Mouse Anti-SCH Recombinant Antibody (clone SCH94.03) (CAT#: HPAB-0007-YJ)

Figure 1 Dose-response relationship between treatment with mAb 28-SCH94.03 and CNS remvelination: area of CNS remvelination (filled circle) and percentage of lesion area with remyelination (open circle) in animals treated with various doses of mAb SCH94.03.

Remyelination was quantitated. Data are the mean values of four or five animals per mAb dose, with the final cumulative dose indicated on the graph; SEM averaged 35% of the mean. There was no statistical difference assessed by one-way ANOVA in the number of demyelinated lesions or the area of demyelination between treatment groups, indicating similar extent of disease in all animals. The number of demyelinated lesions and area of lesions were 33.2 and 1.25 for the 1000 pg group, 3 1.8 and 1.11 for the 100 pg group, 23.8 and 0.54 for the 10 pg group, and 29.0 + 6.5 and 0.74 + 0.20 for the buffer only group (represented as the 0 dose point on the graph). Animals treated with 100 pg of control IgM (MOPC 104E) had remyelination scores similar to control animals treated with buffer only.

Miller, D. J., Sanborn, K. S., Katzmann, J. A., & Rodriguez, M. (1994). Monoclonal autoantibodies promote central nervous system repair in an animal model of multiple sclerosis. Journal of Neuroscience, 14(10), 6230-6238.

Figure 2 Western blot of TMEV proteins.

Lysates from infected L2 fibroblast cells were separated by SDS-PAGE, transferred to nitrocellulose, and blotted with SCH94.03 (lane I), SCH94.32 (lane 2), serum from susceptible mice chronically infected with TMEV (lane 3) and polyclonal rabbit anti-TMEV IgG (lane 4). Molecular weights are indicated on the left in kilodaltons. The position and identification of the major TMEV capsid proteins are indicated on the right. Western blot of lysates from control mock infected L2 cells showed single bands with the serum from chronically infected animals and the polyclonal rabbit anti-TMEV IgG at 32 and 43 kDa, respectively, but no reactivity with SCH94.03 or SCH94.32.

Miller, D. J., Sanborn, K. S., Katzmann, J. A., & Rodriguez, M. (1994). Monoclonal autoantibodies promote central nervous system repair in an animal model of multiple sclerosis. Journal of Neuroscience, 14(10), 6230-6238.

Figure 3 Indirect immunofluorescence of cultured glial cells.

The live surface staining of oligodendrocytes with SCH94.03.

Asakura, K., Miller, D. J., Pease, L. R., & Rodriguez, M. (1998). Targeting of IgMκ antibodies to oligodendrocytes promotes CNS remyelination. Journal of Neuroscience, 18(19), 7700-7708.

Figure 4 Surface staining of live, unfixed primary brain cultures of rat OLs by doublelabel immunofluorescence microscopy with SCH94.03

Asakura, K., Miller, D. J., Murray, K., Bansal, R., Pfeiffer, S. E., & Rodriguez, M. (1996). Monoclonal autoantibody SCH94. 03, which promotes central nervous system remyelination, recognizes an antigen on the surface of oligodendrocytes. Journal of neuroscience research, 43(3), 273-281.

Figure 5 Live cells growing in mixed primary glial cell cultures that were stained on the surface with SCH94.03 by the immunogold technique.

Asakura, K., Miller, D. J., Murray, K., Bansal, R., Pfeiffer, S. E., & Rodriguez, M. (1996). Monoclonal autoantibody SCH94. 03, which promotes central nervous system remyelination, recognizes an antigen on the surface of oligodendrocytes. Journal of neuroscience research, 43(3), 273-281.