Case Western Reserve University

Patent Trials and Appeals Board

Nov 10, 2020

2019006093 (P.T.A.B. Nov. 10, 2020)

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.
14/605,729 01/26/2015 M. Edward Medof CWR-018221US CON-1 7013
68705 7590 11/10/2020
TAROLLI, SUNDHEIM, COVELL & TUMMINO, LLP
1300 EAST NINTH STREET
SUITE 1700
CLEVELAND, OH 44114
EXAMINER
GAMBEL, PHILLIP
ART UNIT PAPER NUMBER
1644
NOTIFICATION DATE DELIVERY MODE
11/10/2020 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):
docketing@tarolli.com
rkline@tarolli.com
PTOL-90A (Rev. 04/07)

UNITED STATES PATENT AND TRADEMARK OFFICE
_________________

BEFORE THE PATENT TRIAL AND APPEAL BOARD
_________________

Ex parte M. EDWARD MEDOF, MICHAEL G. STRAINIC,
and YOUNG A. CHOI

_________________

Appeal 2019-006093
Application 14/605,729
Technology Center 1600
_________________

Before FRANCISCO C. PRATS, JEFFREY N. FREDMAN, and
DEBORAH KATZ, Administrative Patent Judges.

KATZ, Administrative Patent Judge.
DECISION ON APPEAL
Appellant1 seeks our review,2 under 35 U.S.C. § 134(a), of the
Examiner’s decision to reject claims 44–51, 53–55, 57, and 58.3 We have
jurisdiction under 35 U.S.C. § 6(b). We AFFIRM.

1 We use the word “Appellant” as defined in 37 C.F.R. § 1.42. Appellant
identifies the real party-in-interest as Case Western Reserve University.
(Appeal Br. 2.)
2 We consider the Final Office Action issued June 6, 2018 (“Final Act.”), the
Appeal Brief filed February 28, 2019 (“Appeal Br.”), the Examiner’s
Answer issued on June 12, 2019 (“Ans.”), the Reply Brief filed August 12,
2019 (“Reply Br.”).
3 Claims 1–43 have been canceled and claims 52 and 56 withdrawn. (See
Ans. 3.)
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The Examiner rejected claims 44–51, 53–55, 57, and 58 under 35
U.S.C. § 112, first paragraph, for lack of both a sufficient written and a
enabling description. (See Final Act. 2–14.)
The Examiner also rejected claims 44–51, 53–56, 57, and 58 under 35
U.S.C. § 101, as claiming the same invention as claims 1–3, 5–8, 10, 11, and
13–18 of prior U.S. Patent 8,940,299. (See Final Act. 14–15.)
Appellant’s Specification explains that receptors for components of
the complement cascade, called “C5aR” and “C3aR,” can play a role in
attracting phagocytic cells to tumor beds and allowing these cells to ingest
complement opsonized tumor cells. (See Spec. ¶ 3.) Appellant’s claims
recite methods based on the discovery that blocking the complement-
receptor (“C5a/C3a-C5aR/C3aR”) interactions with antagonists can decrease
cancer cell proliferation and induce cancer cell death in a process called
apoptosis. (See id. at ¶ 36.)
Appellant’s independent claim 44 recites:4
A method of inducing apoptosis in a cancer cell expressing a
C3a receptor (C3aR) and a C5a receptor (C5aR), the method
comprising:
administering amounts of a C3a antagonist and a C5a
antagonist directly or locally to the cancer cell;
wherein the amounts of the C3a antagonist and the C5a
antagonist administered to the cancer are effective to induce apoptosis
in the cancer cell, and
wherein the C3a antagonist inhibits C3a mediated C3aR
signaling of the cancer cell and the C5a antagonist inhibits C5a
mediated C5aR signaling of the cancer cell.

