NeuroMab™ Anti-GDNF BBB Shuttle Antibody, Clone HIRmAb

Figure 1. Reduced (left) and non-reduced (right) sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) of chimeric HIRMAb and fusion proteins.

Figure 2 (left panel) Western blot using anti-human IgG primary antibody. (Right panel) Western blot using an anti-human BDNF antibody reactive with the fusion protein or BDNF, but not with the chimeric HIRMAb.

Figure 3 Binding of chimeric HIRMAb or fusion protein replacing [125l]-labeled murine HIRMAb to HIR ECD.

Figure 4 Pharmacokinetics and brain uptake of the fusion protein in adult rhesus monkeys.

Figure 5 Reduced SDS-PAGE and Coomassie blue staining of protein A affinity-purified COS cell chimeric HIRMAb and HIRMAb-GDNF fusion protein.

Figure 6. Binding of COS cell-derived chimeric HIRMAb or HIRMAb-GDNF fusion protein to the extracellular domain (ECD) of HIR is saturable.

Figure 7 Both GDNF and COS cell-derived HIRMAb-GDNF fusion proteins activate luciferase gene expression in a saturable manner

Figure 8 Effect of intracerebral injection of HIRMAb-GDNF and normal saline on stroke volume in rats. serial drama

Figure 9 Western blot using primary antibodies against human IgG (A) or human GDNF (B).

Figure 10 The binding affinity of CHO-derived HIRMAb and CHO-derived HIRMAb-GDNF fusion protein to the extracellular domain of human insulin receptor (HIR) was measured in this ELISA format.

Figure 11 Native polyacrylamide gel electrophoresis of HIRMAb, control human IgG1, or HIRMAb-GDNF fusion protein shows the absence of aggregates in the CHO-derived fusion protein.

Figure 12 Binding of 3H-HIRMAb-GDNF fusion protein to isolated brain capillaries was inhibited by murine HIRMAb.

The HIRMAb-GDNF component of capillary uptake resistant to HIRMAb inhibition represents an endocytic fusion protein.