Yoichiro Iwakura et al.

Patent Trials and Appeals Board

Oct 1, 2019

13580689 - (D) (P.T.A.B. Oct. 1, 2019)

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.
13/580,689 11/20/2012 Yoichiro Iwakura 403481US 1089
22850 7590 10/01/2019
OBLON, MCCLELLAND, MAIER & NEUSTADT, L.L.P.
1940 DUKE STREET
ALEXANDRIA, VA 22314
EXAMINER
JUEDES, AMY E
ART UNIT PAPER NUMBER
1644
NOTIFICATION DATE DELIVERY MODE
10/01/2019 ELECTRONIC
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.
Notice of the Office communication was sent electronically on above-indicated "Notification Date" to the
following e-mail address(es):
OBLONPAT@OBLON.COM
iahmadi@oblon.com
patentdocket@oblon.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
__________

BEFORE THE PATENT TRIAL AND APPEAL BOARD
__________

Ex parte YOICHIRO IWAKURA, NORIYUKI FUJIKADO, and
GUANGYU MA
__________

Appeal 2019-002524
Application 13/580,6891
Technology Center 1600
__________

Before ERIC B. GRIMES, FRANCISCO C. PRATS, and
RACHEL H. TOWNSEND, Administrative Patent Judges.

TOWNSEND, Administrative Patent Judge.

DECISION ON APPEAL
This is an appeal under 35 U.S.C. § 134 involving claims to a method
of treating a disease accompanied by abnormal bone metabolism, which
have been rejected as failing to comply with the written description
requirement and as being obvious. We have jurisdiction under 35 U.S.C.
§ 6(b).
We affirm.

1 We use the word “Appellant” to refer to “Applicant” as defined in 37
C.F.R. § 1.42. Appellant identifies the real party in interest as the University
of Tokyo. (Appeal Br. 2.)
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STATEMENT OF THE CASE
“Dendritic cells (DCs) play a central role in immune system
regulation.” (Spec. ¶ 2.) DCIR (also called LLIR) is a receptor expressed
on dendritic cells. (Id. ¶¶ 2, 3.) “[T]he mouse DCIR is suggested to act as
an inhibitory receptor and to control the dendritic cell function.” (Id. ¶ 3.)
DCIR has been reported to be involved in development of arthritis and
rheumatoid arthritis (“RA”). (Id.)
Claims 17, 19, 21–24, 26–29, 37, and 38 are on appeal. Claims 17
and 38 are representative and read as follows:
17. A method of treating a disease accompanied by
abnormal bone metabolism selected from the group consisting
of osteoporosis, Paget’s disease, osteitis deformans, and
rheumatoid arthritis in a subject in need thereof, comprising
administering to the subject an antibody or a Fab fragment
thereof wherein the antibody or Fab fragment specifically binds
to human dendritic immunoreceptor (LLIR) or mouse dendritic
cell immunoreceptor Clec4a2, acts as an agonist of a dendritic
cell immunoreceptor and treats the disease, wherein the
antibody or the Fab fragment thereof is not modified with
another molecule or is optionally chemically linked to only
polyethylene glycol (PEG).
38. A method of suppressing osteoclast production in a subject
in need thereof, the method comprising administering an
antibody or a Fab fragment thereof to the subject, wherein the
antibody or Fab fragment specifically binds to human dendritic
immunoreceptor (LLIR) or mouse dendritic cell
immunoreceptor Clec4a2, acts as an agonist of a dendritic cell
immunoreceptor, and inhibits GM-CSF action to suppress
osteoclast production, wherein the antibody or the Fab fragment
thereof is not modified with another molecule or is optionally
chemically linked to only polyethylene glycol (PEG).
(Appeal Br. 2, 4.)

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The following grounds of rejection by the Examiner are before us on
review:
Claims 17, 19, 21–24, 26–29, 37, and 38 under 35 U.S.C. § 112, first
paragraph as failing to comply with the written description requirement.
Claims 17, 19, 21–23, 26–28, 37, and 38 under 35 U.S.C. § 103 as
unpatentable over Iwakura,2 Valladeau,3 Meyer-Wentrup,4 and Vasanthi,5
Claims 24 and 29 under 35 U.S.C. § 103 as unpatentable over
Iwakura, Valladeau, Meyer-Wentrup, Vasanthi, and Chapman.6

