Appeal 2006-2644
Application 10/047,945
diseases and (4) Asthma. It was revealed that the level of IgE
in patients of these disorders is several times higher than the
control normal individuals. . . .
We also found that high levels of IgE caused disruption in the
homeostasis of endogenously present other proteins such as
nerve growth factor, myoglobin, insulin and Adenosine
deaminase. We believe that such disruption in homeostasis for
NGF, myoglobin, insulin and ADA may be manifesting the
symptoms for these disorders.
(Specification 4: 12-21.) The Specification also states that “in humans oral
administration of . . . LT-10 lowers IgE level. We further demonstrated that
by lowering the IgE level, other proteins such as NGF, myoglobin, insulin
and ADA [are]returned to their normal homeostasis” (id. at 5: 9-12).
Thus, as we understand it, the Specification teaches that an elevated
level of IgE disrupts the homeostasis of certain other proteins, leading to the
symptoms associated with disorders such as asthma and diabetes and that
“lowering the IgE level” returns those other proteins to their normal
homeostasis. Notably, the Specification does not state that IgE and LT-10
form a complex that no longer interferes with the homeostasis of NGF,
myoglobin, etc.; rather, the Specification states that “LT-10 lowers IgE level
. . . [and] by lowering the IgE level, other proteins . . . [are] returned to their
normal homeostasis” (emphases added).
Finally, Table 4 does not support Appellants’ claim interpretation.
Table 4 is headed “IgE levels in saliva” (Specification 15: 1); the
Specification concludes that “Glucotrol treatment does not contribute in
lowering IgE levels. It is the LT-10 treatment which causes the lowering of
IgE” (id. at 15: 16-18). The comparison of the Glucotrol and LT-10 results
shows that the experiment was not measuring LT-10-bound IgE versus non-
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