In an initial passive immunization study using wild-type CD1 mice, Mabs 8B4 (to mouse PrP residues 34-52) and 8H4 (to mouse PrP residues 175-185) given immediately after challenge with 139A scrapie by intraperitoneal (IP) injection (50 mg/week), resulted in a significant prolongation of the incubation period with 10% of the 8B4 treated animals remaining disease free in the group challenged with a lower dose of PrP Sc [10] . In another study using higher antibody doses (4000 mg/week IP) of either ICSM 18 (to mouse PrP residues 146-158) or ICSM 35 (to mouse residues 95 to 105), prion infection from a peripheral source was completely prevented if treatment was continued for 7 or 30 days immediately following PrP Sc challenge [9] . Furthermore, a transgenic mouse model that expresses Mab 6H4 is resistant to prion infection via IP injection by a mechanism that involves either perturbation of cellular PrP trafficking/PrP C degradation or disruption of the PrP C -PrP Sc interaction [49] .