摘要
Polysorbate 80 (PS80), a vital stabilizer in biotherapeutic formulations, faces persistent oxidative degradation challenges that threaten drug product stability during storage. While PS80 instability has been studied for decades, the oxidation mechanisms in specific formulation-packaging systems remain poorly understood. This work resolves this knowledge gap by demonstrating that PS80 oxidative degradation occurs exclusively in histidine-buffered formulations stored in glass vials. This phenomenon was found to be driven by four factors: iron (leaching from vials promoted by histidine), histidine, zinc (histidine-introduced) and aluminum (glass-derived). These four interdependent factors exhibited a unique functional synergy: 1) iron as the radical chain initiator; 2) histidine as a pro-oxidative cofactor lowering iron’s catalytic threshold via formation of an iron-histidine complex; 3) zinc and aluminum accelerate Fe 2+ /Fe 3+ redox cycling through distinct potential-specific mechanisms, enhancing the overall catalytic efficiency. This study for the first time provides the systematic evidence of the histidine-glass system as an essential prerequisite for PS80 oxidation and reveals novel mechanistic insights on the interplay between formulation composition and packaging-derived contaminants. The findings establish a predictive framework to mitigate PS80 oxidative degradation, ultimately enhancing the stability and safety of protein therapeutics.
危险品化学品经营许可证(带存储)