Appeal 2007-4148
Application 09/148,012
In addition, even though inhibiting SR-BI was shown to increase
plasma cholesterol levels in transgenic mice, it does not follow that
increasing cholesterol level in a patient having normal SR-BI function will
inhibit SR-BI, and thereby inhibit pregnancy. Appellant has pointed to no
evidence in the record that would show that SR-BI is down-regulated or
inactivated in response to elevated cholesterol levels. Thus, the evidence of
record does not support Appellant’s apparent position that any compound
that elevates cholesterol will inhibit SR-BI.
We affirm the rejection of claim 1 under 35 U.S.C. § 112, first
paragraph, for lack of adequate written description. Claims 2-9, 12, 15, 16,
and 20-22 fall with claim 1.
4. ENABLEMENT
Claims 1-9, 15, 16, and 20-22 stand rejected under 35 U.S.C. § 112,
first paragraph, on the basis that the Specification “does not reasonably
provide enablement for any method of decreasing production of steroids or
inhibiting pregnancy in a mammal” (Answer 3).1 The Examiner reasons that
Appellant has provided no guidance and working examples of
any compounds which act via SR-BI to alter pregnancy other
than those in knockout infertile female mice. In fact, the
specification, estrogen . . . , adenoviral vector encoding SR-BI
. . . , and anti-SR-BI antibody . . . have only been shown to
1 Claim 12 was also subject to this ground of rejection in the Office action
mailed August 15, 2005 but was not included in the statement of rejection in
the Examiner’s Answer. At the same time, the Examiner did not expressly
indicate that the rejection had been withdrawn with respect to claim 12. If
this application is subject to further prosecution, the Examiner should
consider whether claim 12 should be rejected for nonenablement.
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