CXCR3 Activators Inhibit Aberrant Angiogenesis in Eye Disorders

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Solution Overview

Problem

Current methods fail to effectively treat angiogenic disorders of the eye, such as diabetic retinopathy and macular degeneration, by inadequately addressing aberrant angiogenesis, which leads to uncontrolled blood vessel growth and vision loss.

Innovation Solution

Administration of a therapeutically effective amount of a CXCR3 activator, specifically IP-10 or PF4 proteins or their biologically active fragments, to inhibit angiogenesis in the eye, either directly or through medical implants, preventing the formation of new blood vessels and fibrosis.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If current treatment methods are used for angiogenic disorders of the eye, then treatment is provided, but the methods fail to effectively inhibit aberrant angiogenesis and prevent uncontrolled blood vessel growth

Engineering Contradiction:
Improveeffectiveness of treatmentVSAvoidinhibition of aberrant angiogenesis
Core Design Contradiction:
ReliabilityVSProductivity

Solution Approach 1:

The patent changes the molecular target parameter from conventional angiogenesis inhibitors to CXCR3 activators. By activating the CXCR3 receptor pathway, the treatment achieves more effective inhibition of aberrant angiogenesis in eye disorders, transforming the therapeutic parameter to achieve superior clinical efficacy.

Inventive Principle:
Principle #35Parameter changes

Solution Approach 2:

The patent introduces CXCR3 activators as intermediary molecules that mediate the inhibition of angiogenesis. These activators bind to and activate the CXCR3 receptor, which then triggers downstream signaling pathways that prevent abnormal blood vessel formation, serving as a crucial intermediary in the therapeutic mechanism.

Inventive Principle:
Principle #24Intermediary (Mediator)

2Reliability

If CXCR3 activators are administered to inhibit angiogenesis, then aberrant blood vessel growth is prevented, but the complexity of the treatment mechanism increases

Engineering Contradiction:
Improveinhibition of new blood vessel formationVSAvoidtreatment mechanism complexity
Core Design Contradiction:
ReliabilityVSDevice complexity

Solution Approach 1:

The patent extracts and isolates the specific CXCR3 receptor activation pathway from the complex network of angiogenesis regulation. By focusing specifically on activating CXCR3 rather than attempting to modulate multiple angiogenic pathways simultaneously, the treatment simplifies the therapeutic mechanism while maintaining high efficacy in preventing abnormal blood vessel formation.

Inventive Principle:
Principle #2Taking out (Extraction)

3Productivity

If angiogenesis is not adequately controlled, then blood vessel growth proceeds unchecked, but vision loss and disease progression occur

Engineering Contradiction:
Improvecontrol of blood vessel growthVSAvoidvision loss and disease progression
Core Design Contradiction:
ProductivityVSObject-affected harmful factors

Solution Approach 1:

The patent applies preliminary anti-action by activating CXCR3 receptors before aberrant angiogenesis can cause significant damage. The CXCR3 activators are administered to pre-emptively inhibit the formation of abnormal blood vessels, preventing the harmful outcomes of vision loss and disease progression before they occur.

Inventive Principle:
Principle #9Preliminary anti-action

Data Source

PatentUS11406687B2Activators of CXCR3 for the treatment of angiopathies of the eye
Publication Date: 2022.08.09 UNIV OF PITTSBURGH OF THE COMMONWEALTH SYST OF HIGHER EDUCATION

AI summary

The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3 (CXCR3). In some embodiments, the activator of CXCR3 is interferon-γ-inducible 10 kDa protein (IP-10) or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal α-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.