PR1P Peptide Enhances VEGF Signaling for Lung Injury Treatment

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Solution Overview

Problem

Dysregulated VEGF signaling is implicated in various lung disorders, and existing treatments fail to effectively address the underlying issues of VEGF dysregulation and associated lung cell apoptosis.

Innovation Solution

Administration of a peptide comprising an amino acid sequence at least 80% identical to DRVQRQTTTVVA (PR1P), which binds VEGF, increases VEGF binding to VEGF receptors, and stabilizes VEGF from proteolytic degradation, thereby upregulating VEGF signaling and reducing lung cell apoptosis.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If existing treatments are used for lung disorders, then general symptom management is provided, but they fail to effectively address VEGF dysregulation and associated lung cell apoptosis

Engineering Contradiction:

Improveeffectiveness of treatmentVSAvoidability to address VEGF dysregulation

Core Design Contradiction:

ReliabilityVSAdaptability or versatility

Solution Approach 1:

The patent introduces a peptide (DRVQRQTTTVVA or variants) as an intermediary substance that specifically binds to VEGF and enhances its interaction with VEGF receptors. This peptide acts as a mediator to correct the dysregulated VEGF signaling pathway, thereby addressing the root cause of lung cell apoptosis and improving treatment effectiveness for lung disorders

Inventive Principle:

Principle #24Intermediary (Mediator)

Solution Approach 2:

The patent modifies the VEGF signaling pathway parameters by introducing a peptide that increases VEGF binding affinity to VEGF receptors. This parameter change in binding strength and signaling intensity restores proper VEGF pathway function, counteracting the dysregulation that leads to lung cell death

Inventive Principle:

Principle #35Parameter changes

2Reliability

If VEGF signaling is upregulated to reduce lung cell apoptosis, then lung cell survival is improved, but excessive VEGF signaling may cause harmful effects

Engineering Contradiction:

Improvelung cell survivalVSAvoidexcessive VEGF signaling effects

Core Design Contradiction:

ReliabilityVSObject-affected harmful factors

Solution Approach 1:

The patent employs a peptide that provides partial enhancement of VEGF signaling rather than complete activation. By increasing VEGF binding to receptors to a moderate extent, the treatment achieves sufficient signal to improve lung cell survival while avoiding the harmful effects of excessive VEGF signaling

Inventive Principle:

Principle #16Partial or excessive action

Solution Approach 2:

The peptide-based treatment creates a feedback mechanism where enhanced VEGF signaling leads to improved lung cell survival and reduced apoptosis. This feedback loop naturally regulates the signaling intensity, preventing excessive activation while maintaining sufficient signal for therapeutic effect

Inventive Principle:

Principle #23Feedback

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

PR1P effectively upregulates VEGF signaling, reduces apoptosis of lung cells induced by injury or toxicity, and shows promise in treating lung disorders associated with dysregulated VEGF signaling, such as emphysema and COPD.

Implementation Method 1

binds VEGF and increases VEGF binding to VEGF receptors and to endothelial cells

Methodology Applied

Scientific EffectProtein-protein binding:

Implementation Method 2

stabilizes VEGF from proteolytic degradation

Methodology Applied

Scientific EffectProteolytic degradation prevention:

Data Source

PatentUS20250134949A1Prominin-1 peptide for treating lung injury

Publication Date: 2025.05.01 CHILDRENS MEDICAL CENT CORP

AI summary

Described herein are compositions and methods for treating a lung disorder associated with dysregulated VEGF signaling. The PR1P peptide (DRVQRQTTTVVA, SEQ ID NO: 1) and variants thereof are able to enhance VEGF signaling in the lungs and reduce lung cell apoptosis (e.g., induced by toxicity or injury), thus treating the disorder.