CD2 Domain Polypeptide Anti-Angiogenic Agent for Tumor Growth Inhibition
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Solution Overview
Problem
Current methods for inhibiting pathological angiogenesis, particularly in cancer treatment, are limited in effectiveness and specificity, leading to challenges in controlling tumor growth and minimizing toxicity to normal tissues.
Innovation Solution
Development of anti-angiogenic agents, specifically polypeptides derived from domain one of CD2 with altered structures to mimic endogenous anti-angiogenic peptides, which inhibit angiogenesis by inducing apoptosis in endothelial cells while sparing normal cells, combined with chemotherapeutic agents to enhance treatment efficacy.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If conventional anti-angiogenic agents are used to inhibit pathological angiogenesis, then tumor growth is suppressed, but toxicity to normal tissues increases and treatment effectiveness is limited
Solution Approach 1:
The patent applies local quality by designing polypeptides with specific structural modifications (anti-parallel beta-sheet configuration with hydrophobic surfaces) that enable selective binding to pathological endothelial cells. The altered CD2 domain polypeptides exhibit enhanced affinity for activated endothelial cells while sparing normal tissues, achieving localized anti-angiogenic effect at the tumor site without systemic toxicity
Solution Approach 2:
The patent employs parameter changes by modifying the structural parameters of CD2 domain polypeptides through specific mutations and folding configurations. These parameter changes in polypeptide structure (beta-sheet formation, hydrophobic surface exposure) result in altered biological activity with enhanced specificity for pathological angiogenesis while reducing off-target effects
2Productivity
If chemotherapeutic agents are used at higher doses to improve tumor control, then treatment efficacy increases, but toxicity to normal tissues increases
Solution Approach 1:
The patent uses altered CD2 domain polypeptides as intermediary agents that selectively target pathological endothelial cells. These polypeptide intermediaries bind to specific receptors on activated endothelial cells, delivering anti-angiogenic effect locally and enabling reduced chemotherapeutic dosing while maintaining tumor control
Solution Approach 2:
The patent creates modified copies of the CD2 domain with altered structures that mimic and enhance the natural anti-angiogenic activity. These polypeptide copies with specific mutations exhibit improved binding affinity and selectivity, allowing for more effective targeted therapy with lower overall drug doses
3Object-affected harmful factors
If short-lived anti-angiogenic agents are used, then rapid clearance reduces toxicity, but circulation time is insufficient for effective tumor targeting
Solution Approach 1:
The patent applies parameter changes by modifying the physical-chemical parameters of the polypeptides through structural alterations. These changes in polypeptide configuration (molecular weight, surface properties, folding stability) result in optimized pharmacokinetic parameters including extended circulation half-life while maintaining selective targeting capability and reduced systemic toxicity
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
The anti-angiogenic agents effectively inhibit tumor growth by reducing vessel density and tumor weight, with minimal toxicity and prolonged circulation time, potentially allowing for reduced chemotherapeutic doses and improved treatment outcomes.
Implementation Method 1
inhibit angiogenesis by inducing apoptosis in endothelial cells
Data Source
AI summary
Anti-angiogenic agents or polypeptides have an amino acid segment substantially similar to domain one of CD2. The polypeptide has a β-sheet formed by two segments. Methods of using such agents and polypeptide are also included.