Appeal 2007-1614
Application 09/779,447
glycosylation by tunicamycin and the disruption of vascular proliferation or
angiogenesis. Tiganis teaches that the inhibition of glycoproteins by
tunicamycin impairs the cell adhesion and the functional properties of the
endothelial lining of the [blood] vessels” (id.).
From these teachings, the Examiner reasons that “if tunicamycin is a
potent inhibitor of N-glycosylation and . . . this inhibition disrupts [the
endothelial cell proliferation required for] . . . angiogenesis, there is clearly
a reasonable expectation of success in the use of tunicamycin as an agent
which would inhibit angiogenesis” (id.). The Examiner states that a “person
of ordinary skill in the art would have been motivated to use a pyrimidine
nucleoside such as tunicamycin given the prior art’s recognition of
tunicamycin as an inhibitor of the pathway leading to the angiogenic process
of capillary endothelial cell proliferation” (id. at 4). The Examiner
concludes that the dosage regimen recited in the claims “is not patentable
given that one of skill in the art practicing the administration of any medical
compound determines the optimum dosage for each patient, based on a
variety of physical and metabolic factors” (id.).
Appellants argue that the Examiner has “fail[ed] to establish a prima
facie case of obviousness” (Br. 6).2 Specifically, Appellants argue that
Banerjee “nowhere teaches or even remotely suggests that tunicamycin
could be administered to a human patient to inhibit angiogenesis” (id.).
Appellants urge that Tiganis teaches that the administration of tunicamycin
“would cause damage to brain tissue. Given this expected side effect,
Tiganis . . . in no way suggests that tunicamycin be administered to a human
2 Appeal Brief filed November 2, 2006.
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