Appeal 2006-2945
Application 10/041,958
A10. Perera makes “no mention of therapy other than to note that the
[S]higa like toxins may play a role in disease ‘although no direct proof for
the involvement of SLTs in pathogenesis has yet been demonstrated’” (Br.
18-19; Reply Br. 8).
We agree that Perera makes no mention of therapy, and recognizes
that SLTs’ involvement in disease was unknown as of the 1988 publication
date of the reference (Perera, page 2130, col. 2, ll. 21-25). We are, however,
not persuaded that Perera’s acknowledgement of the state of the art in 1988
has any effect on the combination of references as relied upon by the
Examiner which in combination teach the use of human or humanized
antibodies to SLT II, SLT II α-subunit, or β-SLT II subunit for the treatment
of HUS in a human.
A11. Perera teaches “that none of the antibodies reactive only with Stx2
could be used to detect organisms; antibodies to Stx2 which were effective
were only able to be used to detect organisms producing both Stx1 and Stx2.
Accordingly, one would not be led by Perera to use these antibodies in
therapy, nor one would [sic] have a reasonable expectation of success using
just an antibody to Stx2, much less to a single subunit of Stx2” (Br. 19).
There is no requirement in claim 26 that the antibodies detect an
organism. Accordingly, we are not persuaded by Appellants’ assertion.
Further Appellants’ assertion appears to be based on a
misinterpretation of Perera. According to Perera, the “E. coli strains used in
this study included clinical isolates from humans with diarrhea, hemorrhagic
colitis, or hemolytic-uremic syndrome, calves with diarrhea, and pigs with
edema disease. . .” (Perera, page 2127, col. 2, ll. 5-8). Of the 10 SLT II
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