Hovenia dulcis extract activates Wnt pathway for bone formation

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Solution Overview

Problem

Current osteoporosis treatments primarily focus on delaying bone loss rather than promoting bone formation, leading to weak and brittle bones, and there is a need for a more fundamental therapeutic approach that activates bone formation pathways without side effects.

Innovation Solution

A composition containing Hovenia dulcis Thunb. extract, gallocatechin, and methyl vanillate is used to activate the Wnt/β-catenin signaling pathway, promoting bone formation and treating osteoporosis, alopecia, wound healing, and metabolic diseases.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If antiresorptive drugs (bisphosphonates) are used to prevent bone loss, then bone resorption is inhibited, but bones become weak and brittle with continued use

Engineering Contradiction:
Improvebone loss preventionVSAvoidbone strength
Core Design Contradiction:
ReliabilityVSStrength

Solution Approach 1:

Instead of inhibiting bone resorption (antiresorptive approach), the patent promotes bone formation through Wnt/β-catenin pathway activation. This inverts the therapeutic strategy from preventing bone breakdown to actively stimulating bone building, thereby improving bone strength while maintaining bone mass.

Inventive Principle:
Principle #13The other way round (Inversion)

Solution Approach 2:

The patent changes the therapeutic parameter from antiresorptive activity to bone formation promotion by activating the Wnt/β-catenin signaling pathway. This parameter change shifts the mechanism of action from inhibiting osteoclasts to stimulating osteoblasts, resolving the contradiction between bone loss prevention and bone strength maintenance.

Inventive Principle:
Principle #35Parameter changes

2Productivity

If Wnt/β-catenin signaling pathway is activated, then bone formation is promoted, but the pathway is also associated with cancer development

Engineering Contradiction:
Improvebone formation rateVSAvoidcancer risk
Core Design Contradiction:
ProductivityVSObject-affected harmful factors

Solution Approach 1:

The patent uses natural compounds (Hovenia dulcis extract, gallocatechin, methyl vanillate) as intermediaries to activate the Wnt/β-catenin pathway. These natural mediators provide a safer activation mechanism compared to synthetic compounds, potentially reducing cancer risk while maintaining bone formation benefits.

Inventive Principle:
Principle #24Intermediary (Mediator)

Solution Approach 2:

The patent employs natural, readily available compounds from Hovenia dulcis fruit as temporary, low-risk activators of the Wnt pathway. These natural compounds offer a short-term, low-toxicity approach to pathway activation, contrasting with potent synthetic compounds that may have long-term cancer risks.

Inventive Principle:
Principle #27Cheap short-living objects (Disposable)

Data Source

PatentUS11219656B2Method of using composition containing <i>Hovenia dulcis </i>Thunb. extract as active ingredient for prevention and treatment of bone diseases
Publication Date: 2022.01.11 IND ACADEMIC COOP FOUND YONSEI UNIV
  • US11219656B2 patent drawing
  • US11219656B2 patent drawing
  • US11219656B2 patent drawing

AI summary

The invention relates to a composition containing extracts of the fruit of Hovenia dulcis Thunb., gallocatechin, and methyl vanillate as active ingredients for preventing and treating bone disease. The extracts of the fruit of Hovenia dulcis Thunb., the gallocatechin, and the methyl vanillate according to the present invention are natural materials and thus cause no side effects, and may activate the Wnt/β-catenin pathway to promote bone formation rather than inhibiting bone decomposition, and therefore may be effective in treating osteoporosis and related diseases. In addition, the extracts of the fruit of Hovenia dulcis Thunb., the gallocatechin, and the methyl vanillate according to the present invention may have the effects regrowing hair and preventing and treating wounds and metabolic diseases related to the activation of Wnt/β-catenin pathway.