Ex Parte Krieger et al - Page 3


               Appeal No. 2006-1993                                                  Page 3                 
               Application No. 10/147,651                                                                   

               over claims 1-9 of U.S. Patent No. 6,437,215.  See Final Rejection, mailed March             
               16, 2005, page 2.  After careful review of the record and consideration of the               
               issues before us, we reverse the rejections under 35 U.S.C. § 112, first                     
               paragraph, and under 35 U.S.C. § 102(b).  Because appellants do not contest                  
               the obviousness-type double patenting rejection, see Appeal Brief, page 18, that             
               rejection is summarily affirmed.  Finally, we raise other issues that the examiner           
               may wish to address upon return of the application.                                          
                                              BACKGROUND                                                    
                      “The present invention is generally in the area of transgenic animal                  
               models of atherosclerosis, methods for screening for inhibitors acting via                   
               interaction with the SR-BI scavenger receptor, and compositions obtained                     
               thereby.”  Specification, page 1.  “SR-BI might play a major role in transfer of             
               cholesterol from peripheral tissues, via HDL, into the liver and steroidogenic               
               tissues, and that increased or decreased expression in the liver or other tissues            
               may be useful in regulating uptake of cholesterol by cells expressing SR-BI,                 
               thereby decreasing levels in foam cells and deposition at sites involved in                  
               atherogenesis.”  Id. at 6-7.                                                                 
                      According to the summary of the invention,                                            
                            Transgenic animals that do not express functional SR-BI and                     
                      ApoE develop severe atherosclerosis, by age four weeks in                             
                      transgenic mice.  Moreover, these animals exhibit progressive heart                   
                      dysfunction starting by age four-six weeks, and die by age nine                       
                      weeks.  Pathology shows extensive fibrosis of the heart and                           
                      occlusion of coronary arteries.  The occlusion appears to be due to                   
                      atherosclerosis, since fat deposition is in the walls.  These animals                 
                      are good models for the following diseases, and for screening of                      
                      drugs useful in the treatment and/or prevention of these disorders:                   





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