CCR5 Antagonist for Th1 and Th2 Inflammatory Disease Treatment

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Solution Overview

Problem

Current treatments for Th1 and Th2 mediated diseases, such as COPD, fail to adequately address the inflammatory responses driven by IFN-γ and IL-13, leading to persistent tissue damage and remodeling without effective healing mechanisms.

Innovation Solution

Administering a CCR5 antagonist, such as a chemical compound, antibody, ribozyme, or antisense nucleic acid, to neutralize CCR5 signaling in the lung, thereby reducing inflammation and tissue alterations induced by IFN-γ or IL-13.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Object-affected harmful factors

If CCR5 antagonist is administered to neutralize CCR5 signaling, then inflammation and tissue remodeling are reduced, but the ability to treat both Th1 and Th2 mediated diseases is required

Engineering Contradiction:

Improveinflammation and tissue remodelingVSAvoidapplicability to Th1 and Th2 diseases

Core Design Contradiction:

Object-affected harmful factorsVSAdaptability or versatility

Solution Approach 1:

The CCR5 antagonist is designed to treat both Th1 and Th2 mediated diseases through a single mechanism. The patent demonstrates that CCR5 signaling is involved in both Th1 (IFN-γ driven) and Th2 (IL-13 driven) inflammatory pathways, allowing one antagonist to address multiple disease types including COPD, asthma, and chronic bronchitis.

Inventive Principle:

Principle #6Universality (Multi-functionality)

2Object-affected harmful factors

If CCR5 signaling is neutralized to reduce inflammation, then tissue damage is ameliorated, but the underlying mechanisms of IFN-γ and IL-13 induced pathology must be understood

Engineering Contradiction:

Improvetissue damageVSAvoidmechanistic understanding of IFN-γ and IL-13 pathways

Core Design Contradiction:

Object-affected harmful factorsVSDifficulty of detecting and measuring

Solution Approach 1:

The CCR5 antagonist serves as an intermediary to block the downstream effects of both IFN-γ and IL-13 signaling. By targeting CCR5, which is activated by chemokines downstream of both Th1 and Th2 pathways, the antagonist effectively interrupts the common pathway leading to tissue damage without requiring direct modulation of IFN-γ or IL-13 themselves.

Inventive Principle:

Principle #24Intermediary (Mediator)

3Ease of operation

If current treatments are used for Th1 and Th2 mediated diseases, then some symptomatic relief is achieved, but persistent tissue damage and remodeling continue without effective healing

Engineering Contradiction:

Improvesymptomatic reliefVSAvoidprevention of persistent tissue damage

Core Design Contradiction:

Ease of operationVSReliability

Solution Approach 1:

The invention extracts and targets the specific CCR5 signaling pathway that is common to both Th1 and Th2 mediated tissue damage. By selectively blocking CCR5, the treatment removes the harmful inflammatory signaling while preserving other immune functions, thereby preventing persistent tissue remodeling that continues with current broad-spectrum treatments.

Inventive Principle:

Principle #2Taking out (Extraction)

Data Source

PatentUS7943130B2Methods and compositions relating to CCR5 antagonist, IFN-γ and IL-13 induced inflammation

Publication Date: 2011.05.17 YALE UNIVERSITY

AI summary

The present invention includes compositions and methods for the treatment of Th1 and/or Th2 medicated inflammatory diseases, relating to inhibiting CCR5. This is because the present invention demonstrates, for the first time, that expression of IFN-γ, IL-13, and CCR5 mediates and/or is associated with Th1 and/or Th2 inflammatory diseases and that inhibiting CCR5 treats, and even prevents, the diseases. Thus, the Invention relates to the novel discovery that inhibiting CCR5 treats and prevents Th1 and/or Th2 mediated inflammatory disease.