2 Iwakura et al., US 2009/0202440 A1, published Aug. 13, 2009. The
Examiner refers to this as the ’440 publication. We, however, refer to it as
Iwakura herein.
3 Valladeau et al., US 6,277,959 B1, issued Aug. 21, 2001. The Examiner
refers to this as the ’959 patent. We, however, refer to it as Valladeau
herein. The Examiner also relies on GenBankAccession # AAH96565,
available at https://www.ncbi.nlm.nih.gov/protein/AAH96565.1, to
demonstrate that SEQ ID NO:8 of this reference is mouse Clec4a2. (Non-
Final Action 6.)
4 Meyer-Wentrup, F., et al., DCIR is endocytosed into human dendritic cells
and inhibits TLR8-mediated cytokine production, 85 J. Leukocyte Biology,
518–25 (2009). The Examiner also relies on an R&D Systems product
information sheet for the Murine anti-human DCIR mAb clone 216110 from
R&D systems described in this reference, which information sheet indicates
the antibody is unconjugated. This R&D Systems information sheet further
references the immunogen used to obtain the antibody is a recombinant
human DCIR Accession #Q9UMR7. The Examiner cites to the UniProt
Accession #Q9UMR7, available at
https://www.ncbi.nlm.nih.gov/protin/59797977?sat=11&satkey=7804620,
but does not indicate for what purpose it is being relied upon in the rejection.
(Non-Final Action 5–7.)
5 Vasanthi, P., et al., Role of tumor necrosis factor-alpha in rheumatoid
arthritis: a review, 10 APLAR J of Rheumatology, 270–74 (2007).
6 Chapman, A.P., et al. Therapeutic antibody fragments with prolonged in
vivo half-lives, 17 Nature Biotechnology, 780–83 (1999).
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DISCUSSION
Lack of Adequate Written Description
The Examiner notes that the claims are “drawn to a method
employing genus of antibodies that function to bind to human dendritic cell
immunoreceptor LLIR or mouse Clec4a2, and also function as agonist of the
dendritic cell immunoreceptor, inhibit GM-CSF action, and suppression of
osteoclast production and/or treatment of disease.” (Non-Final Action7 3.)
The Examiner finds that the claims encompass a large genus of structurally
and functionally distinct antibodies. (Id.) In particular, the Examiner finds
that the antibodies can be from human, rat, or mouse, can have different
VH/VL and CDR sequences, can bind to human or mouse LLIR/Clec4a2 at
different epitopes with different functions such as inhibiting GM-CSF action
or suppressing osteoclasts. (Id.) The Examiner finds that while three
particular mouse monoclonal antibodies that bind to mouse dendritic cell
immunoreceptor Clec4a2 and inhibit osteoclast differentiation and suppress
TNF-alpha production are disclosed in the Specification, neither the
structure nor the amino acid sequence of those antibodies is disclosed. (Id.)
Moreover, the Examiner finds that the Specification fails to disclose a
correlation between the structure of one of those antibodies, or any other,
and the functions claimed, i.e., “suppressing osteoclasts, inhibiting GM-CSF
action, or treating diseases.” (Id.) The Examiner further explains that “[t]he
mechanistic studies cited by Appellant do not provide any information as to
the actual structures of the antibodies that would function as claimed.”
(Ans. 9.) The Examiner concludes that in light of the scant disclosure in

