Tie-2 Activator Reduces Intraocular Pressure

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Solution Overview

Problem

Current treatments for elevated intraocular pressure and ocular hypertension associated with glaucoma are inadequate in effectively reducing pressure within the eye, leading to potential permanent vision loss if not diagnosed or treated promptly.

Innovation Solution

Administration of a therapeutically-effective amount of a Tie-2 activator, which activates Tie-2 signaling by inhibiting human protein tyrosine phosphatase beta (HPTPβ), thereby reducing intraocular pressure by promoting protein phosphorylation and stabilizing the vasculature associated with the trabecular meshwork.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If conventional treatments for elevated intraocular pressure are used, then the treatment can be administered, but the pressure reduction is inadequate and vision loss risk remains high

Engineering Contradiction:
Improveeffectiveness of pressure reductionVSAvoidvision loss risk
Core Design Contradiction:
ReliabilityVSObject-affected harmful factors

Solution Approach 1:

The patent changes the molecular target parameter from conventional IOP-lowering agents to Tie-2 activators that modulate angiopoietin signaling. This parameter change enables superior pressure reduction (0.1-9 mmHg) by activating Tie-2 receptor signaling, which stabilizes the trabecular meshwork vasculature and improves aqueous humor outflow, thereby reliably reducing intraocular pressure and mitigating vision loss risk.

Inventive Principle:
Principle #35Parameter changes

2Reliability

If Tie-2 activator is administered, then intraocular pressure is effectively reduced, but the mechanism of action involves complex protein phosphorylation and vascular stabilization

Engineering Contradiction:
Improvepressure reduction efficacyVSAvoidmechanism complexity
Core Design Contradiction:
ReliabilityVSDevice complexity

Solution Approach 1:

The patent uses Tie-2 activators as intermediary substances that bind to and activate the Tie-2 receptor. This intermediary mechanism simplifies the overall therapeutic approach by focusing on a single activated pathway (angiopoietin-Tie-2 signaling) that cascades into multiple beneficial effects including protein phosphorylation, vascular stabilization, and improved aqueous humor outflow, thereby achieving reliable pressure reduction through a coordinated biological response.

Inventive Principle:
Principle #24Intermediary (Mediator)

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 Tie-2 activator effectively reduces intraocular pressure by 0.1 mmHg to 9 mmHg, providing a therapeutic benefit in treating glaucoma and ocular hypertension, thereby mitigating the risk of vision loss.

Implementation Method 1

activates Tie-2 signaling by inhibiting human protein tyrosine phosphatase beta (HPTPβ), thereby reducing intraocular pressure by promoting protein phosphorylation

Methodology Applied
Scientific EffectProtein phosphorylation:

Data Source

PatentUS12171751B2Methods of treating intraocular pressure with activators of Tie-2
Publication Date: 2024.12.24 EYEPOINT INC
  • US12171751B2 patent drawing
  • US12171751B2 patent drawing
  • US12171751B2 patent drawing

AI summary

Disclosed herein are compounds effective for activation of Tie-2 and inhibition of HPTP-beta. The compounds can provide effective therapy for eye conditions associated with angiogenesis, for example, intraocular pressure, ocular hypertension, and glaucoma.