CD47- and CD36-binding peptides antagonize the NO delay in platelet aggregation. Washed human platelets (2 × 10⁵ platelets/μL) were incubated in Tyrode buffer in the presence of thrombin (0.2 U/mL) and exogenous NO (DEA/NO 10 μM) for 5 minutes. Peptide sequences were derived from relevant domains of TSP1 including 7N3 (FIRVVMYEGKK, 10 μM) and control peptides p604 (FIRGGMYEGKK, 10 μM) and p605 (FIRVAIYEGKK, 10 μM, A), and p7N3 (0.1-10 μM, B), and absorbance was determined under high shear, or p459 (4N1–1, RFYVVMWK, 10 μM, C) and 4N1K (KRFYVVMWKK, 10 μM, D), and absorbance was determined under low shear conditions. Washed human platelets in Tyrode buffer (2 × 10⁵ platelets/μL) were incubated in the presence of thrombin (0.2 U/mL) and exogenous NO (DEA/NO 10 μM) for 5 minutes. Peptide sequences were derived from TSP1, including p7N3 and p907 (GDGV[D-I]TRIR, E) (10 μM) and aggregation was determined under high shear, and p906 (VTAGGGVQKRSRL, F; 10 μM) and p246 (KRFKQDGGWSHWSPWSS, G; 10 μM), and absorbance was measured under low shear. Human platelets were pretreated with TSP1-based peptides p907 and p7N3 (10 μM) before adding DEA/NO (10 μM), and cGMP levels were determined (H). Data are representative of at least 3 experiments (A-G). Results are the mean (± SD) of at least 3 experiments (H).