We also observed an anti-inflammatory effect for dPGS10 at a concentration of 10 µg/mL in the inflamed bronchial epithelium model. We believe that this effect results from the strong affinity of dPGS10 to FN, which we observed by SPR measurements. As this concentration of dPGS10 already exhibits significant anticoagulant activity, further optimization of the polymers would be necessary to target FN in type 2 inflammation. In contrast, the potent effects of heparin, HS and polyglycerol sulfates on T cells arise in the ng/mL range, and the concentrations necessary for IL-13 reduction are comparable to those required for the novel small-molecule TSLPR inhibitor BP79, with its IC50 of 23 ng/mL for IL-13 reduction in CD4 + T-cells. The current clinically approved inhibitors of type 2 inflammation are JAK1 and JAK2 inhibitors, glucocorticoids and monoclonal antibodies targeting TSLP, IL5, IL-4/IL-13Ra, and IgE. While these drug classes offer a variety of therapy options for TH2-driven inflammation, further options are still