Butanetap Therapy for Infection-Driven Neurological Damage

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Solution Overview

Problem

Viral, bacterial, fungal, protozoan, or parasitic infections lead to overproduction of neurotoxic proteins, causing neurological damage and neurodegenerative diseases such as Alzheimer's, Parkinson's, and other conditions by increasing iron levels and triggering a toxic cascade in the brain.

Innovation Solution

Administering Butanetap or its analogues in therapeutically effective amounts to inhibit or treat neurological damage by maintaining heavy metal homeostasis and reducing neurotoxic protein production.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If the brain produces amyloid beta to kill or trap microbes during infection, then the brain is protected from infection, but amyloid plaques build up triggering tau tangles and chronic inflammation leading to neurodegeneration

Engineering Contradiction:
Improvebrain protection from infectionVSAvoidneurotoxic protein overproduction
Core Design Contradiction:
ReliabilityVSObject-generated harmful factors

Solution Approach 1:

The patent converts the harmful overproduction of amyloid beta and tau proteins into a beneficial outcome by using small molecule compounds that specifically inhibit the toxic effects of these proteins while preserving their protective antimicrobial function. The compounds transform the pathological cascade into a controlled protective response.

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

Solution Approach 2:

The patent changes the concentration parameter of neurotoxic proteins by administering small molecule compounds that reduce amyloid beta and tau protein levels to therapeutic ranges, thereby preventing neurodegeneration while maintaining sufficient levels for microbial protection.

Inventive Principle:
Principle #35Parameter changes

2Quantity of substance

If iron levels increase during brain infection, then microbial growth is supported, but neurotoxic protein translation is upregulated causing nerve cell death

Engineering Contradiction:
Improveiron availabilityVSAvoidneurotoxic protein synthesis
Core Design Contradiction:
Quantity of substanceVSObject-generated harmful factors

Solution Approach 1:

The patent changes the iron metabolism parameter by administering compounds that regulate iron homeostasis in the brain, thereby preventing the upregulation of neurotoxic protein translation while maintaining sufficient iron for microbial defense mechanisms.

Inventive Principle:
Principle #35Parameter changes

3Reliability

If neurons overproduce amyloid beta and tau proteins to trap microbes, then infection is contained, but the toxic cascade causes chronic inflammation and nerve cell death

Engineering Contradiction:
Improveinfection containmentVSAvoidbrain tissue integrity
Core Design Contradiction:
ReliabilityVSStability of the object's composition

Solution Approach 1:

The patent changes the concentration parameter of amyloid beta and tau proteins to therapeutic levels using small molecule compounds, thereby containing infections while preventing the toxic cascade that leads to chronic inflammation and nerve cell death.

Inventive Principle:
Principle #35Parameter changes

Solution Approach 2:

The patent introduces small molecule compounds as intermediary substances that mediate between the protective immune response and the toxic effects, allowing the brain to contain infections without suffering neurodegenerative damage.

Inventive Principle:
Principle #24Intermediary (Mediator)

Data Source

PatentUS12582632B2Inhibition of neurological injuries due to infections via administration of Butanetap and analogs thereof
Publication Date: 2026.03.24 ANNOVIS BIO INC
  • US12582632B2 patent drawing
  • US12582632B2 patent drawing
  • US12582632B2 patent drawing

AI summary

The invention relates to methods of inhibiting or treating neurological damage in a human who is infected by or at risk of infection by a virus, a bacterium, a fungus, a protozoan or a parasite that can cause neurological damage, comprising administering to a human a compound selected from the group consisting of Formula (I), Formula (II), Formula (III) or Formula (IV) or pharmaceutically acceptable salts thereof.