Systemic toxicity and short half-lives of native cytokines lead to high clinical failure rates. These innovations engineer specific protein-receptor binding affinities and polymer conjugation to ensure targeted therapeutic action without off-target immune activation.
The enzymatic activity of IL4I1 catabolizes essential amino acids to produce metabolites that inhibit T-cell activation and promote immune evasion. Neutralizing this metabolic pathway prevents the biochemical silencing of the host immune response within the tumor site.