Appeal 2007-4148
Application 09/148,012
affect SR-BI and to alter cholesterol and lipoprotein levels, but
have not been shown to inhibit pregnancy in a mammal.
(Answer 4.) The Examiner also finds that the exemplified “method of
knocking out a gene in an embryonic stem cell is not comparable to a
method of altering fertility . . . in a developed mammal” (id.).
The Examiner concludes that, because of the paucity of guidance and
working examples, and the “lack of predictability as to which compounds
affecting steroid levels will inhibit pregnancy, . . . undue experimentation is
necessary to practice the claimed invention” (id. at 5).
We agree with the Examiner that the Specification does not provide
sufficient guidance to enable practice of the full scope of the claimed
method without undue experimentation. The Specification discloses that
transgenic mice that do not express SR-BI at all are infertile; the
Specification discloses no other examples of inhibiting pregnancy by
inhibiting SR-BI. The Specification provides no guidance regarding what
level of SR-BI expression above zero is sufficient to inhibit pregnancy.
The Specification provides no guidance or working examples that
would enable those skilled in the art to achieve 100% inhibition of SR-BI in
a developed animal expressing SR-BI. The Specification’s example
showing in vitro inhibition of SR-BI activity describes using SR-BI-binding
antibodies to achieve up to 85% inhibition of HDL uptake (Specification 62:
26-28), up to 70% inhibition of HDL-selective cholesteryl ester uptake (id.
at 63: 26-28), and up to 50% inhibition of cell association with HDL (id. at
64: 12-14), and up to 78% inhibition of steroid production (id. at 65: 21-23)
in murine adrenocortical cells. The record provides an inadequate basis on
which to extrapolate these in vitro results to what could be achieved in vivo,
9
Page: Previous 1 2 3 4 5 6 7 8 9 10 11 12 13 14 Next
Last modified: September 9, 2013