4 Claim 44 has been modified by adding indentations to separate elements of
the recited method.
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(Appeal Br. 23.) Independent claim 48 is similar to claim 44. (See Appeal
Br. 24.) Independent claim 55 is also similar, but is limited to antibodies
against C3a and C5a as the antagonists to induce apoptosis. (See id. at 25.)
Appellant elected antibodies against C3a and C5a as the species of
C3a antagonist and C5a antagonist and melanoma as the species of cancer to
be reviewed for prosecution. (See Ans. 3; see Response to Election
Requirement filed June 29, 2017.)
Written Description
The written description requirement of 35 U.S.C. § 112, first
paragraph, requires us to determine “whether the disclosure of the
application relied upon reasonably conveys to those skilled in the art that the
inventor had possession of the claimed subject matter as of the filing date.”
Ariad Pharm., Inc., v. Eli Lilly & Co., 598 F3d 1336, 1351 (Fed. Cir. 2010).
“The purpose of [the written description] provision is to ensure that the
scope of the right to exclude, as set forth in the claims, does not overreach
the scope of the inventor’s contribution to the field of art as described in the
patent specification.” Reiffin v. Microsoft Corp., 214 F.3d 1342, 1345 (Fed.
Cir. 2000).
In regard to the unpredictable biotechnology arts, disclosure of one or
only a few species may be insufficient to support a claim to a genus that
encompasses them because “there may be unpredictability in the results
obtained from species other than those specifically enumerated.” Noelle v.
Lederman, 355 F.3d 1343, 1350 (Fed.Cir.2004). When claims recite a
functionally-defined genus, the specification must show sufficient species
with the function to show that the genus was actually invented. See AbbVie
Deutschland GmbH & Co., KG v. Janssen Biotech, Inc., 759 F.3d 1285,
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1299 (Fed. Cir. 2014) (holding claims limited to the functional element “koff
rate constant of 1x10-2s-1 or less” lacked written description support because
the specification described only one type of antibody). The Federal Circuit
has
held that “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.

Id. (quoting Regents of the University of California v. Eli Lilly & Co., 119
F.3d 1559, 1568–69 (Fed. Cir. 1997)).
Appellant’s Specification presents the results of experiments showing
abrogation of C5a/C3a-C5aR/C3aR signaling in tumor cells to induce
apoptosis. (See Spec. ¶¶ 104–105.) First, in Example 3, murine tumors
were cultured in vitro with a mixture of one particular anti-C5a monoclonal
antibody and one particular anti-C3a monoclonal antibody, both
commercially available, and assayed for levels of the indicators of cell death
Fas and FasL, as well as Bcl-2/Bcl-xl and Bax/Bim. (See Id. at ¶¶ 87, 104.)
The experiment also included in vitro treatment with C5aR and C3aR
antagonists. (See id. at ¶ 104.) The Specification states that by 24 hours the
mixture of antibodies resulted in increased expression of Fas and FasL,
down regulation of Bcl-2/Bcl-xl transcripts, and up-regulation of Bax/Bim
transcripts, consistent with increased apoptosis. (See Spec. ¶¶ 36, 104–105,
Figs. 9–12.) Appellant characterizes these results as showing that blocking
the C3a and C5a interactions with their receptors by both C3a antagonists
and C5a antagonists induces apoptosis in cancer cells expressing C3aR and
C5aR. (See Appeal Br. 11.)
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Example 3 also includes the results of experiments in which
melanoma cells were assessed for tumor growth in vivo using SCID and wild
type mice inoculated with tumor cells and administered a mixture of
C5aR/C3aR antagonist or the monoclonal antibodies against C5a and C3a or
both antagonists and antibodies. (See Spec. ¶¶ 106, 107.) The Specification
reports that each treatment protocol prolonged survival of the SCID mice.
(See Spec. ¶ 106.) A combination therapy of antagonist and antibodies
prolonged the survival of inoculated wild type mice. (See Spec. ¶ 107.)
The Examiner finds that the disclosure in Example 3 of one anti-C3a
antibody and one anti-C5a antibody is insufficient to describe the genus of
antibodies recited in the method of claim 44 because the Specification does
not identify information about other antibodies that can inhibit C3a/C5a
mediated signaling and induce apoptosis in cancer cells. (See Final Act. 4;
see Ans. 5–6.) The Examiner finds that because antibodies were known to
have a high level of polymorphism, one of ordinary skill would conclude
that the inventors were not in possession of structural attributes to induce
apoptosis as required in claim 44. (See Final Act. 6.) To support these
findings, the Examiner cites Rudikoff,5 Colman,6 Kussie,7 and Chen,8 which

