Figure 1.
Effects of ibrutinib, acalabrutinib (ACP-196), and ONO/GS-4059 on static platelet aggregation in blood stimulated by plaque, collagen, TRAP, ADP and AA. Blood samples were incubated for 15 minutes with solvent (DMSO, 0.1%) or Btk inhibitors before stimulation for 10 minutes with plaque (833 µg/mL), collagen (0.1-0.3 µg/mL), TRAP (5 µM), ADP (5µM), AA (0.6 mM), or buffer (no stimulus). Left panels: dose-response curves of ibrutinib (A), acalabrutinib (ACP-196) (B), and ONO/GS-4059 (C) on plaque-induced platelet aggregation. Right panels: effects of ibrutinib (1 µM) (A), ACP-196 (2 µM) (B), and ONO/GS-4059 (2 µM) (C) on plaque-, collagen-, TRAP-, ADP-, and AA-induced platelet aggregation and spontaneous platelet aggregation (no stimulus). Data are mean ± SD (n = 5). *P < .05, **P < .01, ***P < .001, ****P < .0001.

Effects of ibrutinib, acalabrutinib (ACP-196), and ONO/GS-4059 on static platelet aggregation in blood stimulated by plaque, collagen, TRAP, ADP and AA. Blood samples were incubated for 15 minutes with solvent (DMSO, 0.1%) or Btk inhibitors before stimulation for 10 minutes with plaque (833 µg/mL), collagen (0.1-0.3 µg/mL), TRAP (5 µM), ADP (5µM), AA (0.6 mM), or buffer (no stimulus). Left panels: dose-response curves of ibrutinib (A), acalabrutinib (ACP-196) (B), and ONO/GS-4059 (C) on plaque-induced platelet aggregation. Right panels: effects of ibrutinib (1 µM) (A), ACP-196 (2 µM) (B), and ONO/GS-4059 (2 µM) (C) on plaque-, collagen-, TRAP-, ADP-, and AA-induced platelet aggregation and spontaneous platelet aggregation (no stimulus). Data are mean ± SD (n = 5). *P < .05, **P < .01, ***P < .001, ****P < .0001.

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