Appeal No. 2001-0407 Page 11
Application No. 08/460,215
that simply supplying more copies of a functional PKD1 gene would correct the
metabolic deficiency that results in APKD.
Thus, we agree with the examiner that the known pattern of dominant
inheritance of the APKD phenotype suggests that simply supplying more wild-
type protein would not be expected to provide an effective treatment. After all,
the dominant pattern of inheritance indicates that the disease manifests itself
even in the presence of the wild-type protein. We conclude that the examiner
has shown, by a preponderance of the evidence, that practicing the claimed
method would have required undue experimentation. The burden therefore
“shifts to the applicant to provide suitable proofs indicating that the specification
is indeed enabling.” In re Wright, 999 F.2d at 1562, 27 USPQ2d at 1513.
In response to the examiner’s rejection, Appellants have provided no
evidence supporting the specification’s statement that the claimed method would
be “feasible if a particular mutant PKD1 allele, when present in a single copy,
merely causes the level of the PKD1 protein to diminish below a threshold level
necessary for normal function.” Rather, Appellants cite in their brief numerous
scientific papers allegedly showing successful treatment of various disorders via
gene therapy. See page 5. Appellants also submitted a Supplemental Brief,
citing numerous additional references to the same effect. See Paper No. 22,
filed November 20, 1998.
This argument is not persuasive. First of all, most of the references cited
by Appellants were published after the effective filing date of the instant
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