Ex parte KAMBOJ et al.; Ex parte FOLDES et al. - Page 12


                  Appeal No.  1999-2200                                                                                         
                  Application No.  08/896,063                                                                                   
                  GROUNDS OF REJECTION29                                                                                        

                          Claims 23, 25, 26, 37, 39, and 43-45 are rejected under 35 U.S.C.                                    
                  103(a) as being unpatentable over Heinemann in view of Bettler ‘90, Sommer ‘92,                               
                  Puckett and Birnbaumer.                                                                                       
                          We reverse.                                                                                           
                  The rejection under 35 U.S.C.  103(a):                                                                       
                          According to the examiner (Answer30, page 6):                                                         

                                 It would have been obvious to one of ordinary skill in the art at                              
                          the time the invention was made to isolate a human homolog of the rat                                 
                          GluR5-231 sequence disclosed by Bettler [‘90] from a human cDNA                                       
                          library, employing PCR amplification according to Puckett32, and                                      
                          therewith to assay candidate agonists or antagonists of the human                                     
                          receptor, according to Heinemann, because Bettler [‘90] teaches that                                  
                          GluR5 has properties unique among the known glutamate receptors                                       
                          (page 583, col. 2), because Puckett advocates the cloning of human                                    
                          glutamate receptor genes in order to delimit their postulated                                         
                          relationships to a variety of serious pathological conditions, and                                    
                                                                                                                                
                  29 We note the Answer contains a single new grounds of rejection over all appealed                            
                  claims.  This new grounds of rejection was made to incorporate Sommer ‘92 (cited                              
                  by the examiner (Answer, page 4) as new prior art) into the statement of the                                  
                  rejection.                                                                                                    
                  30 Paper No. 23, mailed March 4, 1997,                                                                        
                  31 The examiner states (Answer, page 5) that the GluR5-2 cDNA exhibits 86%                                    
                  residue identify with appellants’ EAA3a SEQ ID NO:1 at the DNA level and the                                  
                  predicted translation products are 98% identical.  The examiner continues that the                            
                  identity between the rat clone of EAA3b is substantially equivalent to EAA3a except                           
                  that it differs at only a single nucleotide, resulting in a change at a single amino acid.                    
                  32 The examiner states (Answer, page 5) “Puckett discloses the cloning of a human                             
                  kainate-binding glutamate receptor, GluHI, which was obtained by PCR                                          
                  amplification using primers derived from the published GluR1 sequence.” The                                   
                  examiner states (Answer, page 14) that “Puckett evidences that PCR was a routine                              
                  and predictable procedure for the retrieval of homologous clones from mammalian                               
                  cDNA libraries.“  Puckett does not teach the isolation of GluR1 by use of PCR.                                
                  Puckett teaches the amplification of a probe [Puckett, page 7557, column 2 and                                
                  page 7558, Results, column 1] which is then used to screen a cDNA library under                               
                  reduced stringency hybridization [Puckett, bridging paragraphs, pages 7557-7558                               
                  and page 7558, Results, column 1].                                                                            

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