Appeal 2006-2945
Application 10/041,958
purified IgG monospecific polyclonal antibodies to SLT II. Accordingly, we
are not persuaded by Appellants’ assertion to the contrary.
A2. Krivan appears to describe only those “SLT forms that cause animal
disease, not . . . the Stx2 form causing HUS” (id.).
This assertion is inconsistent with Krivan’s disclosure. Specifically,
Krivan discloses that “[t]he invention . . . comprises methods and
pharmaceutical compositions for the prevention, amelioration, or treatment
of disease in a human or animal caused by an SLT or by bacteria that
produce an SLT” (Krivan, col. 6, ll. 37-44). As discussed above, Krivan
teaches that HUS is one such disease caused by an SLT or by bacteria that
produce an SLT. Accordingly, we do not find Appellants’ assertion
persuasive.
A3. Krivan does not recognize that different E. coli strains infect different
hosts. Therefore, one cannot extrapolate from reagents in one species, e.g.,
cattle, for use in another, e.g., humans, “since there are differences in the
toxins, and in the host species, [therefore,] cattle and humans which are
infected differently have different diseases” (Br. 15).
It is unclear why Appellants’ attempt to distinguish Krivan by
focusing of the differences between cattle and humans. Krivan recognizes
that cattle respond to SLTs differently than humans and other animals, and
for that reason selected cattle as the animal of choice for producing
antibodies against SLTs. See Krivan, col. 5, ll. 42-53; col. 8, ll. 16-35.
Further, contrary to Appellants’ assertion, no extrapolation is necessary on
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