Appeal 2007-1139
Application 10/052,664
“[a] utility for Npt2B cannot be assigned without knowledge of what disease
is associated with Npt2B dysfunction or what drugs/ligands affect Npt2B
function.” (Id. at 22-23.)
We disagree. First, the Declaration followed the procedures set forth
in the Specification and is used to substantiate the utility set forth in the
Specification, and not to establish a utility. See In re Brana, 51 F.3d 1560,
1566, 34 USPQ2d 1436, 1441 (Fed. Cir. 1995). The Specification clearly
states that the Npt2B polypeptide is a co-transporter of sodium cation and
phosphate anions and is expressed, among other locations, on the surface of
intestinal epithelial cells, i.e. on the apical or intestinal luminal side of the
epithelial cells, providing for the transport of sodium and phosphate ions
from the intestinal lumen into the intestinal epithelial cells. The
Specification also characterizes the polypeptide as a type II transporter. The
Examiner has not brought forth any evidence or argument as to why one
skilled in the art would not find credible the asserted function of the Npt2B
polypeptide beyond relying on evidence that states that polypeptide function
may not always be predicated on sequence homology.
As to the Examiner’s assertion that a utility for Npt2B cannot be
assigned without knowledge of what disease is associated with Npt2B
dysfunction or what drugs/ligands affect Npt2B function, the Specification
teaches that Npt2B is involved in the absorption of Pi from the intestine. As
such, the reduction or inhibition of Npt2B activity in a host would limit or
stop Pi transport, thus reducing plasma Pi levels. The Specification also sets
forth disease states that are characterized by the presence of
hyperphosphatemia where reduction in plasma Pi levels is desirable, which
disease states include: hyperparathyroidism, hypocalcemia, vitamin D
9
Page: Previous 1 2 3 4 5 6 7 8 9 10 11 12 13 Next
Last modified: September 9, 2013