Ex Parte Nakamura et al

Board of Patent Appeals and Interferences

Nov 2, 2010

11584649 (B.P.A.I. Nov. 2, 2010)

UNITED STATES PATENT AND TRADEMARK OFFICE
UNITED STATES DEPARTMENT OF COMMERCE
United States Patent and Trademark Office
Address: COMMISSIONER FOR PATENTS
P.O. Box 1450
Alexandria, Virginia 22313-1450
www.uspto.gov
APPLICATION NO. FILING DATE FIRST NAMED INVENTOR ATTORNEY DOCKET NO. CONFIRMATION NO.
11/584,649 10/23/2006 Akira Nakamura 31671-237175 5524
26694 7590 11/02/2010
VENABLE LLP
P.O. BOX 34385
WASHINGTON, DC 20043-9998
EXAMINER
BERTOGLIO, VALARIE E
ART UNIT PAPER NUMBER
1632
MAIL DATE DELIVERY MODE
11/02/2010 PAPER
Please find below and/or attached an Office communication concerning this application or proceeding.
The time period for reply, if any, is set in the attached communication.
PTOL-90A (Rev. 04/07)

UNITED STATES PATENT AND TRADEMARK OFFICE
__________

BEFORE THE BOARD OF PATENT APPEALS
AND INTERFERENCES
__________

Ex parte AKIRA NAKAMURA,
TOSHIHIRO NUKIWA, and TOSHIYUKI TAKAI
__________

Appeal 2010-005047
Application 11/584,649
Technology Center 1600
__________

Before ERIC GRIMES, LORA M. GREEN, and JEFFREY N. FREDMAN,
Administrative Patent Judges.

GREEN, Administrative Patent Judge.

DECISION ON APPEAL1
This is a decision on appeal under 35 U.S.C. § 134 from the
Examiner’s rejection of claim 8. We have jurisdiction under 35 U.S.C.
§ 6(b).

1 The two-month time period for filing an appeal or commencing a civil
action, as recited in 37 C.F.R. § 1.304, or for filing a request for rehearing,
as recited in 37 C.F.R. § 41.52, begins to run from the “MAIL DATE”
(paper delivery mode) or the “NOTIFICATION DATE” (electronic delivery
mode) shown on the PTOL-90A cover letter attached to this decision.
Appeal 2010-005047
Application 11/584,649

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STATEMENT OF THE CASE
Claim 8 is the only claim on appeal, and reads as follows:
8. A method for diagnosing Goodpasture’s syndrome at the early
stage characterized in that a Fcγ receptor IIB gene is extracted
from human test cells and is examined whether there is any
deficiency in the function of said gene.

The following ground of rejection is before us for review:
Claim 8 stands rejected under 35 U.S.C. § 112, first paragraph, for
lack of enablement.
We affirm.
ISSUE
Has the Examiner established by a preponderance of the evidence that
the Specification fails to enable a method of diagnosing Goodpasture’s
syndrome at the early stage as set forth by claim 8?

FINDINGS OF FACT
FF1 The Specification teaches:
Goodpasture’s syndrome, which has the combination of
diffuse alveolar hemorrhage, glomerulonephritis, and the
appearance of antikidney glomerular basement membrane
antibody, is similar as a clinical feature with Wegener's
granulomatosis, systemic necrotizing vasculitis, systemic lupus
erythematosus (SLE) and the like, and is believed that
antibodies common to the kidney glomerular basement
membrane and alveolar epithelium basement membrane exist in
the patient’s serum, which bind to the target tissues and induce
lesion of inflammation based on type II hypersensitivity
reaction. Aside from the characteristics of the above-mentioned
clinical feature, the diagnosis of Goodpasture’s syndrome is
made by proving the deposition of immunoglobulin (hereinafter
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“Ig”) on the kidney glomerular basement membrane, where
most of the anti basement membrane antibodies belong to the
IgG fraction, and in recent years, it has been identified as an
autoantibody to a part of the α3 chain of type IV collagen.

(Spec. 1-2 (references omitted).)
FF2 The Specification teaches further that immune and other cells have
receptors that recognize and bind the Fc portion of Ig, one of which is the
FcγRII, which has low affinity to the IgG of the monomer, but binds to
polyvalent IgG. (Id. at 2.)
FF3 The Specification teaches further that when a FcγRII knockout mouse
is immunized with type IV collagen, the mouse is a model for Goodpasture’s
syndrome. (Id. at 4.)
FF4 Based on those findings, the Specification teaches:
Onset of Goodpasture’s syndrome is possible when there is a
deficiency in the function of Fcγ RIIB in the expression
product, and as mentioned above, a method for diagnosing
Goodpasture’s syndrome at the early stage becomes possible by
examining whether there is any deficiency in the function of
Fcγ RIIB gene.

