Figure 4
Figure 4. Biocompatibility of UHRAs compared with other polyP inhibitors. (A) The ability of UHRA compounds, protamine, and PEI (tested at 1 or 2 mg/mL) to activate complement in human serum was measured by sheep erythrocyte complement consumption assay. Heat-aggregated human immunoglobulin G (IgG; 1 mg/mL) and PBS were the positive and negative controls, respectively. UHRAs did not activate complement compared with buffer controls, whereas protamine and PEI showed high levels of complement activation. (B) The ability of UHRA compounds, protamine, and PEI (tested at 1 and 2 mg/mL) to activate platelets in human PRP was measured by flow cytometry for expression of platelet activation marker CD62P. Bovine thrombin (at 1 IU/mL) was used as the positive control, and PBS alone was used as the negative control (buffer control). UHRAs showed low levels of platelet activation compared with PEI. +ve, positive.

Biocompatibility of UHRAs compared with other polyP inhibitors. (A) The ability of UHRA compounds, protamine, and PEI (tested at 1 or 2 mg/mL) to activate complement in human serum was measured by sheep erythrocyte complement consumption assay. Heat-aggregated human immunoglobulin G (IgG; 1 mg/mL) and PBS were the positive and negative controls, respectively. UHRAs did not activate complement compared with buffer controls, whereas protamine and PEI showed high levels of complement activation. (B) The ability of UHRA compounds, protamine, and PEI (tested at 1 and 2 mg/mL) to activate platelets in human PRP was measured by flow cytometry for expression of platelet activation marker CD62P. Bovine thrombin (at 1 IU/mL) was used as the positive control, and PBS alone was used as the negative control (buffer control). UHRAs showed low levels of platelet activation compared with PEI. +ve, positive.

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