Ex Parte Tzipori et al - Page 14

                  Appeal  2006-2945                                                                                            
                  Application 10/041,958                                                                                       
                  A10.  Perera makes “no mention of therapy other than to note that the                                        
                  [S]higa like toxins may play a role in disease ‘although no direct proof for                                 
                  the involvement of SLTs in pathogenesis has yet been demonstrated’” (Br.                                     
                  18-19; Reply Br. 8).                                                                                         
                          We agree that Perera makes no mention of therapy, and recognizes                                     
                  that SLTs’ involvement in disease was unknown as of the 1988 publication                                     
                  date of the reference (Perera, page 2130, col. 2, ll. 21-25).  We are, however,                              
                  not persuaded that Perera’s acknowledgement of the state of the art in 1988                                  
                  has any effect on the combination of references as relied upon by the                                        
                  Examiner which in combination teach the use of human or humanized                                            
                  antibodies to SLT II, SLT II α-subunit, or β-SLT II subunit for the treatment                                
                  of HUS in a human.                                                                                           

                  A11.  Perera teaches “that none of the antibodies reactive only with Stx2                                    
                  could be used to detect organisms; antibodies to Stx2 which were effective                                   
                  were only able to be used to detect organisms producing both Stx1 and Stx2.                                  
                  Accordingly, one would not be led by Perera to use these antibodies in                                       
                  therapy, nor one would [sic] have a reasonable expectation of success using                                  
                  just an antibody to Stx2, much less to a single subunit of Stx2” (Br. 19).                                   
                          There is no requirement in claim 26 that the antibodies detect an                                    
                  organism.  Accordingly, we are not persuaded by Appellants’ assertion.                                       
                          Further Appellants’ assertion appears to be based on a                                               
                  misinterpretation of Perera.  According to Perera, the “E. coli strains used in                              
                  this study included clinical isolates from humans with diarrhea, hemorrhagic                                 
                  colitis, or hemolytic-uremic syndrome, calves with diarrhea, and pigs with                                   
                  edema disease. . .” (Perera, page 2127, col. 2, ll. 5-8).  Of the 10 SLT II                                  

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