Appeal No. 1997-4275
Application No. 08/253,217
administration of the TNF antibody after the administration of LPS provides, at best,
questionable benefit to the treated mice. Beutler would reasonably appear to recognize
this in the stated conclusion which emphasized the criticality of timing of the administration
of the antibody. Further, we do not agree that Beutler would reasonably suggest a
treatment of patients with a bacterial infection which could result in sepsis using the
antibody to TNF to prevent or ameliorate the effect of LPS. As acknowledged by the
examiner “the experiments performed in Beutler et al. were done to determine if TNF
mediated the lethal effects of LPS, not to treat the sepsis and prevent death in the mice in
which they administered the LPS.” (Answer, page 9).
Beutler states (page 871, col. 1):
These data give evidence for the role of cachectin/TNF in
mediating the lethal effects of LPS. Cachectin/TNF is clearly
only one of the mediators responsible for the numerous
pathological effects evoked by LPS, since the passively
immunized mice become febrile, and continue to appear ill
and distressed. It is possible, for example, that cachectin/TNF
acts in concert with other mediators . . . in order to elicit the
lethal effect of LPS.
While Beutler may speculate about the “potential utility” of passive immunization with
antisera to cachectin/TNF in animals with shock. . . .” (page 871, column 1, last
paragraph), Beutler stops short of describing such a treatment or of suggesting that such a
treatment would likely be beneficial in the treatment or prevention of sepsis.
Thus, we conclude that Beutler does not evince the use of antibodies to TNF for the
treatment or prevention of sepsis in a patient with a bacterial infection. The examiner's
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