Appeal No. 2002-1367 Page 3
Application No. 08/981,964
Kirsch is cited for describing a method for identifying sterol biosynthesis
inhibitors wherein a test compound is contacted with a host cell transformed with
a reporter construct. The rejection acknowledges that the methods of Kirsch
“differ from those claimed . . . only in that the sterol biosynthetic gene promoter of
the methods of Kirsch is that of the lanosterol 12-α-demethylase gene while the
promoter of the reporter construct of the claimed methods is that of the
acetoacetyl-CoA thiolase gene.” Examiner’s Answer, page 4.
Servouse is cited by the rejection for teaching
that acetoacetyl-CoA thiolase is the first enzyme of the ergosterol
biosynthesis pathway of yeast, that the activity of this enzyme is
induced by ergosterol starvation and repressed by ergosterol
excess and that the depression of activity in the presence of excess
sterol is likely due to reduced enzyme synthesis since there is no
detectable in vitro inhibition by ergosterol. As such one of ordinary
skill in the art would have reasonably expected that regulation of
acetoacetyl-CoA thiolase activity occurs at least in part by
regulation of the transcription of the acetoacetyl-CoA thiolase gene.
Id. at 4-5.
Dequin and Hiser are cited for teaching the nucleic acid sequence from
Saccharomyces encoding the acetoacetyl-CoA thiolase gene “which includes in
each case several hundred nucleotides of the region 5' to the coding sequence of
the gene which would be reasonably expected to contain the sequences
necessary for regulation of transcription of the gene.” Id. at 5.
The rejection concludes:
Therefore, it would have been obvious to one of ordinary skill
in the art to replace the lanosterol 14-α-demethylase gene
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