Appeal 2007-1068
Application 10/015,394
“PRO1760 scored positive as [an] inhibitor of glucose or FFA (free fatty
acid) uptake in rat adipocyte cells” (id. at 4), but argues that the
Specification does not explain how PRO1760 would be useful in treating
diabetes, obesity, hyper- or hypo-insulinemia, as asserted in the
Specification, “because in these conditions little or no glucose is entering the
cells to begin with” (id.). Rather, the Examiner argues, “one skilled in the
art would want to enhance glucose uptake” in these conditions (id. at 7).
Appellants argue that “[t]he fact that PRO1760 inhibits glucose
uptake does not make it useless in such treatment. One of skill in the art
would readily understand that a protein which inhibits glucose uptake into
adipocytes is a useful therapeutic target, since blocking the function of this
protein would decrease the inhibition, and thus increase glucose uptake into
adipocytes” (Brief 4, emphasis in original). Appellants argue that “[o]ne of
skill in the art would further understand that antagonists to the PRO1760
polypeptide include antibodies, such as the claimed antibodies which
specifically bind the PRO1760 polypeptide” (id.).
This argument does not persuade us that the Examiner’s rejection
should be reversed. To satisfy the requirements of § 101, a utility must be
one that makes the invention useful to the public in its current form, not
potentially useful in the future after further research. See Fisher, 421 F.3d at
1370, 76 USPQ2d at 1230. While it might be reasonable to infer that a
given stimulator of glucose uptake would enhance glucose uptake in
diabetes, obesity, hyper- and hypo-insulinemia, even if the stimulator had no
specific role in any of those conditions, it does not follow that blocking the
activity of a glucose uptake inhibitor would enhance glucose uptake - unless
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