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. 2017 Jun 9;9(6):945–958. doi: 10.1080/19420862.2017.1336592

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© 2017 The Author(s). Published with license by Taylor & Francis Group, LLC

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

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Figure 7. — Functional characterization of ACT017 in vitro. (A) Isotherm binding curve of ACT017 to immobilized GPVI-Fc. (B) Inhibition of GPVI-Fc binding to immobilized collagen by increasing concentrations of ACT017. (C) In vitro binding of ACT017 conjugated to Alexa488 to human platelets analyzed by flow cytometry (red: whole blood; black: PRP). (D) Typical residual platelet aggregation as the ratio of the response in the presence of ACT017 to the response without ACT017 as a function of ACT017 concentration (Black: residual intensity, Gray: residual velocity). The insert shows a typical aggregation curve obtained after pre-incubation of human PRP with increasing concentrations of ACT017 (0–10 μg/mL).