2-(3,4-dihydroxyphenyl)ethyl 3-hydroxybutanoate for Aortic Endothelial Protection

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Solution Overview

Problem

Current treatments for atherosclerosis, a major contributor to cardiovascular diseases, are often ineffective in preventing or reversing the inflammatory and mitochondrial damage that lead to this condition, highlighting the need for new substances that can improve aortic endothelial cell function.

Innovation Solution

The compound 2-(3,4-dihydroxyphenyl)ethyl 3-hydroxybutanoate is developed, which inhibits inflammatory responses in aortic endothelial cells, reduces IL-6 mRNA levels, protects mitochondrial function, and increases mitochondrial complex I protein expression, thereby preventing the development of atherosclerosis.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If conventional treatments for atherosclerosis are used, then existing therapeutic approaches are applied, but they are ineffective in preventing or reversing inflammatory and mitochondrial damage

Engineering Contradiction:
Improveeffectiveness of treatmentVSAvoidinflammatory and mitochondrial damage
Core Design Contradiction:
ReliabilityVSObject-affected harmful factors

Solution Approach 1:

The patent converts the harmful inflammatory response and mitochondrial damage caused by saturated fatty acids into a beneficial target for treatment. By identifying that these harmful processes are driven by specific molecular pathways, the invention develops compounds that specifically inhibit these pathways, thereby converting the understanding of harm into a basis for therapeutic benefit through targeted anti-inflammatory and mitochondrial protective effects

Inventive Principle:
Principle #22Blessing in disguise (Convert harm into benefit)

Solution Approach 2:

The patent applies parameter changes by modifying the chemical structure to create 2-(3,4-dihydroxyphenyl)ethyl 3-hydroxybutanoate, which has optimized pharmacological properties. The compound's specific molecular parameters (functional groups, stereochemistry, molecular weight) are designed to achieve optimal binding affinity to inflammatory and mitochondrial targets, thereby improving treatment effectiveness while reducing side effects

Inventive Principle:
Principle #35Parameter changes

2Reliability

If new substances are developed to improve aortic endothelial cell function, then anti-atherosclerotic effects are achieved, but the complexity of drug development increases

Engineering Contradiction:
Improveanti-atherosclerotic effectVSAvoiddrug development complexity
Core Design Contradiction:
ReliabilityVSDevice complexity

Solution Approach 1:

The patent achieves multi-functionality with 2-(3,4-dihydroxyphenyl)ethyl 3-hydroxybutanoate, which simultaneously exhibits anti-inflammatory effects, mitochondrial protective effects, and anti-atherosclerotic properties. This single compound addresses multiple pathological mechanisms of atherosclerosis, thereby reducing the need for complex combination therapies and simplifying the overall treatment approach while maintaining high reliability

Inventive Principle:
Principle #6Universality (Multi-functionality)

Data Source

PatentUS10947179B22-(3,4-dihydroxyphenyl)ethyl 3-hydroxybutanoate, composition, and method for improving function of aortic endothelial cell
Publication Date: 2021.03.16 XI AN JIAOTONG UNIV
  • US10947179B2 patent drawing
  • US10947179B2 patent drawing
  • US10947179B2 patent drawing

AI summary

The disclosure relates to a compound, 2-(3,4-dihydroxyphenyl)ethyl 3-hydroxybutanoate, for improving aortic endothelial cell function and use thereof. The compound is capable of inhibiting inflammatory response of the human aortic endothelial cells caused by a saturated fatty acid, and preventing an occurrence and progression of atherosclerosis. The compound is capable of reducing human aortic endothelial inflammation caused by a saturated fatty acid, for example, reducing the mRNA levels of interleukin-6 (IL-6), and is capable of effectively protecting the function of mitochondria in human aortic endothelium from being damaged by a saturated fatty acid, for example, increasing the expression of mitochondrial complex I.