NEK10 Kinase Activation for Impaired Mucociliary Clearance

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Solution Overview

Problem

Bronchiectasis, a syndrome of pathological airway dilation associated with impaired mucociliary clearance, lacks effective therapeutic targets for modulating mucociliary transport, and its regulation remains incompletely understood.

Innovation Solution

Administering wild-type NEK10 or hyperactive NEK10 mutants, such as NEK10S684D, to enhance mucociliary clearance by regulating the motile ciliary proteome and promoting ciliary length and function.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If conventional therapies are used for bronchiectasis, then general respiratory support is provided, but mucociliary clearance remains impaired and no specific therapeutic target is addressed

Engineering Contradiction:

Improvemucociliary clearance functionVSAvoidavailability of therapeutic targets

Core Design Contradiction:

ReliabilityVSEase of manufacture

Solution Approach 1:

The patent changes the molecular parameter by introducing NEK10 kinase, a previously unidentified therapeutic target, to modulate mucociliary transport. This specific kinase parameter provides a new mechanism for improving mucociliary clearance function that was previously unavailable through conventional therapies.

Inventive Principle:

Principle #35Parameter changes

Solution Approach 2:

NEK10 acts as an intermediary molecule that regulates the motile ciliary proteome and connects upstream signaling to downstream ciliary function. By targeting this intermediary kinase, the therapy addresses the specific mechanism of mucociliary clearance impairment in bronchiectasis.

Inventive Principle:

Principle #24Intermediary (Mediator)

2Productivity

If NEK10 is administered to enhance mucociliary clearance, then ciliary length and motile ciliary transport are improved, but the complexity of targeting a previously unknown kinase pathway increases

Engineering Contradiction:

Improvemucociliary transport efficiencyVSAvoidtherapeutic mechanism complexity

Core Design Contradiction:

ProductivityVSDevice complexity

Solution Approach 1:

The NEK10 kinase serves as a self-regulating therapeutic target that, when activated, automatically regulates the motile ciliary proteome and enhances ciliary function. The kinase's endogenous regulatory mechanisms provide self-service functionality, reducing the need for complex external control systems.

Inventive Principle:

Principle #25Self-service

3Reliability

If inactivating mutations in NEK10 are present, then bronchiectasis syndrome develops with impaired mucociliary clearance, but the mechanism of action was previously unknown

Engineering Contradiction:

Improveciliary functionVSAvoidunderstanding of regulation mechanism

Core Design Contradiction:

ReliabilityVSLoss of information

Solution Approach 1:

The patent performs preliminary identification and characterization of NEK10 kinase as the critical regulator of mucociliary transport. By establishing the kinase's role before developing therapies, the research prevents loss of information about the mechanism and provides a foundation for future treatments.

Inventive Principle:

Principle #10Preliminary action

Data Source

PatentUS12605428B2Kinase NEK10 and its use in treating and diagnosing bronchiectasis and other respiratory disorders

Publication Date: 2026.04.21 THE GENERAL HOSPITAL CORP

AI summary

Aspects of the present disclosure provide compositions comprising NEK10 for example, wild-type NEK10 or a hyperactive NEK10 mutant such as NEK10S684D, and methods of using such for treating a respiratory disorder such as bronchiectasis.