Appeal 2007-1040
Application 09/960,708
considered to be inherent in the prior art methods” (Answer 3, alteration
original). We disagree.
We understand the Examiner’s argument to be that since
“[a]ngiogenesis is an early event in the development of chemically induced
skin tumors” (Bolontrade title), by inhibiting tumor formation Jiang’s
method inherently results in the inhibition of angiogenesis/vascular
development. The problem with the Examiner’s rationale is that the method
of claims 8-11, 15-18, 35, 37, 39, 40, and 44 require the systemic
administration of a Ca2+/calcineurin/NF-ATc inhibitory agent (e.g.,
FK506). Jiang teaches that systemic administration of immunosuppressants,
such as FK506 and cyclosporin A, “promotes carcinogenesis in parallel with
the suppression of T cell functions” (Jiang 69, col. 2, ll. 49-51). Therefore,
the inherency argument relied upon by the Examiner is directly refuted by
the express teachings in Jiang. In contrast, Jiang teaches that it is the topical
administration of FK506 that resulted in the inhibition of tumor formation
(Jiang 67: abstract).
For the foregoing reasons we reverse the rejection of claims 8-11,
15-18, 35, 37, 39, 40, and 44 under 35 U.S.C. § 102(b) as anticipated by
Jiang.
OBVIOUSNESS:
Claims 36-44, 46, and 47 stand rejected under 35 U.S.C. § 103 as
being unpatentable over the combination of Jiang and Flanagan.
According to the Examiner, since the prior art “teaches the
interchangeable use of [c]yclosporin A and Fk506 and rapamycin based on
their biological properties . . . [a person of ordinary skill in the art at the time
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