Galectin Candidate Therapeutic for Modulating Immune Response

Regulates Inflammation and Immune Responses at Lower Doses Than Other Galectin Therapeutics

This fusion protein is composed of galectin-1 and galectin-3 and is a candidate therapeutic for modulating immune responses and treating inflammation. The global autoimmune disease therapeutics market should reach $1.5 billion by 2025. Galectins are promising therapeutic candidates for managing immune responses and inflammation because they can alter the phenotype and function of immune cells. Currently, galectin-1 and galectin-3 variants are used separately as therapeutics, but both require high doses that are expensive and impractical for clinical use.

Researchers at the University of Florida have developed a fusion protein composed of galectin-1 and galectin-3 that is a candidate therapeutic for regulating immune responses and controlling inflammation. This new candidate therapeutic displays greater binding ability, better immunomodulatory potency, and requires lower doses to be effective than other galectin therapeutics.

Application

New galectin therapeutic with lower minimum effective dose and better binding in immune response regulation than other galectin therapeutics

Advantages

• Is effective at lower doses compared to other galectin therapeutics, reducing costs and enabling practical application in clinical settings
• Fusion protein has high anchoring capacity, reducing off-target effects and potentially increasing the length of time that the therapeutic is effective in the body
• Can be expressed well in E. coli, lending to scalability and easing the required purification process

Technology

This candidate therapeutic for regulating immune responses and controlling inflammation is a fusion protein comprised of one galectin-1 polypeptide and one galectin-3 polypeptide. This protein dimer has a better binding affinity and lower effective dosing requirement than current galectin candidate therapeutics, and it was more effective than other galectin therapeutics at inducing T-cell apoptosis critical for regulating immune responses.