Ex Parte Morikawa et al - Page 8


                 Appeal No. 2006-3200                                                         Page 8                  
                 Application No.  10/196,428                                                                          
                 rheumatoid arthritis.  Brief, page 7, Luchetti “show[s] a correlation between                        
                 elevated PTX3 gene expression and rheumatoid arthritis. . . .”  Therefore, the                       
                 evidence of record supports the finding that Chao’s rheumatoid arthritis patient                     
                 population is the same as the patient population in Appellants’ claimed invention.                   
                 In this regard, we remind Appellants that “[i]t is a general rule that merely                        
                 discovering and claiming a new benefit of an old process cannot render the                           
                 process again patentable.”  In re Woodruff, 919 F.2d 1575, 1578, 16 USPQ2d                           
                 1934, 1936 (Fed. Cir. 1990).  On this record, Appellants have simply discovered                      
                 that by practicing Chao’s method of treating rheumatoid arthritis patients with a                    
                 composition comprising an HMG-CoA reductase suppressor, such as                                      
                 pravastatin, PTX3 gene expression is suppressed.  At best, Appellants have                           
                 recognized the underlying mechanism through which Chao’s method operates.                            
                 See e.g., Specification, page 2,                                                                     
                        [The] PTX3 gene is constantly expressed in synovial cells of a                                
                        rheumatoid arthritis patient and [ ] this expression is suppressed by                         
                        inte[r]feron-γ (IFN-γ) or transforming growth factor-β (TGF-β) . . . .                        
                        Moreover, PTX3 also takes part in a disorder via a complement                                 
                        pathway in an autoimmune disease, especially rheumatoid arthritis,                            
                        because it binds to C1q, one of complement components, to                                     
                        activate the complement pathway . . . .                                                       
                               Suppression of PTX3 gene expression, therefore,                                        
                        suppresses worsening of an autoimmune disease, especially                                     
                        rheumatoid arthritis and further, results in its treatment.                                   
                 In our opinion, the evidence of record does not support Appellants’ assertion that                   
                 the discovery of the underlying mechanism through which Chao’s method                                
                 operates, or the new benefit of Chao’s method is nonobvious in view of the                           
                 combination of prior art relied upon.                                                                







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