Appeal No. 2001-0407 Page 10
Application No. 08/460,215
acceptable carrier such as phosphate buffered saline, saline,
deionized water, or the like. Typically, the compositions are added
to a retained physiological fluid such as blood or synovial fluid. The
amount administered will be empirically determined using routine
experimentation. Other additives, such as stabilizers, bactericides,
and the like, may be included in conventional amounts.
Pages 23-24. Appellants’ specification also concedes that the claimed method
would only 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; in this case,
increasing the gene dosage by supplementing with additional
normal copies of the PKD1 gene should correct the functional
defect.
Page 23 (emphasis added).
As the examiner correctly noted, the specification does not indicate what
form(s) of APKD are associated with such mutants, or even that such PKD1
mutants exist. See the Examiner’s Answer, page 7. Thus, the specification’s
“guidance” in this respect seems to be merely hopeful speculation: if the
mechanism by which PKD1 mutants cause APKD is similar to the mechanism by
which most recessive mutations cause disease, then APKD could be treated by
using gene therapy to supply additional functional PKD1 gene product. No
evidence in support of the speculative mechanism is provided.
Thus, the nature of the claimed method suggests that it is nonenabled,
because the claimed method is based on a mechanism that is at odds with the
observed inheritance pattern of the disease to be treated. Neither the prior art of
record nor any evidence disclosed in the specification supports an expectation
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