Fig. 4.
Fig. 4. Time course of ancrod treatment of all 12 subjects (mean, SD, 95th percentile). / (A) DesA-profibrin; (B) desAA-fibrin; (C) Mab 2B5-aFDP-D ELISA. Release of one fibrinopeptide A from fibrinogen results in the formation of desA-profibrin. DesA-profibrin is detected by combining an antibody against the neo–N-terminus of the fibrin α-chain (MAb 2B5) with an antibody against fibrinopeptide A. Infusion of ancrod results in an increase in desA-profibrin in plasma, followed by a gradual decrease, and a more shallow second peak. At increasing plasma concentrations of ancrod, less desA-profibrin is generated in favor of desAA-fibrin. The Mab 2B5 epitope appears to be accessible without KSCN sample pretreatment, as exemplified by the result of the ELISA system combining MAb 2B5 with an antibody against the fibrin(ogen) D-domain, using native samples without KSCN sample pretreatment.

Time course of ancrod treatment of all 12 subjects (mean, SD, 95th percentile).

(A) DesA-profibrin; (B) desAA-fibrin; (C) Mab 2B5-aFDP-D ELISA. Release of one fibrinopeptide A from fibrinogen results in the formation of desA-profibrin. DesA-profibrin is detected by combining an antibody against the neo–N-terminus of the fibrin α-chain (MAb 2B5) with an antibody against fibrinopeptide A. Infusion of ancrod results in an increase in desA-profibrin in plasma, followed by a gradual decrease, and a more shallow second peak. At increasing plasma concentrations of ancrod, less desA-profibrin is generated in favor of desAA-fibrin. The Mab 2B5 epitope appears to be accessible without KSCN sample pretreatment, as exemplified by the result of the ELISA system combining MAb 2B5 with an antibody against the fibrin(ogen) D-domain, using native samples without KSCN sample pretreatment.

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