Appeal No. 1999-1732
Application No. 08/308,879
DISCUSSION
The answer contains two grounds of rejection, both based on obviousness. We will
address the obviousness rejection in reverse order, addressing the rejection over
Kopchick first.
The Answer relies on the Kopchick reference for teaching growth hormone receptor
antagonists, and specifically for teaching that the mutant in which the glycine at position
120 has been mutated to arginine (G120R) is a growth receptor antagonist. With respect
to the use of using such growth hormone antagonists to treat breast cancer, the Kopchick
reference states:
It has been suggested that long-activity somatostatin analogues may
have value in the control of breast and prostate cancers. Manni, Biotherapy,
4:31-36 (1992). Manni hypothesizes that they could inhibit tumor growth by a
number of mechanisms, including inhibiting growth hormone secretion.
Growth hormone is implicated because it is lactogenic and because it
elevates IGF-1 levels. We suggest that the growth hormone antagonists of
the present invention may be used in the treatment of cancers whose growth
is facilitated by endogenous growth hormone or IGF-1.
Kopchick, Col. 3, line 60-Col. 4, line 2 (emphasis added). The reference, however,
presents no examples, nor does it provide in vitro or in vivo data, wherein the disclosed
growth hormone antagonists are administered to breast cancer cells that express prolactin
receptors, as required by claim 1.
Based on this single paragraph in the Kopchick reference, the Answer concludes
that “it would have been obvious to a person of ordinary skill in the art to administer [growth
4
Page: Previous 1 2 3 4 5 6 7 8 9 10 11 Next
Last modified: November 3, 2007