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Updated: Jan 29, 2026

Drug-Induced Sleep Endoscopy DISE with Target Controlled Infusion TCI and Bispectral Analysis in Obstructive Sleep Apnea

Drug-Induced Sleep Endoscopy DISE with Target Controlled Infusion TCI and Bispectral Analysis in Obstructive Sleep Apnea

Published on: December 6, 2016

Rationally Designed Dual Kinase Inhibitors for Management of Obstructive Sleep Apnea-A Computational Study.

Kosi Gramatikoff¹, Miroslav Stoykov², Mario Milkov²

¹Research Institute, Medical University "Prof. Dr. Paraskev Stoyanov", 55 Marin Drinov Str., 9002 Varna, Bulgaria.

|January 28, 2026

Summary

This summary is machine-generated.

This study identifies the CK1δ-PINK1 signaling pathway as a key target for obstructive sleep apnea (OSA) drug discovery. Novel dual kinase inhibitors were rationally designed, offering a new precision therapeutic approach for OSA management.

Keywords:

Nigella sativa PINK1 casein kinase 1 delta (CK1δ)comorbidities dual kinase inhibitors network pharmacology neurodegeneration obstructive sleep apnea plant alkaloids precision therapeutics rational drug design

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Last Updated: Jan 29, 2026

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Published on: January 26, 2019

Area of Science:

Biochemistry
Pharmacology
Computational Biology

Background:

Obstructive sleep apnea (OSA) affects over a billion adults globally, presenting significant comorbidities like cardiovascular disease and cognitive decline.
Current pharmacological treatments for OSA are limited, and traditional omics approaches face challenges in therapeutic translation due to gene overlap with other diseases.
A novel top-down, comorbidity-driven strategy is proposed to identify actionable molecular targets for OSA.

Purpose of the Study:

To identify molecular targets for OSA management using a comorbidity-driven approach.
To develop rational dual kinase inhibitors for OSA by targeting the CK1δ-PINK1 signaling cascade.
To establish a generalizable workflow for drug discovery in complex, multimorbid diseases.

Main Methods:

A five-tier modeling workflow including comorbidity network analysis and disease module identification.
Mechanistic pathway reconstruction of the CK1δ-(HIF1A)-PINK1 signaling cascade.
Molecular docking of *Nigella sativa* alkaloids and reference inhibitors against CK1δ and PINK1, followed by rational design and computational validation of novel dual inhibitors.

Main Results:

Network analysis identified a discrete OSA disease module involving CK1δ and PINK1, linking circadian disruption and neurodegeneration.
Specific *Nigella sativa* alkaloids showed potent binding to CK1δ and PINK1.
Rationally designed dual inhibitors (ICL, PFL) exhibited superior binding affinities compared to reference compounds, indicating enhanced therapeutic potential.

Conclusions:

The CK1δ-PINK1 axis is validated as a therapeutic target for OSA through a comorbidity-driven translational framework.
Rationally designed dual inhibitors represent advanced precision therapeutics for OSA's complex pathophysiology.
The developed five-tier workflow offers a scalable template for discovering drugs targeting complex, multimorbid conditions.