Appeal 2007-1068
Application 10/015,394
other than anaerobic lactate production, possibly oxidation or lipogenesis”
(Mueller II 530, col. 2), “[r]ather than glucose uptake per se” (id. at 531, col.
1), based on “the multiple known biological actions of vanadium” (id. at
537, col. 2).
Similarly, Mueller I teaches that “[t]he competitive inhibition [of
leptin secretion] produced by 2-DG could be reversed by the addition of a
high concentration of glucose, suggesting that 2-DG did not inhibit leptin
secretion via a nonspecific toxic effect” (Mueller I 557, col. 1), while “the
inhibition by phloretin was not reversed by glucose, as phloretin is not a
competitive inhibitor” (id.).
Appellants have not explained how the observation that PRO1760
inhibits glucose uptake in adipocytes, with nothing more, is useful in
investigating leptin regulation - especially as the evidence of record shows
that leptin secretion can be inhibited by both inhibitors and stimulators of
glucose uptake. That being the case, the mere identification of PRO1760 as
a glucose uptake inhibitor does not provide a specific, well-defined, and
particular benefit with respect to investigating leptin regulation.
We therefore conclude that neither the Specification’s disclosure, nor
the extrinsic evidence relied on by Appellants, satisfies the utility
requirement of 35 U.S.C. § 101 with respect to PRO1760, or antibodies that
specifically bind it. The rejections of claims 28-35 and 38-40 under
35 U.S.C. §§ 101 and 112, first paragraph, are affirmed.
7
Page: Previous 1 2 3 4 5 6 7 8 Next
Last modified: September 9, 2013