Appeal No. 1998-0350
Application No. 08/453,937
the examiner argues that Sandset would have led those skilled in the art to
expect LACI and heparin to act synergistically in vivo, because Sandset teaches
that administration of heparin, alone, resulted in a several-fold increase in LACI3
activity in patients. Id.
The examiner’s argument is not persuasive. It is true that Sandset
teaches that “[a]fter intravenous injection [of heparin], EPI activity increased
dose-dependently.” See the abstract. Sandset’s data, however, led him to
“conclude that EPI probably is produced in endothelial cells and may be released
by heparin.” Id. Sandset therefore would have led those skilled in the art to
expect that administration of heparin would lead to an increase in plasma LACI
activity as a result of releasing endogenous LACI into the blood. However,
Sandset does not suggest that heparin increases the activity of LACI already in
circulation. That is, Sandset suggests that heparin increases the level, and
therefore the activity, of LACI in plasma by releasing stored LACI from
endothelial cells, but Sandset does not suggest that heparin affects the activity of
LACI after the LACI is present in the plasma. Thus, while Sandset would have
led those skilled in the art to expect administration of heparin alone to cause an
increase in plasma LACI levels, Sandset would not have motivated those skilled
in the art to combine LACI and heparin and administer them together as an
anticoagulant composition.
In addition, even if the prior art supported a prima facie case of
obviousness, Appellant’s specification presents evidence that the claimed
3 Sandset refers to LACI by its alternative name of extrinsic pathway inhibitor, or EPI.
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