Agrin nLG3 and ActR2B Inhibitor Compound for Muscle Performance
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Solution Overview
Problem
Current therapies lack a comprehensive solution to address the overall loss of muscle performance, despite individual approaches improving muscle mass or maintaining neuromuscular junctions, as existing methods fail to effectively counteract the decline in muscle function across various pathological disorders.
Innovation Solution
A compound comprising the nLG3 domain from the C-terminus of agrin and proteins or antibodies that inhibit ActR2B-induced signaling activity in the presence of myostatin, linked by specific entities, is administered to improve muscle performance by enhancing muscular endurance without significant muscle mass increase or acetylcholine receptor clustering.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Quantity of substance
If therapies target muscle mass increase or neuromuscular junction maintenance individually, then specific muscle function aspects are improved, but overall muscle performance decline is not effectively counteracted
Solution Approach 1:
The patent combines two distinct therapeutic mechanisms into a single compound: the nLG3 domain (which maintains neuromuscular junctions) and the ActR2B inhibitor (which prevents muscle atrophy). This merging allows simultaneous improvement of both neuromuscular junction maintenance and muscle mass preservation, thereby addressing overall muscle performance decline more effectively than individual therapies
2Quantity of substance
If ActR2B signaling is inhibited to prevent muscle atrophy, then muscle mass is maintained, but muscle satellite cell activation and performance improvement are limited
Solution Approach 1:
By combining the nLG3 domain with the ActR2B inhibitor, the compound simultaneously activates muscle satellite cells (through nLG3) and prevents muscle atrophy (through ActR2B inhibition). This dual mechanism overcomes the limitation of using only ActR2B inhibitors, achieving both muscle mass maintenance and enhanced muscle performance
3Reliability
If nLG3 domain is used to maintain neuromuscular junctions, then neuromuscular function is preserved, but muscle mass increase and performance improvement are insufficient
Solution Approach 1:
The compound merges the nLG3 domain (for neuromuscular junction maintenance) with the ActR2B inhibitor (for muscle mass preservation and satellite cell activation). This combination ensures that neuromuscular function is preserved while simultaneously promoting muscle mass increase and performance improvement, overcoming the insufficiency of using nLG3 alone
Applied Scientific Principles
This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.
Function Achieved in This Case
The compound significantly improves muscular endurance, as demonstrated by experimental methods, without proportional increase in internal organ size, specifically activating muscle satellite cells and improving muscle performance in both young and aged mice models.
Implementation Method 1
The compound comprises the nLG3 domain from the C-terminus of agrin and proteins or antibodies that inhibit ActR2B-induced signaling activity
Implementation Method 2
proteins or antibodies that inhibit ActR2B-induced signaling activity in the presence of myostatin
Data Source
AI summary
A compound comprising at least two components, a first component being the nLG3 or (h)nLG3 domain from the C-terminus of mouse or human agrin, and at least one second component, selected from proteins or an antagonistic antibody that inhibit ActR2B-induced signaling activity in the presence of myostatin, the components being linked by means of linking entities.Such compounds are effective treatments for neuromuscular diseases and problems.