Mutated CD200 Protein Binding Affinity for Autoimmune Treatment
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Solution Overview
Problem
Current treatments for autoimmune diseases are inefficient, requiring high doses and failing to provide adequate clinical efficacy, due to the limitations of wild-type CD200 proteins in binding to the CD200 receptor.
Innovation Solution
Development of mutated CD200 proteins with increased affinity for the CD200 receptor, specifically at amino acid residues 130 and 131, and their use in fusion proteins or pharmaceutical compositions to enhance immunosuppressive effects.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If wild-type CD200 proteins are used for treatment, then the treatment can be administered, but the binding affinity to CD200 receptor is insufficient leading to inadequate clinical efficacy
Solution Approach 1:
The patent applies parameter changes by mutating specific amino acid residues (positions 130 and/or 131) in the CD200 protein sequence to alter its binding properties. These mutations change the physical-chemical parameters of the protein to achieve higher binding affinity and longer residence time on the CD200 receptor, directly resolving the contradiction between insufficient efficacy and inadequate binding affinity.
2Reliability
If high doses of wild-type CD200 are administered to achieve adequate efficacy, then clinical effect may be improved, but the treatment cost and burden increase
Solution Approach 1:
By mutating amino acid residues 130 and/or 131, the patent changes the binding parameters of CD200 to achieve longer residence time on the receptor. This parameter change allows lower doses to achieve the same therapeutic effect, reducing the quantity of substance required while maintaining clinical efficacy.
3Device complexity
If wild-type CD200 is used, then the treatment approach is simple, but the residence time on receptor is short reducing effectiveness
Solution Approach 1:
The patent changes the molecular parameters of CD200 through targeted mutations at positions 130 and/or 131, which directly increases the residence time on the CD200 receptor. This parameter modification enhances the duration of action without adding complexity to the treatment approach, as it still uses a single protein therapeutics.
Data Source
AI summary
The invention relates generally to mutant CD200 proteins which bind with greater affinity to the CD200 receptor than wild-type CD200, in particular the invention relates to a mutated CD200 protein comprising a mutation at amino acid residue position 130 and/or 131. This invention also relates to a fusion protein comprising the protein as defined herein fused to a non-CD200 protein encoding portion via an optional linker portion, a pharmaceutical composition comprising the protein as defined herein and uses thereof.