5 Rudikoff et al., “Single amino acid substitution altering antigen-binding
specificity,” PNAS 79:1979–83 (1982).
6 Colman, “Effects of amino acid sequence changes on antibody-antigen
interaction,” Research in Immunology 145:33–36 (1994).
7 Kussie et al., “A Single Engineered Amino Acid Substitution Changes
Antibody Fine Specificity,” J. Immunol. 152:146–52 (1994).
8 Chen et al., “Enhancement and destruction of antibody function by somatic
mutation: unequal occurrence is controlled by V gene combinatorial
associations,” EMBO J. 14:2784–94 (1995).
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teach that even minor amino acid changes can affect the antigen-binding
characteristics of an antibody. (See Final Act. 6.)
The Examiner also finds that the disclosure of a single anti-C3a
antibody/anti-C5a antibody pair in Appellant’s Specification fails to
sufficiently describe the full scope of claim 44 because inducing apoptosis in
cancer cells through complement is complex, involving many different
pathways with potentially disparate effects. (See id. at 7.) In support, the
Examiner cites to two post-filing date publications: Rutkowski9 and
Darling.10 (See id. at 7.) Rutkowski teaches that complement components
can play complicated roles in the tumor microenvironment, including direct
and antibody-dependent cell mediated cytotoxic defenses against tumors.
(See Rutkowski at 1460.) Darling teaches that C5a agonists can be useful in
the effectiveness of tumor vaccines and that, in general, the full roll of C5a
in tumorigenesis is unknown, possibly being concentration dependent at the
tumor site. (See Darling 7–9.) Darling indicates that even in 2015, well
after Appellant’s earliest filing date in 2008, “additional studies [were]
warranted to confirm and compare the effects of C5a at various
concentrations, and perhaps in diverse microenvironment, in regard to its
pro- and antitumor activity.” (Darling 9.) Given the unpredictable effects of
anti-C3a and anti-C5a antibodies and the complexity of the complement
pathways targeted, the Examiner concludes that a single experiment with
one set of antibodies does not provide sufficient written description support

9 Rutkowski et al., “Cancer and the Complement Cascade,” Mol. Cancer
Res. 8:1453–65 (2010).
10 Darling et al., “Immunological Effects and Therapeutic Role of C5a in
Cancer,” Expert Rev. Clin. Immunol. 11:255–63 (2015).
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for the full scope of claim 44, encompassing any antibody against C3a and
against C5a. (See Final Act. 8.)
Appellant argues that the Examiner errs because the Specification
allows persons of ordinary skill in the art to recognize that Appellant was in
possession of C3a antagonists and C5a antagonists and because the
Specification shows that administration of a C3a antagonist and a C5a
antagonist would induce apoptosis in cancer cells expressing C3aR and
C5aR. (See Appeal Br. 7.) Appellant argues that the disclosure of
representative compositions or of distinguishing structural features common
to members of the claimed genus can be sufficient written description
support. (See id., citing Lilly, 119 F.3d at 1568.) According to Appellant,
C3a antagonists and C5a antagonists were well known to skilled artisans at
the time of filing and were commercially available. (See Appeal Br. 8–11,
citing Spec. ¶ 87.) Appellant argues further that Example 3 demonstrates
that the combination of anti-C3a antibody and anti-C3b antibody disabled
C5a-receptor and C3a-receptor signal transduction and induced apoptosis
and, thus, those in the art would have recognized that the inventors were in
possession of the claimed method. (See Appeal Br. 11, citing Spec. ¶¶ 101–
108.)
Appellant’s arguments are unpersuasive because they do not
sufficiently address the Examiner’s findings, based on Rudikoff, Colman,
Kussie, and Chen, that not all anti-C3a or anti-C5a antibodies will
necessarily have the same effects given that even small differences in
antibodies can cause disparate actions. Appellant also fails to sufficiently
address the Examiner’s findings, based on Rutkowski and Darling, that
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interactions with the complement pathway are not always predictable and
can be affected by variables such as the concentration of components.
Appellant argues that although claim 44 encompasses antibodies,
Appellant is not claiming antibodies to a newly characterized antigen and,
therefore, Amgen Inc. v. Sanofi, 872 F.3d 1367 (Fed. Cir. 2017), cited by the
Examiner, is not controlling. (See Appeal Br. 11; see Reply Br. 3.) We
disagree because the holding of Amgen is not based merely on the newness
of the antigen, but also on the functional language recited in the claim at
issue. See Amgen, 872 F.3d at 1378 (“We cannot say that this particular
context, involving a ‘newly characterized antigen’ and a functional genus
claim to corresponding antibodies, is one in which the underlying science
establishes that a finding of ‘make and use’ (routine or conventional
production) actually does equate to the required description of the claimed
products.” (emphasis added)). The claim at issue in Amgen recites not just
an antibody, but one that binds to certain residues of a biological protein and
“blocks binding” of that protein to another. Id. at 1372. Thus, like
Appellant’s current claims, the claims at issue in Amgen are characterized by
their function.
Centocor Ortho Biotech, Inc. v. Abbott Labs., 636 F.3d 1341 (Fed.
Cir. 2011), is similarly informative for the written description issues of
Appellant’s claims. In that case, the court explained:
Claiming antibodies with specific properties, e.g., an antibody that
binds to human TNF-α with A2 specificity [indicating the ability to
bind TNF-α in a specific location], can result in a claim that does not
meet written description even if the human TNF-α protein is disclosed
because antibodies with those properties have not been adequately
described.

