GRIMES, Administrative Patent Judge, dissenting in part.
I agree that the cited references would not have led those skilled in the art
to administer an HMG-CoA reductase inhibitor to patients having sitosterolemia.
In my opinion, however, the evidence of record would have suggested using
ezetimibe to treat sitosterolemia to those skilled in the art. I would reverse the
rejection of the claims that require administering an HMG-CoA reductase inhibitor
but affirm the rejection of the remaining claims.
The claims are directed to a method of treating sitosterolemia by
administering a sterol absorption inhibitor, ezetimibe being the elected species.
The examiner rejected the claims as obvious in view of Rosenblum and
Belamarich. Belamarich discloses that
[t]he metabolic defect [underlying sitosterolemia] is related to a five-
fold or greater increase in intestinal absorption of dietary plant
sterols compared with subjects who do not have sitosterolemia.
Failure to excrete plant sterols in the bile has also been implicated
as a contributing factor.
Page 977, right-hand column. Belamarich also teaches that
[p]atients with sitosterolemia are frequently hypercholesterolemic
. . . , however, the hypercholesterolemia of sitosterolemia is
responsive to cholesterol-lowering diets, bile acid binding resins,
and ileal bypass surgery.
Id.
Belamarich reports that treating a patient with a combination of a low-
sterol diet and cholestyramine, a bile acid binding resin, “evoked a 40% decrease
in plasma cholesterol and a 42% reduction of plasma sitosterol concentration.
These findings confirm previous observations of the effectiveness of
cholestyramine in sitosterolemia.” Page 980, left-hand column.
Page: Previous 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 Next
Last modified: September 9, 2013