Appeal 2007-4148
Application 09/148,012
Appellant argues that, in addition to antibodies that bind murine
SR-BI, the Specification describes adenoviral vectors that encode SR-BI and
transgenic animals made by inactivating SR-BI in embryonic stem cells (Br.
8-9).
These disclosures do not contribute to the description of the claimed
method. Adenoviral vectors encoding SR-BI result in overexpression of
SR-BI, the opposite effect from that required by claim 1. (Specification 40:
26-29 (mice infected with an SR-BI-encoding adenovirus transiently
overexpress SR-BI).) Inactivating the SR-BI gene in transgenic animals
results in “inhibiting uptake, binding or transport of cholesteryl ester by
SR-BI,” but Appellant has not begun to explain how this method could be
practiced on a living, mammalian patient – as required by claim 1 – who can
hardly be generated from embryonic stem cells.
Appellant also argues that “the many compounds that already exist for
regulating cholesterol levels . . . can be used to inhibit pregnancy or decrease
steroidal overproduction via the modulation of SR-BI expression or activity”
(Br. 9). Appellant argues that a “different degree of description is required
where compounds are known and one only needs to provide the criteria for
their selection and use – a degree clearly met by appellant” (id. at 10).
We do not find this argument persuasive. The record provides no
basis to expect that compounds that lower plasma cholesterol levels would
inhibit SR-BI activity, since elimination of SR-BI activity results in elevated
plasma cholesterol. (Specification 50:10-13.) Those skilled in the art would
therefore expect that inhibition of SR-BI activity by an administered
compound would also result in elevated plasma cholesterol levels.
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