7 The Non-Final Action is dated March 27, 2018.
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Appellant’s Specification that “one of skill in the art would conclude that
Applicant was not in possession of the structural attributes of a
representative number of species possessed by the members of the genus of
dendritic cell immunoreceptor antibodies with the claimed specificity and
functional attributes, broadly encompassed by the claimed invention.” (Id.
at 5.)
We agree with the Examiner’s factual findings and conclusion that the
claimed methods are not adequately described. Appellant does not argue the
claims separately. We address claim 17 as representative.
A description adequate to satisfy 35 U.S.C. § 112, first paragraph,
must “‘clearly allow persons of ordinary skill in the art to recognize that [the
inventor] invented what is claimed.”’ Ariad Pharms., Inc. v. Eli Lilly & Co.,
598 F.3d 1336, 1351 (Fed. Cir. 2010) (en banc). A patent disclosure is
sufficient if it “reasonably conveys to those skilled in the art that the
inventor had possession of the claimed subject matter as of the filing date,”
based on an “objective inquiry into the four corners of the specification.” Id.
A “sufficient description of a genus . . . requires the disclosure of either a
representative number of species falling within the scope of the genus or
structural features common to the members of the genus so that one of skill
in the art can ‘visualize or recognize’ the members of the genus” and not just
“a generic statement of an invention’s boundaries.” Id. at 1349–1350 (citing
Regents of the University of California v. Eli Lilly & Co., 119 F.3d 1559,
1568–69 (Fed. Cir. 1997)); Amgen Inc. v. Sanofi, 872 F.3d 1367, 1373 (Fed.
Cir. 2017).
We agree with the Examiner that the number of antibodies
encompassed by the claim for use in the method of treatment is a large
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genus. Claim 17 sets forth three functional requirements for the antibodies
that are within the scope of the claim. The first is that it “specifically binds
to human dendritic immunoreceptor (LLIR) or mouse dendritic cell
immunoreceptor Clec4a2.” The second is that the antibody “acts as an
agonist of a dendritic cell immunoreceptor.” And the third function is that
the antibody treats “a disease accompanied by abnormal bone metabolism
selected from the group consisting of osteoporosis, Paget’s disease, osteitis
deformans, and rheumatoid arthritis.” Appellant’s Specification states that
antibodies for use in the claimed invention, include monoclonal, polyclonal
and antibody mutants and derivatives. (Spec. ¶ 27.) And, as the Examiner
pointed out in the Answer, and Appellant does not dispute, “antibodies is
intended to encompass mouse antibodies, human antibodies, rat antibodies,
camel antibodies and bird antibodies as well as chimeric or humanized
antibodies.” (Ans. 10; see Spec. ¶ 28.)
The Specification describes production of antibodies to DCIR in
Example 5. (Spec. ¶¶ 62–66.) Some of the antibodies produced were
determined to have a higher DCIR binding ability than that of keratan sulfate
II (KS-II), a native ligand for DCIR and to more highly suppress TNF-alpha
production (Spec. ¶¶ 8, 67 (identifying hybridoma strains “3, 4, and 5 . . . in
Figure 12”)), and others promoted TNF-alpha compared to KS-II (id. ¶ 67
(identifying hybridoma strains “1 and 2 . . . in Figure 12”). The
Specification states that the former “are useful as DCIR agonists that
enhance DCIR activity,” where the latter “are useful as DCIR antagonists
that suppress DCIR activity.” (Id.) The Specification further notes that the
“[t]he hybridoma supernatants (DCIR agonist (3, 4, 5 strains in Figure 13))
showing higher DCIR binding abilities than that of keratan sulfate in
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Example 5 suppressed osteoclast differentiation, compared with keratan
sulfate” whereas the supernatants of 1 and 2 strains “promoted osteoclast
differentiation, compared with keratan sulfate.” (Id. ¶ 68.)
Thus, Appellant’s Specification describes producing mouse antibodies
to mouse Clec4a2 and evaluating the antibodies from monoclonal hybridoma
culture supernatant for DCIR-binding ability and assessing agonistic as
compared to antagonistic activity by measuring TNF-alpha production
(Spec. 46–54.) However, it does not disclose the structure or amino acid
sequence of any antibodies produced. Nor does it name those antibodies or
indicate that the antibodies were deposited in a public depository. Enzo
Biochem, Inc. v. Gen-Probe Inc., 323 F.3d 956, 965 (Fed. Cir. 2002)
(“[R]eference in the specification to a deposit in a public depository, which
makes its contents accessible . . . constitutes an adequate [written]
description . . .”).
Indeed, Appellant does not dispute that no structure of the antibodies
