Appeal No. 1999-2330
Application No. 08/219,200
specification). There is no objective evidence that CD28Ig was tested in
this in vitro system or other experimental in vitro or in vivo systems that
would be predictive of the therapeutic methods encompassed by the
claims. There is insufficient objective evidence that accurately reflects the
relative efficiency of the claimed methods to inhibit T cell proliferation or to
prevent binding of CD28 receptor to B7 antigen, commensurate in scope
with the therapeutic methods encompassed by the claimed invention.
As evidentiary support for lack of enablement the examiner relies on Kahan for
establishing that no in vitro assay predicts or correlates with in vivo immuno-
suppressive efficacy. Answer, page 3. Blazar is relied on as teaching that issues such
as tissue distribution, half-life, affinity and avidity obtained with various CD28-B7-
specific reagents might prove to be highly important in achieving graft vs. host disease
(GVHD) protection. According to the examiner, Blazar discloses that anti-CD80 (B7-1)
or anti-CD86 (B7-2) antibodies were ineffective in preventing T cell CD8-mediated
GVHD lethality, that each antibody was partially effective in CD4-mediated GVHD and
that the combination of anti-CD80 and anti-CD86 antibodies were effective in
preventing GVHD lethality in murine experimental models. Id.
The examiner also relies on Perrin for the disclosure that, in contrast to the
effective treatment of disease with CTLA-4 Ig; anti-CD80 (B7-1) attenuated the first
clinical disease episode but not the relapse, anti-CD86 (B7-2) had no significant effect
on the course of disease, and the combined treatment with anti-CD80 plus anti-CD86
resulted in the exacerbation of disease. Id.
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