Ameliorative effects and adverse events caused by 17C02-based molecules and 3G8 in an antibody-mediated model of ITP. FcγR-humanized mice were treated with an IV administration of either deglycosylated full-length 17C02 or deglycosylated full-length 3G8 (81 μg/mouse; 540 μM/mouse), 17C02-albumin (50 μg/mouse; 540 μM/mouse), deglycosylated full-length IgG1 and IgG2 isotype controls (81 μg/mouse; 540 μM/mouse), or albumin alone (35.1 μg/mouse; 540 μM/mouse). (A) Decreases in rectal temperature were evaluated as an indicator of an inflammatory adverse event comparing 0-minute (pretreatment) with 15-, 30-, and 45-minute posttreatment conditions. Data are presented as mean ± standard deviation (n = 5-7). The statistical analysis was performed by a 2-way ANOVA and Sidak multiple comparisons test (∗∗∗P < .001). (B) ITP was then induced in mice with 15 μL of a rabbit antiplatelet serum 2 hours after the anti-FcγRIIIA therapeutic intervention. Additional mice were either left untreated (Untreated) or treated with the antiplatelet serum alone (Nil) as comparative controls. Data are presented as mean ± standard deviation (n = 6). The statistical analysis was performed by a 1-way ANOVA and Tukey multiple comparisons test (∗∗∗P < .001). (C) The ability of FcγRIIIA-blocking reagents and controls to directly induce thrombocytopenia (as an adverse event) was evaluated 2 hours after treatment. The antiplatelet serum alone (15 μL/mouse) was used as a positive control. Deglycosylated mouse IgG1 (degly-mIgG1) and IgG2a (degly-mIgG2a) isotype controls were used as negative controls for amelioration. Data are presented as mean ± standard deviation (n = 5). The statistical analysis was performed using Kruskal-Wallis and Dunn multiple comparison test (∗P < .05; ∗∗P < .01).