Appeal No. 2001-1499 Page 15
Application No. 08/957,654
Rao stated that their “results suggest[ed] that the degradation of AT, by as
yet unidentified enzymes, leads to loss of this inhibitor in wounds that eventually
feature extensive FN degradation.” Page 576, right-hand column. Finally, in the
paragraph cited by the examiner, Rao stated that their results
may have relevance for the treatment of chronic wounds. Several
studies demonstrated a beneficial effect for topical FN on leg ulcers
and non-healing corneal ulcers. Intact FN may be required for the
healing of chronic wounds. The [data] suggest that the degradation
of AT precedes the degradation of FN in chronic wounds. . . . AT
effectively prevented the degradation of FN by chronic wound fluid
serine proteinases. Therefore, topical AT may inhibit FN degrading
enzymes and increase the concentration of intact and functional FN
in chronic wounds.
Page 577, left-hand column.
I agree with the examiner that the combined disclosures of Gillis and Rao
would have rendered claims 1 and 7 prima facie obvious. Specifically, it would
have been obvious to a person of ordinary skill in the art to modify Gillis’ IL-1-
based method and composition for treating chronic wounds, by adding alpha-1-
antitrypsin, in the amount shown by Rao to effectively inhibit proteinase activity in
vitro (150-600 µg/ml). Motivation to combine the teachings of the references is
provided by Gillis, who specifically suggests including alpha-1-antitrypsin in the
IL-1-containing composition (column 4, lines 52-65) and by Rao, who teaches
that inhibition of proteinase activity prevents fibronectin degradation, and that
fibronectin contributes to wound healing (pages 572 and 577, left-hand
columns).
Rao also shows that 150-600 µg/ml alpha-1-antitrypsin effectively
prevented fibronectin degradation in vitro by proteinases in chronic wound fluid.
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