Appeal No. 2005-0410
Application No. 09/902,461
IV. Claims 1-9 and 11-23 stand rejected under 35 U.S.C. § 103(a) as being
unpatentable over Bijvoet in view of Fuller.
V. Claims 1-9 and 11-23 stand rejected under 35 U.S.C. § 103(a) as being
unpatentable over Fuller.
We have carefully considered the respective positions of both the appellant and
the examiner and find ourselves in substantial agreement with that of the appellant.
Accordingly, we reverse Rejections I-V.
Background
The specification discloses that glycogen storage disease type II (GSD-II, a.k.a.
Pompe disease or acid maltase deficiency) “is a fatal genetic muscle disorder caused
by a deficiency of acid "-glucosidase (GAA), a glycogen degrading lysosomal enzyme.”
Specification, p. 1, lines 7-9. The specification further discloses that this “deficiency
results in lysosomal glycogen accumulation in almost all tissues of the body, with
cardiac and skeletal muscle being the most seriously affected.” Id., lines 12-14. The
specification still further discloses:
Clinically, GSD-II encompasses a range of phenotypes differing as to age
of onset, organs involved and clinical severity, generally correlating with the
residual amount of GAA activity. In its most severe presentation (infantile
GSD-II, or Pompe disease, in which less than 1% of normal GAA activity is
present), infants are affected by a hypertrophic cardiomyopathy, generalized
muscle weakness and hypotonia secondary to massive glycogen accumulation in
cardiac and skeletal muscles . . . The disease progresses rapidly, with death
from cardiac failure usually occurring by 1 year of age. Juvenile (1-10% of
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