Appeal No. 2006-2466 Page 5
Application No. 09/835,759
2. Anticipation
The examiner has rejected claims 1, 2, and 7-10 under 35 U.S.C. § 102(b) as
anticipated by Noguchi,1 as evidenced by page 11 of the specification and by
Trinchieri.2 The examiner argues that Noguchi teaches “a composition comprising a
nonamer p53 peptide (234CM) (i.e., tumor-associated antigen) in QS-21 adjuvant, and
IL-12, which is reasonably interpreted as an effector of B cell depletion,” and that
Trinchieri provides evidence that “IL-12 induces or promotes a TH1 response and
inhibits a TH2 type or humoral/antibody response (see Figures 1 and 2).” Examiner’s
Answer, page 4.
Specifically, the examiner argues that “the claims are drawn to some unknown
‘immunotherapeutic composition’ identified solely by its principal biological activity, i.e.,
effecting B cell depletion. The specification defines B cell depletion broadly at page 8
. . . , which includes blocking of B cell function, inhibiting the proliferation of B cells, and
inhibiting the differentiation of B cells to plasma cells.” Examiner’s Answer, page 6.
The examiner argues that Figures 1 and 2 of Trinchieri “provide extrinsic evidence that
IL-12 acts as a negative regulator of TH2 promoting cytokines, such as IL-5, which
functions in the proliferation and differentiation of B cells.” Id. Thus, the examiner
argues that IL-12 “necessarily inhibit[s] B cell proliferation and differentiation” and is
therefore “an effector of B cell depletion.” Id., page 7.
1 Noguchi et al., “Influence of interleukin 12 on p53 peptide vaccination against established Meth A
sarcoma,” Proc. Natl. Acad. Sci USA., Vol. 92, pp. 2219-2223 (1995).
2 Trinchieri, “Interleukin-12 and its role in the generation of TH1 cells,” Immunology Today, Vol. 14, No.7,
pp. 335-338 (1993).
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