Appeal No. 1999-1245
Application No. 08/245,282
matter and reveal a reasonable expectation of success to one reasonably skilled in the
art.
The examiner argues in the Final Rejection (Paper No.13, page 4), that
“Vandenberghe teaches that herbimycin A inhibits a protein tyrosine kinase and one of
skill would expect that inhibition of protein kinase would affect the PI 3-kinase and
ultimately the D3 phosphoinositide production.” If this is the examiner’s position, it
remains that the examiner establish, with appropriate evidence, that the inhibitor of
tyrosine kinase described by Vandenberghe would have the same specificity, and also
act on PI 3-kinase. Appellant’s specification, page 6, lines 34-35 would appear to
distinguish between inhibitors of PI 3-kinase and inhibitors of tyrosine kinase activity,
such as herbimycin A. However, if the examiner’s supposition is correct regarding the
ability of herbimycin A to inhibit PI 3-kinase, Vandenberghe would appear to anticipate
claim 1.3
At best, the statement of the rejection establishes that individual parts of the
claimed invention were known in the prior art. Okada describe the role of PI3K in
insulin induced glucose transport and antilipolisis in rat adipocytes but does not address
T-cell activation. Ward 1993 would appear to suggest that activation of PI3K and
subsequent D-3 lipid metabolism may be important signaling events in CD-28 mediated
3 Note that the specification, page 9, line 34, indicates that a phorbol ester
(PMA) stimulates a T cell. Vandenberghe, page 953, column 1, would appear to
suggest that herbimycin A inhibits PMA stimulation.
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