Appeal No. 2004-1259
Application No. 09/832,355
protein of Yoon et al. for the purpose of making a cytotoxic fusion protein
to be used to treat either KS or glioma/glioblastomas. The artisan would
have been motivated to do so by the disclosures of Gill et al. and
Rockwell et al. that the VEGF receptors are ‘markers’ for those tumors,
and would have been particularly motivated to use the 121 amino acid
form of VEGF, as it is the shorter of the soluble forms... and the art
generally recognizes the utility of using smaller molecules where possible,
for example see Yoon et al. Accordingly, the invention, taken as a whole,
is prima facie obvious over the cited prior art.
Appellants argue that one of ordinary skill in the art would not be motivated to
substitute VEGF for EGF in the fusion protein of Yoon. Brief, page 10. Appellants
argue that Yoon teaches away from such a substitution because VEGF is an agent that
promotes tumor angiogenesis and one of ordinary skill in the art seeking to kill tumor
cells in accordance with the disclosure of Yoon would not be motivated to substitute
VEGF for EGF “in as much as the VEGF peptide portion would enhance tumor cell
survival by promoting tumor angiogenesis.” Id, pages 10-11.
The examiner responds to appellants, arguing, “[a]lthough VEGF would, alone,
be contraindicated for administration to a tumor, as a fusion protein with angiogenin, it
would be expected to be cytotoxic... and thus not cause angiogenesis and further tumor
growth.” Answer, page 25.
We agree with the examiner that Yoon does not teach away from the substitution
of VEGF for EGF in its fusion protein. Both the EGF receptor and the VEGF receptor
are tyrosine kinase receptors. See, e.g., Rockwell, Column 1, lines 60-66. Yoon
teaches that EGF is a tumor marker for epithelial carcinoma cells and CHO-K1 cells.
Gill and Rockwell teach that VEGF is a tumor marker for KS and glioma/glioblastoma.
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