Ex Parte Du et al

Board of Patent Appeals and Interferences

Jan 14, 2010

10316145 (B.P.A.I. Jan. 14, 2010)

UNITED STATES PATENT AND TRADEMARK OFFICE
__________

BEFORE THE BOARD OF PATENT APPEALS
AND INTERFERENCES
__________

Ex parte YANSHENG DU, MARTIN R. FARLOW,
and RUYU DU
__________

Appeal 2009-004284
Application 10/316,145
Technology Center 1600
__________

Decided: January 14, 2010
__________

Before ERIC GRIMES, JEFFREY N. FREDMAN, and STEPHEN WALSH,
Administrative Patent Judges.

FREDMAN, Administrative Patent Judge.

DECISION ON REQUEST FOR REHEARING
Appellants have requested rehearing (reconsideration) of the Decision
entered October 5, 2009. That Decision affirmed the Examiner’s rejection
of claims 1-18 and 22 under 35 U.S.C. § 103(a).
Appellants' request has been granted to the extent that the Decision
has been reconsidered, but such request is denied with respect to making any

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Application 10/316,145

modifications to the Decision affirming the Examiner's rejection under
35 U.S.C. § 103(a).
DISCUSSION
Appellants first argue that the previous Decision misapprehended
Bergmann. Specifically, Appellants argue that “Bergmann explicitly stated
that ‘in neonatal cardiomyocytes and in H9c2 cells, specific inhibition of
NF-kB resulted in increased sensitivity of TNF-α-induced apoptosis’”
(Req. Recons. 2-3). Appellants argue that “[i]n other words, the
aforementioned test results demonstrated accuracy of the hypothesis
Bergmann intends to test, i.e., inhibition of NF-κΒ promotes heart cell
death” (id. at 3). Appellants conclude that “Bergmann provides
experimental data, which contradicts Nunokawa relied on by the Examiner”
(id.).
We have reviewed our Decision in light of these arguments. However,
we are not persuaded that our Decision was in error. In our Decision, we
addressed Bergmann, and correctly noted that Bergmann does not
specifically contradict Nunokawa’s disclosure that NF-κB inhibitors would
be effective in treating heart disease (Dec. 9). Bergmann, in a cellular
model, shows that “inhibition of NF-κB resulted in increased sensitivity of
TNF-α-induced apoptosis” (Bergmann 1229, col. 1). Bergmann uses an
artificial cell culture system in which exogenous TNF-α is applied to
cardiomyocytes which are subjected to transfection with a viral vector
expressing a particular IκB inhibitor (Bergmann 1227, col. 1). Bergmann
does not show any results from animal models, nor does Bergmann show
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that NF-kB inhibitors fail to treat heart disease in an animal or human
model.
Contrast Bergmann’s indirect teachings with the specific teaching by
Nunokawa that the “present invention therefore provides preventive or
therapeutic agents for myocarditis, dilated cardiomyopathy and heart failure
comprising NF-κB inhibitor as an active ingredient” (Nunokawa, col. 4, ll.
8-11; FF 7; Dec. 6). Nunokawa teaches that “the present inventors have
discovered, surprisingly, that compounds with an inhibitory effect on NF-κB
suppress cardiac necrosis and infiltration of inflammatory cells into normal
cardiac of [sic, or?] heart tissue” (Nunokawa, col. 3, l. 67 to col. 4, l. 3; FF 5;
Dec. 6). Nunokawa demonstrates, in animal models, that several different
NF-kB inhibitory test compounds functioned to increase survival rates in a
murine myocarditis model (Nunokawa, col. 166-168, Examples 2-6).
In weighing the suggestive power of Bergmann and Nunokawa, we
reasonably found that the specific and direct teaching of Nunokawa that NF-
κB inhibitors treat cardiac disease was more persuasive than Bergmann’s
artificial cell culture system regarding the reasonable expectation of success
in using NF-κB inhibitors to treat cardiac disease.
Appellants’ second argument relates to the obviousness of applying
CAPE to the treatment of Parkinson’s disease (Req. Recons. 4-5).
Appellants specifically argue that “the number of potential solutions for
treating PD is infinite” (id. at 4). Appellants also argue that “a skilled
artisan would not know how exactly a particular NF-κb inhibitor (e.g.,
CAPE) would act in human brains” (id. at 5).
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We have reviewed our Decision in light of these arguments. However,
we are not persuaded that our Decision was in error. In our Decision, we
specifically addressed the obvious to try argument, noting that “the prior art
provides sufficient specificity to demonstrate that NF-κB inhibitors protect
PC-12 cells (FF 16) and NF-κB inhibitors would reasonably be expected to
be useful in the treatment of neurological diseases” (Dec. 17). CAPE is a
specific NF-kB inhibitor which is a member of a class of compounds taught
to treat Parkinson’s disease (FF 12, 13, 18; Dec. 12-13) and CAPE was
specifically taught in the prior art as an NF-kB inhibitor that may be useful
for treatment of neurologic diseases (FF 15; Dec. 13). The prior art
therefore reduces Appellants’ “infinite” set of treatments down to NF-kB
inhibitors useful for neurologic diseases and CAPE is specifically identified
as such an NF-kB inhibitor (FF 15; Dec. 13). Thus, there are reasonably
understood to be a finite number of species for treatment of Parkinson’s
disease based upon the teachings of the prior art.
We also note that absolute predictability is not required, as Kubin
commented that “[r]esponding to concerns about uncertainty in the prior art
influencing the purported success of the claimed combination, this court [in
O'Farrell] stated: ‘[o]bviousness does not require absolute predictability of
success … all that is required is a reasonable expectation of success.”’ In
re Kubin, 561 F.3d 1351, 1360 (Fed. Cir. 2009) (citing In re O'Farrell,
853 F.2d 894, 903-904 (Fed. Cir. 1988)). Appellants’ arguments relating to
the effects of NF-κB inhibitors on the MPTP model were already addressed
by the Teisman reference, which found that NF-κB is not involved in the
MPTP model of Parkinson’s disease (FF 22; Dec. 14-15). Teismann does
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note that NF-κB activation is experimentally associated with Parkinson’s
disease (FF 23; Dec. 15). Thus, the MPTP model does not replicate
Parkinson’s disease with regard to NF-κB expression.
We continue to conclude that there would have been a “reasonable
expectation of success” in applying a known NF-κB inhibitor to Parkinson’s
disease, since Parkinson’s disease was known to be associated with
overexpression of NF-κB and inhibition of NF-κB was protective in a
known model system of Parkinson’s disease (FF 15-17, 21, 23, 24; Dec. 13-
15).
SUMMARY
We have carefully reviewed the original opinion in light of
Appellants’ request, but we find no point of law or fact which we
overlooked or misapprehended in arriving at our Decision. To the extent
relevant, Appellants’ request amounts to a reargument of points already
considered by the board.
Therefore, Appellants’ request has been granted to the extent that the
Decision has been reconsidered, but such request is denied with respect to
making any modifications to the Decision affirming the Examiner's rejection
under 35 U.S.C. § 103(a).

REHEARING DENIED

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