Appeal No. 1999-1245
Application No. 08/245,282
then be used to inhibit or stimulate T cell responses. Such screening assays, once
identified, can be routinely used by those of ordinary skill in the art to screen
compounds for activity. The examiner has advanced no specific reasoning as to why
the compound screening assays outlined in the specification would be unsuccessful in
identifying other similar agents, which can act as inhibitors of PI3K.
In addition, appellant argues, citing examples 2 and 5 of the specification, that
appellant’s specification shows that treatment of T-cells according to the methods of the
invention (e.g., using a phosphatidylinositol 3-kinase inhibitor) inhibits T-cell responses
such as the production of D-3 phosphatidylinositides or cytokine product, e.g.,
interleukin-2, and cell proliferation induced by CD28 ligation in vitro. Brief, page 9.
More specifically, the specification teaches methods for modulating T-cell response in,
for example, a subject suffering from an autoimmune disease or other disorder
associated with an abnormal immune response, or a transplant recipient. Such
methods as taught in the specification starting on page 8, line 31, include the
administration of an agent which modulates production of D-3 phosphoinositides at a
dose for a period of time sufficient to induce T-cell unresponsiveness. Brief, page 9.
It is appellant's position that successful in vitro testing for a particular
inhibitory/therapeutic activity in an accepted in vivo model establishes a significant
probability that in vivo testing for this particular inhibitory and/or therapeutic activity will
be successful. Appellant offers Sato, a publication after his filing date, as evidence that
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