Tranilast Formulation for Amyloid Fibril Formation Control

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Solution Overview

Problem

Existing treatments are ineffective in suppressing or inhibiting amyloid fibril formation, which leads to amyloidosis and associated diseases such as Alzheimer's and Parkinson's, and there is a need for a formulation that can dissolve or eliminate amyloid fibrils effectively.

Innovation Solution

Tranilast or its pharmacologically acceptable salts are used as an active ingredient in a formulation to suppress or inhibit amyloid fibril formation by promoting dissolution or discharge of amyloid fibrils in vivo.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If existing treatments (clioquinol, curcumin, tannic acid, hemin, melatonin, 4,5-dianilinophthalimide, L-DOPA, hexadecyl-N-methylpiperidinium, congo red) are used to suppress amyloid fibril formation, then some suppression effect is achieved, but none of these compounds have been proven to effectively dissolve or eliminate existing amyloid fibrils in vivo

Engineering Contradiction:
Improveeffectiveness of amyloid fibril suppressionVSAvoidability to dissolve or eliminate existing amyloid fibrils
Core Design Contradiction:
ReliabilityVSAdaptability or versatility

Solution Approach 1:

The patent applies parameter changes by using tranilast at specific dosage ranges (200-600 mg/day) to achieve both suppression of new amyloid fibril formation and dissolution of existing fibrils, transforming the therapeutic outcome from merely inhibiting formation to actively eliminating deposits

Inventive Principle:
Principle #35Parameter changes

2Object-affected harmful factors

If tranilast is used at low doses, then side effects are minimized, but the ability to dissolve or eliminate amyloid fibrils is insufficient

Engineering Contradiction:
Improveside effects of treatmentVSAvoideffectiveness of amyloid fibril dissolution
Core Design Contradiction:
Object-affected harmful factorsVSReliability

Solution Approach 1:

The patent applies partial or excessive action by using tranilast at doses higher than typical antiallergic treatment (200-600 mg/day versus usual lower doses), which exceeds the threshold for simple inhibition and achieves active dissolution of amyloid fibrils while remaining within the safe tolerance range of the drug

Inventive Principle:
Principle #16Partial or excessive action

3Reliability

If high doses of tranilast are used to enhance amyloid fibril dissolution, then therapeutic effect is improved, but risk of side effects increases

Engineering Contradiction:
Improvetherapeutic effect against amyloidosisVSAvoidside effects at high dosage
Core Design Contradiction:
ReliabilityVSObject-affected harmful factors

Solution Approach 1:

The patent applies self-service by utilizing tranilast's inherent dual mechanism (inhibition of formation and promotion of dissolution) at optimized doses, allowing the drug to work through its own pharmacological properties without requiring combination therapy or complex administration protocols, thereby achieving high therapeutic effect with acceptable side effect profile

Inventive Principle:
Principle #25Self-service

Data Source

PatentEP4039255B1Amyloid fiber formation limiter or inhibitor
Publication Date: 2025.10.15 OMOIDESOUZOU
  • EP4039255B1 patent drawingFigure 1A~1H
  • EP4039255B1 patent drawingFigure 2A~2G
  • EP4039255B1 patent drawing

AI summary

The object of the present invention is to provide a formulation with the effect of effectively suppressing or inhibiting amyloid fibril formation by the dissolution, elimination (discharge), etc. of amyloid fibril formation in vivo. If an agent for suppressing or inhibiting an amyloid fibril formation comprising tranilast or a pharmacologically acceptable salt thereof as an active ingredient is administered by a method such as oral administration, amyloid fibril formation can be effectively suppressed or inhibited in vivo as a result of effects such as amyloid fibril dissolution or elimination (discharge). Therefore, it is possible to prevent or treat amyloid plaques, in which amyloid fibrils formed by the aggregation of amyloid protein have been deposited, and to prevent or treat diseases arising from amyloid fibril deposition, that is, diseases arising from the deposited amyloid fibrils themselves and diseases that cause dysfunction of organs or tissues as a result of amyloid fibril deposition.