Appeal No. 2000-1783 Page 7
Application No. 08/817,719
was surely unsurprising.@ Brief, page 6.
In our view, the reasons cited in support of the examiner=s rejection do not
provide a reasonable basis to question the adequacy of the disclosure provided for the
claimed invention, and the evidence of record is insufficient to support the examiner=s
conclusion that Ait would take undue trials and errors to practice the claimed invention.@
Answer, page 5. Accordingly, the rejection of the claims under the first paragraph of
35 U.S.C. ' 112 is reversed.
Obviousness
There are three separate rejections of the claims; each relies, at least in part, on
the same four references (Flores-Romo, Bonnefoy, Bansal and Armant) in the
alternative, so we will discuss the rejections together.
Flores-Romo teaches that CD23 is a low-affinity IgE receptor and that it interacts
specifically with CD21, thereby modulating IgE production. In an in vivo model of an
allergen-specific IgE response, administration of CD23-specific antibody resulted in up
to 90 percent inhibition of antigen-specific IgE synthesis. Because IgE mediates many
allergic responses, Flores-Romo suggests that CD23 Acould be important in allergic
disease.@ Abstract.
Similarly, Bonnefoy teaches that anti-CD23 antibodies inhibit antigen-specific IgE
response in atopic patients (i.e., patients with IgE-associated type 1 allergies).
ASince [Bonnefoy] and [Flores-Romo] teach that anti-CD23 inhibits the
production of anti-IgE responses,@ the examiner concludes that Aone with skill in the art
. . . would be motivated to administer anti-CD23 antibody to autoimmune diseases
mediated by IgE such as asthma as is claimed in claims 14 and 21.@ Answer, page 6.
However, appellant points out that Aallergic asthma is an IgE-related disease,@
but A[i]ntrinsic non-atopic asthma,@ the form of asthma encompassed by the claims, Ais
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