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Id. at 1352. Even though claim 44 encompasses antibodies to known
antigens, it requires certain functions of these antibodies. Under Amgen,
Centocor, and similar cases,11 Appellant must present sufficient evidence
that one of ordinary skill would have understood the inventors were in
possession of not just one antibody that binds C3a and one antibody that
binds C5a, but a representative number of antibodies demonstrating
possession of the full scope of antibodies with the functional characteristic
of being “effective to induce apoptosis in the cancer cell” and of inhibiting
C3a mediated C3aR and C5a mediated C5aR signaling in the cancer cell.
We are not persuaded that the disclosure of one antibody pair
meeting the claimed functional limitations in Example 3 of the Specification
is sufficient. Even if other antibodies were known, Appellant does not direct
us to evidence that all other anti-C3a and anti-C5a antibodies, or indeed any
other antibodies, would result in an induction of apoptosis in cancer cells.
(Contra Reply Br. 5, citing Spec. ¶ 41.) Given the variability of different

11 See AbbVie, 759 F3d at 1299; see also Ariad Pharm., Inc. v. Eli Lilly &
Co., 598 F.3d 1336, 1350 (Fed. Cir. 2010) (“We have also held that
functional claim language can meet the written description requirement
when the art has established a correlation between structure and function.
But merely drawing a fence around the outer limits of a purported genus is
not an adequate substitute for describing a variety of materials constituting
the genus and showing that one has invented a genus and not just a species. .
. . In fact, this case similarly illustrates the problem of generic claims. The
claims here recite methods encompassing a genus of materials achieving a
stated useful result, i.e., reducing NF-κB binding to NF-κB recognition sites
in response to external influences. But the specification does not disclose a
variety of species that accomplish the result.”) (citations omitted).

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antibodies, the complexity of the complement pathway, and the general
unpredictability of the art the Examiner demonstrates by citing research, we
are not persuaded that one of ordinary skill would understand the inventors
were in possession of the full scope of claim 44 without some definition of
structure-function relationship between anti-C3a and anti-C5a antibodies and
induction of apoptosis or inhibition of C3a and C5a signaling. We are not
persuaded that those of ordinary skill would know which other anti-C3a and
anti-C5a antibodies would meet these functional requirements because
Appellant’s Specification does not provide evidence that any other
antibodies would do so.
Because Appellant fails to persuade us that claim 44, limited to the
elected species of an antibody as the C3a antagonist and an antibody as the
C5a antagonist, is supported by a sufficient written description, we would
not be persuaded that the full scope of claim 44, encompassing any C3a and
C5a antagonist, is supported by a sufficient written description. In addition,
because Appellant does not argue for the separate patentability of any of the
claims rejected for a lack of sufficient written description, we are not
persuaded that any other claims are sufficiently supported.
Accordingly, the Examiner did not err in rejecting Appellant’s
currently pending claims under 35 U.S.C. § 112, first paragraph.
Enablement
The Examiner rejects all of Appellant’s claims as lacking an enabling
disclosure under 35 U.S.C. § 1112, first paragraph. (See Final Act. 8–14.)
A patent specification must enable one of ordinary skill in the art “to
practice the claimed invention without undue experimentation.” Nat’l
Recovery Techs., Inc. v. Magnetic Separation Sys., Inc., 166 F.3d 1190, 1196
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(Fed. Cir. 1999) (emphasis omitted). Whether undue experimentation would
be required is determined by analyzing a number of factors, including
(1) the quantity of experimentation necessary, (2) the amount of
direction or guidance presented, (3) the presence or absence of
working examples, (4) the nature of the invention, (5) the state of
the prior art, (6) the relative skill of those in the art, (7) the
predictability or unpredictability of the art, and (8) the breadth of
the claims.

