Appeal 2007-1139
Application 10/052,664
deficiency, soft tissue or metastatic calcification, and the like, and of
particular interest is the reduction in plasma Pi levels to treat
hyperphosphatemia resulting from renal insufficiency, e.g. caused by renal
disease resulting in at least impaired renal functions.
We also find that such a utility would be credible to the skilled artisan.
Appellants rely on Peerce (“Inhibition of human intestinal brush border
membrane vesicle Na+-dependent phosphate uptake by phosphophloretin
derivatives,” Biochem. Biophys. Res. Comm., Vol. 301, pp. 8-12 (2003))
(Br. 13), which states at page 8 that "[a] pharmacological method of
reducing intestinal phosphate absorption may provide a more palatable
approach to reducing serum phosphate and may slow the progression of
moderate chronic renal failure to end-stage renal failure.” Even though
Peerce was published after the filing date of the instant application, we find
the quoted statement to be indicative of the state of the art at the time of
filing. For Example, Feild (EP 0875569, published November 4, 1998,
submitted in the IDS dated January 17, 2002), states that:
Phosphate retention has been shown to play a critical role
in the development of uremic bone disease. Blockade of
intestinal absorption of phosphate could provide an important
target for prevention of uremic bone disease in patients who
have end stage renal disease (ESRD) and possibly a target for
slowing the progression of the renal disease itself. Patients with
ESRD cannot excrete phosphate, and they develop
hyperphosphatemia, secondary hyperparathyroidism and uremic
bone disease. Current treatment of these patients involves
dietary phosphate restriction and phosphate binders, both of
which have severe drawbacks. Blockade of phosphate
absorption with a specific inhibitor of the intestinal phosphate
transporter would provide a major advance in the treatment of
these patients.
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