IGFBPL1 Mediator for Optic Nerve Regeneration

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Solution Overview

Problem

Current methods for stimulating nerve regeneration and repair after injury, particularly involving insulin growth factor 1 (IGF-1), have been unsuccessful due to incomplete understanding of IGF-1's mechanisms in postnatal and adult neuronal cell survival and nerve regeneration.

Innovation Solution

The discovery that insulin-like growth factor binding protein-like 1 (IGFBPL1) promotes axon outgrowth in retinal ganglion cells through regulation of the IGF-1 signaling pathway, with compounds that increase or stabilize IGFBPL1 activity or expression reversing developmental loss of axon regenerative capacity.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Productivity

If IGF-1 is administered to stimulate nerve regeneration, then nerve growth should be promoted, but the mechanism is incomplete and unsuccessful in postnatal and adult stages

Engineering Contradiction:

Improvenerve regeneration efficiencyVSAvoidmechanism understanding completeness

Core Design Contradiction:

ProductivityVSReliability

Solution Approach 1:

The patent identifies IGFBPL1 as a critical intermediary molecule that mediates IGF-1's effects on neuronal survival and axon growth. By discovering this intermediate component in the IGF-1 signaling pathway, the patent resolves the incomplete mechanism understanding and enables successful nerve regeneration therapy in postnatal and adult stages where IGF-1 alone failed

Inventive Principle:

Principle #24Intermediary (Mediator)

2Productivity

If IGF-1 signaling is activated to promote axon growth, then nerve regeneration improves, but optic nerve degeneration occurs without proper regulation

Engineering Contradiction:

Improveaxon growth rateVSAvoidoptic nerve degeneration

Core Design Contradiction:

ProductivityVSObject-affected harmful factors

Solution Approach 1:

The patent utilizes intravitreal administration to change the delivery parameters of IGFBPL1, achieving high local concentration in the eye while maintaining systemic safety. This parameter change enables effective promotion of axon growth and prevention of optic nerve degeneration without the harmful effects associated with unregulated IGF-1 signaling

Inventive Principle:

Principle #35Parameter changes

3Reliability

If intravitreal administration is used to deliver IGFBPL1, then local efficacy in the eye is improved, but delivery system complexity increases

Engineering Contradiction:

Improvelocal treatment efficacyVSAvoidadministration method complexity

Core Design Contradiction:

ReliabilityVSDevice complexity

Solution Approach 1:

The patent employs intravitreal injection which is a minimally invasive, self-contained delivery method that directly administers IGFBPL1 to the vitreous humor of the eye. This approach achieves high local efficacy without requiring complex delivery systems, surgical implants, or external control mechanisms, thereby resolving the contradiction between efficacy and complexity

Inventive Principle:

Principle #25Self-service

Data Source

PatentUS12295985B2Methods of reducing severity of glaucoma by intravitreal administration of insulin-like growth factor binding protein-like 1 (IGFBPL1)

Publication Date: 2025.05.13 SCHEPENS EYE RESEARCH INSTITUTE INC

AI summary

Disclosed is a method of promoting neuronal growth by administering IGFBPL-1, or an agent that increases or stabilizes IGFBPL-1 activity to a subject in need thereof, e.g., a subject in need of treating optic nerve degeneration.