic, diagnostic, and imaging efficacy by disrupting intercellular junctions, allowing better targeting and distribution of treatments to previously inaccessible areas.
Implementation Method 1
AdB-2/3 fiber multimers or their functional equivalents, which bind to desmoglein-2 (DSG2) receptors, triggering the transient opening of intercellular junctions
Implementation Method 2
Ads internalize into the cell through endocytosis
Data Source
Figure 1a~1g
Figure 2a~2i
Figure 3a~3g
AI summary
The present invention provides compositions and methods for treating disorders associated with epithelial tissues.