for use in the claimed method is disclosed. Instead, Appellant contends only
that the Specification provides sufficient description that the disclosed
agonist antibodies function to suppress osteoclast differentiation. (Appeal
Br. 7–8 (referring in part to Example 7).) While the Federal Circuit has
recognized that “the written description requirement can in some cases be
satisfied by functional description,” it has made clear that “such functional
description can be sufficient only if there is also a structure-function
relationship known to those of ordinary skill in the art.” In re Wallach, 378
F.3d 1330, 1335 (Fed. Cir. 2004); see also Enzo Biochem, 323 F.3d at 964
(holding that the written description requirement would be satisfied “if the
functional characteristic of preferential binding . . . were coupled with a
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disclosed correlation between that function and a structure that is sufficiently
known or disclosed”); Amgen, 872 F.3d at 1378 (holding that an “adequate
written description must contain enough information about the actual
makeup of the claimed products”).
Such is not the case here, as Appellant’s arguments in the Appeal
Brief make clear. (See, e.g., Appeal Br. 7–10.) Appellant argues that “there
are many antibodies which can be linked to the specific receptor (DCIR) to
induce an agonistic signal[]” (Appeal Br. 8) and that “[a] skilled person in
the art would easily identify the claimed agonistic antibodies by
differentiating osteoclasts by using bone marrow cells derived from DCIR-
deficient mouse or derived from WT mouse” (id. at 9). However, as the en
banc decision in Ariad made clear, to satisfy the statutory requirement of a
description of the invention, it is not enough for the specification to show
how to make and use the invention, i.e., to enable it. Ariad, 598 F.3d at
1345–46, 1347–48.
Appellant does not identify a structure-function relationship for the
antibodies disclosed as agonists and which can function in the additional
manner recited by the claim. And, as the Examiner notes, Appellant argues
that “certain species of DCIR antibodies were known in the art” but that
those “antibodies do not possess the same function as the claimed
antibodies.” (Ans. 9; Appeal Br. 11–12.) Thus, it cannot be disputed, as the
Examiner pointed out, that there is not a well-known correlation between
structure and function to support the claimed genus of antibodies. (Ans. 9.)
Appellant’s argument that the claim recites sufficient specificity to
describe the genus of antibodies that may be used in the claimed method
(Appeal Br. 8) misunderstands the written description rejection, which is
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that the Specification fails to reasonably convey to one of ordinary skill in
the art that the inventors had possession of the broad genus of antibodies
embraced by the claim. The argument, however, does confirm the
Examiner’s position that the genus of antibodies being claimed is vast.
Claim 17 and Appellant’s Specification here is similar to the claims
and disclosure in University of Rochester v. G.D. Searle & Co., 358 F.3d
916 (Fed. Cir. 2004), where the claims were found to be inadequately
described. In that case, claims directed to a method of selectively inhibiting
the COX-2 enzyme by administering a non-steroidal compound that
selectively inhibits the COX-2 enzyme, were found inadequately described
where the patent Specification at issue there did not describe any specific
compound capable of performing the claimed method and the skilled artisan
would not be able to identify any such compound based on the
Specification’s functional description. Id. at 927–28. As the Federal Circuit
in Ariad summed up, the claims in University of Rochester “merely recite a
description of the problem to be solved while claiming all solutions to it and
. . . cover any compound later actually invented and determined to fall
within the claim’s functional boundaries—leaving it to the pharmaceutical
industry to complete an unfinished invention.” Ariad, 598 F.3d at 1353. In
the Application before us, claim 17 recites a number of diseases for
treatment by an antibody that specifically binds a human or mouse dendritic
cell immunoreceptor and is agonistic thereof, but the Specification does not
provide a structural description of even a single specific antibody that
performs that disease-treating function, much less a representative number
of species falling within the scope of the genus, or structural features
common to the members of the genus so that one of skill in the art could
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visualize or recognize a priori (i.e., without carrying out experimentation to
determine whether the antibody in hand functioned as claimed) antibodies
