NeuroMab™ Anti-ERBB2 Antibody(NRP-0422-P1225)

Figure 1 shows a competitive ligand binding assay comparing the displacement of125I-C5a by the humanized 7F3 antibody and mouse 7F3 from hC5aR on human neutrophils.

Figure 10 shows CD11b on neutrophils against PBS control after humanized anti-C5aR antibodies hAb-G or hAb-J or C5a were incubated with human whole blood for 20 minutes.

Figure 11 shows that hAb-Q (also known as anti-C5aR ab) by itself does not stimulate superoxide production by solid-phase bound human neutrophils, but in contrast triggers C5a production. It is a character who expresses acting skills.

Figure 12 is a graph showing disease progression in an inflammatory arthritis model. After intraperitoneal administration of 10 mg/kg anti-hC5aR antibodies G, M and N on day 5, reversal of K/BxN serum-induced inflammation in hC5aR knock-in mice (n = 6 per group) was the group mean clinical change in fractions.

Figure 13 is a graph showing disease progression in an inflammatory arthritis model. Mean clinical scores of K/BxN serum-induced inflammation reversal in hC5aR knock-in mice (n = 4-5 per group) after intraperitoneal administration of 1-10 mg/kg anti-hC5aR antibodies C and J on day 5.

Figure 14 shows occupied C5aR levels over time following in vivo administration of various doses of humanized anti-C5aR antibody, control antibody or PBS.

Figure 2 shows saturable binding of anti-C5aR antibody to human neutrophils at 4°C, plotted on the x-axis on a log 10 (upper panel) and linear (lower panel) scale.

Figure 3 shows humanized anti-C5aR mAbs hAb-J and Q or anti-C5aR mAb S5/1 (5 μg/g) against peptide PEP1 coated on ELISA plates at various dilutions. Figure 2 is a combination of diagrams | m1) representing the coupling.

Figure 4 shows a chemotaxis assay: migration of human neutrophils to 1 nM C5a in the presence of 5 μg/ml 7F3 and various humanized 7F3 antibodies.

Figure 5 shows the inhibition of C5a-driven migration of h5aR/L1.2 transfected cells by parental mouse antibody 7F3 and humanized antibodies J and Q.

Figure 6 shows that C5a-induced chemotaxis of human neutrophils was inhibited after pre-incubation with high concentration of humanized anti-C5aR antibody hAb-Q.

Figure 7 shows the inhibition of C5a-induced chemotaxis of human neutrophils by anti-C5aR antibodies hAb-Q (solid diamonds) and 7F3 (white squares). Mean (± standard error) results from 4 independent experiments are shown as the percentage of maximum migration (upper panel) or mean number of migrated cells (lower panel) for control samples without antibody. Units on the x-axis are log 10 Ab concentrations in μg/m1.

Figure 8 shows the inhibition of C5a-induced CD11b expression on human neutrophils pre-incubated with various concentrations of humanized anti-C5aR antibody hAb-Q.

Figure 9 shows CD11b on neutrophils after humanized anti-C5aR antibodies hAb-Q and hAb-J, PBS or granulocyte activator fMLP were incubated with human whole blood for 1 hour.