Appeal 2007-1068
Application 10/015,394
the inhibitor is involved in the decreased uptake seen in those conditions in
the first place. In the absence of any evidence that PRO1760 is involved in
the decreased glucose uptake seen in diabetes, obesity, hyper- or hypo-
insulinemia, the purely hypothetical possibility that blocking its inhibitory
activity with antibodies might be useful in treating any of these conditions is
too tenuous to establish “a significant and presently available benefit to the
public” (Fisher, 421 F.3d at 1371, 76 USPQ2d at 1230).
Relying on Mueller I1 and Mueller II2 as evidence, Appellants also
argue that “PRO1760, as an inhibitor of adipocyte glucose uptake, . . . has
utility as a pharmacological tool for investigation of leptin regulation” (Brief
4), just like other inhibitors of glucose uptake “already known and used in
the art such as 2-DG [(2-deoxy-D-glucose)], phloretin, and cytocholasin B”
(id.), as well as stimulators like metformin and vanadium (id.).
We do not find this argument persuasive either. As both Mueller
references make clear, all of these inhibitors and stimulators inhibited leptin
secretion under assay conditions (Mueller I 557, col. 1; Mueller II 530, col.
2), and their usefulness as pharmacological tools in investigating leptin
regulation depends upon an understanding of their mechanisms of action.
For example, Mueller II suggests that “the effect of glucose utilization to
stimulate leptin production involves the metabolism of glucose to a fate
1 W.M. Mueller et al., “Evidence That Glucose Metabolism Regulates
Leptin Secretion from Cultured Rat Adipocytes,” Endocrinology, Vol. 139,
No. 2, pp. 551-558 (1998), made of record January 10, 2005.
2 W.M. Mueller et al., “Effects of Metformin and Vanadium on Leptin
Secretion from Cultured Rat Adipocytes,” Obesity Research, Vol. 8, No. 7,
pp. 530-539 (October 2000), made of record January 10, 2005.
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