Antisense Oligonucleotide Inhibits MS Lesion Conversion
Find Innovative SolutionsGenerate Solutions
Solution Overview
Problem
Current treatments for multiple sclerosis, particularly for patients with active lesions and progressive disease, are inadequate in reducing the conversion of active lesions to persistent black holes, a marker of axonal loss and permanent tissue damage, and in altering the course of established lesions to slow disease progression.
Innovation Solution
Administration of a pharmaceutical composition containing a specific oligonucleotide, 5′-MeCMeUG AGT MeCTG TTT MeUMeCMeC AMeUMeU MeCMeU-3′, which inhibits the conversion of active brain lesions into hypointense T1-weighted lesions, thereby reducing axonal loss and disability progression.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If conventional treatments are used for multiple sclerosis, then general disease management is achieved, but the conversion of active lesions to persistent black holes is not sufficiently reduced
Solution Approach 1:
The patent employs antisense oligonucleotides that specifically bind to and inhibit the expression of adhesion molecules (such as VCAM-1 and ICAM-1) involved in the pathogenesis of multiple sclerosis. This molecular-level parameter change prevents the conversion of active lesions to persistent black holes by blocking the inflammatory cascade and axonal damage processes, thereby reducing harmful effects while maintaining disease management.
2Productivity
If existing therapies are administered, then symptomatic relief is provided, but the course of established lesions cannot be altered to slow disease progression
Solution Approach 1:
The antisense oligonucleotides act preliminarily by preventing the formation and progression of lesions before they become established permanent damage. By targeting adhesion molecules early in the inflammatory process, the treatment alters the course of lesions at an early stage, slowing disease progression before irreversible damage occurs.
Solution Approach 2:
The patent changes the molecular parameters of the disease process by inhibiting specific adhesion molecules through antisense oligonucleotide binding. This molecular intervention alters the biological parameters of lesion development and progression, enabling modification of the disease course rather than merely managing symptoms.
3Object-affected harmful factors
If current MS treatments are used, then general disease control is maintained, but neureoprotective effects are insufficient
Solution Approach 1:
The antisense oligonucleotides act as molecular intermediaries that block the interaction between inflammatory cells and neural tissue by inhibiting adhesion molecule expression. This intermediary action prevents the harmful effects of inflammation on neurons and glial cells, providing enhanced neuroprotection while maintaining overall disease control.
Data Source
AI summary
A method for treating a patient suffering from multiple sclerosis, including progressive forms of multiple sclerosis, comprising periodically administering a pharmaceutical composition comprising a therapeutically effective amount of OLIGONUCLEOTIDE I to the patient, thereby treating the patient.