within the genus. Accordingly, we agree with the Examiner that the instant
disclosure is insufficient to satisfy the written description requirement.
II
Obviousness
According to the Examiner, the claims “broadly encompass any DCIR
agonist antibody that functions to treat rheumatoid arthritis [RA].” (Non-
Final Action 8.) The Examiner explains that internalization is a type of
agonist activity for DCIR because it induces endocytosis of bound ligands.
(Id. (citing Meyer-Wentrup (“MW”)).) The Examiner further notes that
according to the Specification “DCIR agonist antibodies . . . also function to
inhibit TNF-alpha production (see paragraphs 67 and 20–23, in particular).”
(Id.)
With this understanding of the claims, the Examiner finds that
Iwakura teaches that it was known that DCIR (also known as LLIR) can
serve as an inhibitory receptor to regulate dendritic cell function, and that
lack of DCIR is linked to exacerbation of RA. (Non-Final Action 5 (citing
Iwakura 1–2, 4, and 9).) The Examiner further notes that Iwakura teaches
that “a substance that activates DCIR (i.e., agonists) can be used as a remedy
for autoimmune arthritis.” (Id. at 5–6.)
The Examiner further states that Iwakura teaches that “DCIR plays a
role in regulation of differentiation of osteoclast cells and that a lack of
DCIR protein activity is linked to osteoporosis and bone loss.” (Id. at 6.)
Additionally, according to the Examiner, Iwakura teaches that DCIR
signaling negatively controls cytokine signal transduction through GM-CSF
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and that “GM-CSF may exacerbate arthritis by stimulating proliferation of
dendritic cells.” (Id.)
The Examiner recognizes that Iwakura does not teach DCIR agonist
antibodies but finds that such antibodies were known in the art and that the
use of such antibodies in the method of treatment of RA taught by Iwakura
would have been obvious in light of MW and Valladeau. (Id. at 6–7.) The
Examiner explains that MW teaches agonist antibodies (monoclonal
antibody clone 216110) that trigger DCIR which induce receptor
internalization and inhibit the production of inflammatory cytokines such as
TNF-alpha by dendritic cells. (Id. at 6.) The Examiner notes that MW
teaches that this activity “points to an important role for DCIR in limiting
DC mediated immune activation, and that manipulation of DCIR could be of
use [to] treat immune mediated diseases.” (Id.)
The Examiner finds that Valladeau teaches producing antibodies to
mouse Clec4a2. (Id.) The Examiner further notes that Valladeau teaches
administering the agonist antibodies “to a subject for modulating antigen
presentation and immunological responses.” (Id.)
As with the written description rejection discussed above, Appellant
does not separately address the claims. However, we find that separate
issues are presented by the various independent claims. Claim 17 for
example, in contrast to claim 38, only requires that the antibody
administered to treat RA, a disease accompanied by abnormal bone
metabolism, specifically binds to human or mouse dendritic immunoreceptor
and acts as an agonist thereof. Claim 38, on the other hand, requires a
method of suppressing osteoclast production where the antibody
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administered not only binds to a human or mouse dendritic immunoreceptor
and acts as an agonist thereof, but also suppresses osteoclast production.8
Appellant argues that Iwakura “only suggest[s] that DCIR relates to
bone metabolism” and that it would not have been expected from that
publication “that the agonistic anti-DCIR antibodies can inhibit osteoclast
differentiation directly,” i.e., “in a TNF-independent manner.” (Appeal Br.
14–15.) We do not find this argument persuasive as to claim 17 since that
claim does not require inhibition of osteoclast differentiation, much less that
such inhibition be in a TNF-independent manner. Claim 17 requires that the
disease to be treated by an antibody or Fab fragment thereof that specifically
binds to human or mouse LLIR and is an agonist thereof is one that is
accompanied by abnormal bone metabolism, and that the disease is treated
with the antibody or fragment thereof. The claim includes RA as one such
disease. There is no stated limitation regarding osteoclasts in this claim.
Thus, it is irrelevant to claim 17 and the Examiner’s rejection thereof
whether Iwakura teaches that the agonist antibody inhibits osteoclast
differentiation.
Nevertheless, we find that the Examiner has not established a prima
facie case of obviousness of claim 17 because we conclude the cited prior art
would not have provided one of ordinary skill in the art with a reasonable
expectation of treating RA with an agonist antibody that specifically binds to
human or mouse dendritic immunoreceptor. “[T]he examiner bears the

