Figure 1.

Inhibitory properties of glenzocimab. (A) Glenzocimab inhibits collagen-induced platelet activation. Washed human platelets were preincubated with glenzocimab or the 3J24 Fab (50 μg.mL⁻¹) before activation was triggered by the addition of collagen (25 μg.mL⁻¹) during 15 minutes at room temperature. Exposure of P-selectin was assessed by flow cytometry using a fluorescein isothiocyanate-coupled anti–P-selectin. Mean fluorescence intensities are shown. Data are the mean ± SD of 3 experiments made in triplicate. Statistical analysis was performed using one-way analysis of variance followed by a Tukey multiple comparisons test; ∗∗∗P < .001. (B) Glenzocimab inhibits GPVI dimerization and clustering. Box plot showing the effect of glenzocimab (50 μg.mL⁻¹) on the molecular brightness (cpm s⁻¹) of GPVI-eGFP alongside the molecular brightness (cpm s⁻¹) of monomeric CD86-eGFP and dimeric CD28-eGFP control receptors in transfected HEK293T cells. For all box plots, center lines represent the median; box limits indicate the 25th and 75th percentiles and whiskers extend to minimum and maximum points. Significance was measured with Kruskal-Wallis with a Dunn post-hoc test in which P ≤ .05. FCS measurements were taken in 35 to 49 cells from 3 independent experiments. (C) Glenzocimab inhibits fibrin-induced platelet aggregation. Washed human platelets were preincubated with vehicle (red curve), 9μM eptifibatide (green curve), or glenzocimab (50 μg.mL⁻¹) before aggregation was initiated by the addition of a solubilized fibrin (200 μg.mL⁻¹). NS, not significant; SD, standard deviation.