Appeal No. 1998-2088
Application 08/372,712
of the inflammatory monokine, tumor necrosis factor-a (TNF-a) mediates the
biologic effects caused by bacterial endotoxins (see first column, page 319). Fisher
further teaches that TNF-a has a central role as a mediator of sepsis by producing
proinflammatory activities but this cytokine also induces other inflammatory
mediators. Because of this major role, Fisher states TNF-a has become a primary
target of immune-based therapies (Id., pages 324-325). Wispé also teaches that
TNF-a is a potent mediator of immune function and inflammation (see page 1954)
and that TNF-a activity affects ARDS (Adult respiratory distress syndrome) by
inhibiting the production of pulmonary surfactant proteins (see page 1958). These
references show that a nexus between TNF-a activity and inflammation was well
known in the art. In addition, the references as well as Appellants’ specification
(see for example, page 57) teach that TNF-a activity induces other secondary
cytokines which further mediate inflammation. Unlike the Examiner, we find no open
endedness since the claim is drawn to inhibiting TNF-a activity which results in
inflammation. That the inflammation caused by TNF-a activity may be implicated in
several different diseases does not make the claim indefinite.
With regard to the Examiner’s concern that there is an apparent lack of
specific values for TNF-a levels which renders the claims indefinite, we again turn to
the guidance provided by Mattison, 509 F.2d at 565, 184 USPQ at 486. In
Mattison, the PTO was similarly concerned about a lack of absolute values which
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