Appeal 2007-1139
Application 10/052,664
polypeptide into mammalian cells, and teaches methods of assaying for
Na/Pi transporter activity (id. at 29-30).
The Specification teaches further that antibodies that bind to Npt2B
may be used to reduce or inhibit Npt2B activity in a host, and thus limit or
stop Pi transport, and thus reduce plasma Pi levels (id. at 19-21, 25).
According to the Specification, “[d]isease conditions resulting from
abnormally high Npt2B activity are those characterized by the presence of
hyperphosphatemia and include: hyperparathyroidism, hypocalcemia,
vitamin D deficiency, soft tissue or metastatic calcification, and the like. Of
particular interest is the use of the subject methods to treat
hyperphosphatemia resulting from renal insufficiency, e.g. caused by renal
disease resulting in at least impaired renal functions, and the like.” (Id. at
27.)
DISCUSSION
UTILITY
Claim 1 stands rejected under 35 U.S.C. § 101 on the grounds that the
claimed invention is not supported by either a specific and substantial utility
or a well-established utility.
The Examiner notes that the Specification discloses that the Npt2B
polypeptide of SEQ ID NO:1 is a human intestinal sodium phosphate co-
transporter, and that the Specification also discloses disorders in inorganic
phosphate (Pi) metabolism and that methods of treating such disorders are
varied (Answer 4).
The Examiner asserts, however, that “[m]embers of the sodium
phosphate co-transporter family are highly divergent in their effects and
ligand specificity.” (Id.) Moreover, according to the Examiner, “[t]here is
4
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