8 Independent Claim 37 is similarly directed to a method of treating a
disease such as RA and does not require the administered antibody suppress
osteoclast production. Independent claim 19 is similar to claim 38 in
requiring suppression of osteoclast production by the administered antibody.
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initial burden, on review of the prior art . . . , of presenting a prima facie
case of unpatentability.” In re Oetiker, 977 F.2d 1443, 1445 (Fed. Cir.
1992).
While Iwakura teaches that “DCIR is involved in development or
aggravation of autoimmune diseases” (Iwakura ¶ 66), it does not disclose,
contrary to the Examiner’s position (Non-Final Action 5–6), that any DCIR
agonist can be used as a remedy for autoimmune arthritis. Rather, Iwakura
discloses that one
can screen a substance that facilitates activity of DCIR protein,
that is, a preventive/remedy for autoimmune diseases . . . by co-
culturing the peptide [having an amino acid sequence identical
or substantially identical to DCIR protein], the partial peptide
or the salt thereof with a candidate substance, and comparing
the activity of DCIR protein under presence or absence of the
candidate substance.
(Iwakura ¶ 64; see also id. ¶ 59.) Iwakura also states, in conjunction with
the fact that “[t]he inventors clarified for the first time that DCIR is involved
in development or aggravation of autoimmune diseases,” and knowing that
“DCIR is one of inhibitory regulators in immune system, playing a role to
suppress immune response under physiological condition,” that:
Therefore, by administering a peptide comprising an amino acid
sequence identical or substantially identical to DCIR protein
(soluble extracellular protein moiety, in particular), or a partial
peptide or salt thereof, inhibitory signals in immune system
may be inhibited, activating immune system. Therefore, the
peptide, the partial peptide or salt thereof can be used as a
remedy for various infections caused by various viruses,
bacteria, fungi or protozoa.
(Id. ¶ 66.) The ultimate goal of Iwakura might be stated as:
The purposes of the invention are to provide a DCIR defective
(KO) mouse (DCIR-/- mouse) to elucidate the role of DCIR in
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development of autoimmune diseases including arthritis, to
demonstrate the usefulness of the DCIR-/- mouse as a disease
model animal, to provide a method to screen a
preventive/remedy for autoimmune diseases using the DCIR-/-
mouse, and to provide a preventive/remedy for the autoimmune
diseases using the screening method.
(Id. ¶ 9.) Nonetheless, there is no disclosure of using the DCIR defective
mouse model to “develop [an] effective method and drug for treatment and
diagnosis” of bone and cartilage disease such as RA (id. ¶ 15). Iwakura
discloses at most a method for screening for substances that are agonists that
may in turn be tested for the ability to prevent or remedy autoimmune
diseases (id. ¶ 59), though it does not disclose a method for testing for the
ability to treat autoimmune disease.
In light of the foregoing, we disagree with the Examiner that Iwakura
would have motivated one of ordinary skill in the art with a reasonable
expectation of success in choosing agonist antibodies disclosed in MW or
Valladeau as therapeutics for autoimmune arthritis, such as RA.
As to claim 38, contrary to the Examiner’s position (Non-Final Action
6), Iwakura does not teach that DCIR definitively plays a role in regulation
of differentiation of osteoclast cells. Instead, based on observations made in
male DCIR-/- mouse of the heel joint showing increased calcification
compared to wild type mouse and showing that cartilage was replaced with
bone as well as observing that femur bone mass was decreased, it was
posited that “DCIR may play a role in bone metabolism, regulation of
differentiation and proliferation of cartilage cells, osteoblast and osteoclast
cells.” (Iwakura ¶ 130.) Based on this observation, Iwakura states that the
“DCIR-/- mouse can serve as a good model mouse of osteoporosis.” (Id.)
In short, Iwakura indicates that
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since the DCIR protein defective animal develops autoimmune
diseases, a gene coding DCIR protein or a partial sequence
thereof is effective as a diagnostic agent of autoimmune
diseases or osteoporosis. The invention provides a diagnostic
agent of autoimmune diseases or osteoporosis[.]
(Id. ¶ 63.) While it is true that Iwakura teaches that lack of DCIR protein
activity where DCIR is defective is linked to osteoporosis, we agree with
Appellant that at best Iwakura suggests that DCIR relates to bone
metabolism (Appeal Br. 14). We conclude that Iwakura does not provide a
reasonable expectation of success that an agonist of DCIR protein, much less
an agonist antibody, will suppress osteoclast production simply because it
was observed that DCIR may play a role in regulation of differentiation and
proliferation of cartilage cells, osteoblast and osteoclast cells. Thus, we
disagree with the Examiner that Iwakura would have motivated one of
ordinary skill in the art with a reasonable expectation of success in choosing
agonist antibodies disclosed in MW or Valladeau as agents for suppressing
osteoclast production in patients in need thereof.
In view of the foregoing, we reverse the Examiner’s rejection of
claims 17, 19, 21–23, 26–28, 37, and 38 as being obvious.
Moreover, because the Examiner’s rejection for obviousness of claims
24 and 29 does not remedy the deficiencies noted above, we also reverse the
Examiner’s obviousness rejection of those claims.
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SUMMARY
In summary:
Claims
Rejected
Basis  Affirmed Reversed
17, 19, 21–24, 26–
29, 37, and 38
§ 112, first
paragraph (written
description) 
17, 19, 21–24,
26–29, 37, and
38

17, 19, 21–23, 26–
28, 37, and 38
§ 103 Iwakura,
Valladeau, Meyer-
Wentrup, Vasanthi 
17, 19, 21–23,
26–28, 37, and
38
24 and 29 § 103 Iwakura,
Valladeau, Meyer-
Wentrup, Vasanthi,
and Chapman
24 and 29
Overall Outcome 17, 19, 21–24,
26–29, 37, and
38

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).

AFFIRMED