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. 2022 Aug 1;132(15):e157765. doi: 10.1172/JCI157765

Figure 1. Competitive inhibition against basophil degranulation and IgE-FcεRI interactions.

Figure 1

(A) As determined by CD63 expression on flow cytometry as a basophil activation marker, UB-221, omalizumab, and negative control (anti-Her2 trastuzumab mAb) do not activate isolated primary human basophils, while the positive control anti-IgE 5H2 antibody does. (B) In inhibition of FcԑRI-expressing RBL SX-38 cell degranulation induced by the ovalbumin-IgE (OVA-IgE) complex (mean ± SD, n = 6), UB-221 exhibits 7-fold greater inhibition over omalizumab (IC50: 0.14 vs. 0.94 μg/mL). The results are in line with higher potency in competitive inhibition of IgE-FcεRI interactions shown on ELISA and RBL SX-38 cells. (C) In a representative competitive inhibition assay on ELISA coated with FcεRI, UB-221 inhibits IgE binding with 8-fold greater potency over omalizumab (IC50: 26.1 vs. 214 ng/mL). (D) In competitive inhibition of IgE binding to FcεRI-expressing RBL SX-38 cells (mean ± SD, n = 3), UB-221 inhibits IgE binding with 3-fold greater potency over omalizumab (IC50: 0.035 vs. 0.106 μg/mL).