(Id. at 9.)
FF5 The Specification also presents an example of generation of the
Goodpasture’s syndrome mouse model. (Id. at 12 (Examples 1 and 2).)
FF6 The Examiner’s statement of the rejection may be found at pages 4-8
of the Answer.
FF7 Specifically, the Examiner notes that the nature of the invention is
drawn to a method of diagnosing Goodpasture’s syndrome, wherein a Fcγ
receptor IIB gene is extracted from a test cell and the gene is examined for a
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deficiency in function by examining the function of the expression product.
(Ans. 5.) According to the Examiner, the claim “is directed to a method of
diagnosis and is not directed to a method of determining whether there is a
lesion in the FcγRIIB that could be diagnostic of Goodpasture’s syndrome.”
(Id. at 9.)
FF8 The Examiner notes that while the Specification teaches a model for
Goodpasture’s syndrome, it does not provide “any guidance with respect to
the actual role of FcγRIIB in Goodpasture’s in humans that naturally exhibit
the syndrome.” (Id. at 6.)
FF9 The Examiner cites Nakamura2 for its teaching that “the FcγRIIB
deficiency merely renders the mouse susceptible to Goodpasture’s by
creating a permissive environment and that it is likely that contributions
from enhanced effector cell responses to deposited anti collagen type IV
autoantibodies are significant factors in the development of disease.” (Id.
(citing Nakamura, paragraph bridging pp. 903-904).)
FF10 Specifically, Nakamura teaches the “observation that FcγRIIB
deficiency creates a permissive immunological environment for the
development of anti-C-IV autoantibodies offers further support for a role for
this receptor in the mechanism of maintaining tolerance,” as its deficiency
removes an immunological checkpoint, and thus contributes to the
development of autoimmunity. (Nakamura, p. 904, first column.) Based on
the data, Nakamura postulates that alterations in the function or expression

2Nakamura et al., Fcγ Receptor IIB-deficient Mice Develop Goodpasture’s
Syndrome upon Immunization with Type IV Collagen: A Novel Murine
Model for Autoimmune Glomerular Basement Membrane Disease, 191 J.
EXP. MED. 899-905 (2000).
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of the FcγRIIB gene “could be a susceptibility factor in the pathogenesis of
the human disease.” (Id. at 904, second column.)
FF11 The Examiner cites Kalluri3 to demonstrate “that a deficiency in
FcγRIIB is not necessary to model Goodpasture’s Syndrome.” (Ans. 6.)
FF12 Thus, according to the Examiner, “[w]hile the instant specification
demonstrates a role for FcγRIIB in Goodpasture’s syndrome, it fails to
demonstrate a causal link that is necessary to enable the invention as
claimed.” (Id.) The Examiner notes further that while Appellants have
uncovered a new path of investigation, the Specification does not enable a
method of early diagnosis of Goodpasture’s syndrome. (Id. at 9.)

PRINCIPLES OF LAW
“[E]nablement requires that the specification teach those in the art to
make and use the invention without ‘undue experimentation.’ That some
experimentation may be required is not fatal; the issue is whether the amount
of experimentation required is ‘undue.’” In re Vaeck, 947 F.2d 488, 495
(Fed. Cir. 1991) (citation omitted). “Whether undue experimentation is
needed is not a single, simple factual determination, but rather is a
conclusion reached by weighing many factual considerations.” In re Wands,
858 F.2d 731, 737 (Fed. Cir. 1988).
Patent protection is granted in return for an enabling disclosure of an
invention, not for vague intimations of general ideas that may or may not be

3 Kalluri et al., Susceptibility to Anti-Glomerular Basement Membrane
Disease and Goodpasture Syndrome Is Linked to MHC Class II Genes and
the Emergence of T Cell-mediated Immunity in Mice, 100 J. CLIN. INVEST.
2263-2275 (1997).
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workable. See Brenner v. Manson, 383 U.S. 519, 536 (1966) (stating, in
context of the utility requirement, that “a patent is not a hunting license. It is
not a reward for the search, but compensation for its successful
conclusion.”). Tossing out the mere germ of an idea does not constitute
enabling disclosure. “While every aspect of a generic claim certainly need
not have been carried out by an inventor, or exemplified in the specification,
reasonable detail must be provided in order to enable members of the public
to understand and carry out the invention.” Genentech, Inc. v. Novo Nordisk
A/S, 108 F.3d 1361, 1366 (Fed. Cir. 1997).
If mere plausibility were the test for enablement under section
112, applicants could obtain patent rights to ‘inventions’
consisting of little more than respectable guesses as to the
likelihood of their success. When one of the guesses later
proved true, the “inventor” would be rewarded the spoils
instead of the party who demonstrated that the method actually
worked. That scenario is not consistent with the statutory
requirement that the inventor enable an invention rather than
merely proposing an unproved hypothesis.

