Appeal 2007-4148
Application 09/148,012
lowering or cholesterol-raising drugs affect the expression or activity of
SR-BI.
Appellant also argues that “one of skill in the art would understand
from the specification which compounds to use, and how to derive
appropriate doses with minimal routine experimentation to practice the
claimed method and inhibit fertility or treat a disorder characterized by
excessive steroidal production.” (Br. 13.)
Appellant provides no further explanation of the basis for this
assertion. For the reasons discussed above, we disagree that the
Specification provides adequate guidance to enable practice of the full scope
of claim 1 without undue experimentation. The rejection under 35 U.S.C.
§ 112, first paragraph, for lack of enablement is affirmed. Claims 2-9, 15,
16, and 20-22 fall with claim 1.
OTHER ISSUES
If this application is subject to further prosecution, the Examiner
should consider the following issues:
A. Estrogen as SR-BI inhibitor
The Specification states that estrogen administration reduces SR-BI
expression and is therefore an SR-BI inhibitor:
Animals receiving estrogen had significantly reduced levels of
SR-BI expressed in the liver, and elevated levels of SR-BI and
fluorescence in the ovaries. Since administration of estrogen is
associated with a number of side effects, inhibition is more
preferably achieved through the use of agents which inhibit
expression of SR-BI, translation of SR-BI, binding of SR-BI, or
cellular processing mediated by the SR-BI.
(Specification 10: 29 to 11: 6.)
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