Rasmusson v. SmithKline Beecham Corp., 413 F.3d 1318, 1325 (Fed. Cir.
2005).

ANALYSIS
According to Appellants, the “present application is based on the
production of the world’s first disease model for Goodpasture’s syndrome
that develops an autoimmune disease remarkably resembling Goodpasture’s
syndrome.” (App. Br. 5.) Appellants argue that the Examiner appears to be
of the view that the Specification provides no evidence that altered FcγRIIB
activity is correlated with Goodpasture’s syndrome as it presents in humans,
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and thus “appears not to accept the scientific achievements on gene
deficiency mice that have been produced so far.” (Id. at 3.) Appellants
argue that “involvement of FcγRIIB gene in Goodpasture’s is confirmed and
the nexus between altered FcγRIIB activity and Goodpasture’s syndrome is
sufficiently proved.” (Id. at 4.)
Specifically, Appellants argue:
Therefore, even for the mouse model of the present
invention, it has not been specified in the strict sense whether
FcγRIIB is the causal gene or whether it is one of various causal
genes of so called Goodpasture’s syndrome. However, it can
be concluded that FcγRIIB is confirmed to play a considerably
important role in the immune system as a whole, since the
FcγRIIB deficient mouse was observed to demonstrate the same
symptoms as those that emerge in autoimmune diseases that are
thought to be developed due to the disorder in the immune
system control. In fact, the present inventors have
demonstrated ahead of the world based on their production of
the FcγRIIB deficient mouse of the present invention that FcR
has a major role in the allergic response and that there exists a
FcγRIIB-mediated negative feedback mechanism.

(Id. at 6 (emphasis in original).) Appellants assert further that the skilled
artisan who is “interested in prevention and treatment of Goodpasture’s
syndrome should naturally focus on the human FcγRIIB gene given the
above-mentioned results obtained in mice, irrespective of whether the nexus
between the human FcγRIIB gene and Goodpasture’s syndrome has been
shown using human data.” (Id. at 7.)
Appellants’ arguments have been carefully considered, but are not
deemed to be convincing. As noted by the Examiner, Appellants’ claim 8 is
drawn to a method of “diagnosing Goodpasture’s syndrome at the early
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stage,” wherein “a Fcγ receptor IIB gene is extracted from human test cells
and is examined whether there is any deficiency in the function of said
gene.” As also noted by the Examiner, Appellants have not established a
causal link between deficiencies in the FcγRIIB gene and the development
of Goodpasture’s syndrome.
Specifically, Nakamura teaches that a deficiency in FcγRIIB gene
function or expression could be a susceptibility factor in the pathogenesis of
the human disease, but Appellants are not claiming a method of determining
a subject’s susceptibility to developing Goodpasture’s syndrome. Kalluri
further demonstrates that a deficiency in FcγRIIB gene function or
expression is not necessarily a factor in the development of Goodpasture’s
syndrome, providing further support for the Examiner’s finding that
Appellants have not established a causal link between deficiencies in the
FcγRIIB gene with the development of Goodpasture’s syndrome. Thus,
while we agree with Appellants the skilled artisan who is interested in the
prevention and treatment of Goodpasture’s syndrome would focus on the
human FcγRIIB gene given the results obtained in mice reported in the
instant Specification, we conclude the Specification has set forth a promising
line of research in methods that may be used in the further characterization
of Goodpasture’s syndrome, but not an enabling disclosure of the claimed
invention.

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Application 11/584,649

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CONCLUSION OF LAW
We conclude that the Examiner has established by a preponderance of
the evidence that the Specification fails to enable a method of diagnosing
Goodpasture’s syndrome at the early stage as set forth by claim 8.
We thus affirm the rejection of claim 8 under 35 U.S.C. § 112, first
paragraph, for lack of enablement.

TIME PERIOD FOR RESPONSE
No time period for taking any subsequent action in connection with
this appeal may be extended under 37 C.F.R. § 1.136(a)(1)(iv)(2006).

AFFIRMED

cdc

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