In re Wands, 858 F.2d 731, 737 (Fed. Cir. 1988).
Appellant does not argue for the separate patentability of any of the
rejected claims. We focus on claim 48, which recites:
A method of treating cancer in a subject in need thereof, the method
comprising: administering directly or locally to cancer cells
expressing C3aR and C5aR of the subject therapeutically effective
amounts of a C3a antagonist and a C5a antagonist, wherein the
amounts of C3a antagonist and C5a antagonist administered to the
cancer cells induce apoptosis in the cancer cells, and the C3a
antagonist inhibits C3a mediated C3aR signaling of the cancer cell
and the C5a antagonist inhibits C5a mediated C5aR signaling of the
cancer cell.

(Appeal Br. 24.) Claim 55 similarly recites a method of treating cancer in a
subject by administering C3a and C5a antibodies to induce apoptosis. (See
Appeal Br. 25.)
We note at the outset that although Appellant elected melanoma as the
species of cancer for the Examiner’s search, we review the rejection as if the
requirement for an election was withdrawn. (See Ans. 3 (acknowledging the
election of species, but stating that “[u]pon search and in the interest of
compact prosecution, the election of species has been extended to all species
of cancer (e.g., see claims 54, 58).”)
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The Examiner finds that Appellant’s claims are broad, being unlimited
as to antibody or the environment of the cancer cells targeted, as well as
encompassing treatment of cancer in human patients. (See Final Act. 12.)
The Examiner finds further that in vitro studies, like the study presented in
Example 3, would not necessarily reflect the relative efficacy of the claimed
therapeutic strategy to induce apoptosis in cancer with the claimed
antibodies. (See id.) For example, the Examiner notes that treatment of
cancer in human patients may start only after cancer has been established for
some time, a condition not reflected in in vitro experiments. (See id.; see
Ans. 16.)
Furthermore, as discussed above, the Examiner cites to Rutkowski for
its teaching of the complicated roles complement plays in the tumor
microenvironment, including as direct and antibody-dependent cell mediated
cytotoxic defenses against tumors, and to Darling for its teachings that the
full roll of C5a in tumorigenesis was unknown at the time of filing and that
additional studies were warranted even years after filing to understand its
pro- and antitumor activity. (See Final Act. 13; see Ans. 16–18, see
Rutkowski 1460; see Darling 9.) The Examiner concludes:
The specification describes experimental models that do not provide
sufficient predictability of treating cancer as well as inhibiting
C3a/C5a mediated signaling and inducing apoptosis in cancer cells
that reflect the complexity and unpredictability of achieving such
results in tumor microenvironment by a broad range of cancer cells
encompassed by the scope of the claimed methods. This description of
experimental models without more is a starting point, a direction for
further research.

(Ans. 19.)
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Appellant argues that the amount of direction or guidance disclosed in
the Specification is sufficient to enable a skilled artisan to make and use the
method of claim 48 using only routine experimentation. (See Appeal Br.
13.) Appellant argues that the Specification shows that in certain cancer
cells expressing C3aR and C5aR, that C3aR and C5aR signaling promotes
cancer cell survival and that inhibition of this signaling can induce
apoptosis. (See id. at 14, citing Spec. ¶¶ 35–37, 101; see Reply Br. 7.)
Appellant argues further that Example 3 is a working example of blocking
C3a and C5a interactions with their receptors by administering antagonists
against the receptors. (See Appeal Br. 15.) Appellant concludes:
Thus, the specification of the present application clearly allows one
skilled in the art to recognize what is claimed based on the disclosure
of the . . . specific C3a antagonists and C5a antagonists, the fact that
C3a antagonists and C5a antagonists were well known at the time of
filing the application, the described mechanism of action the C3a
antagonists and C5a antagonists, and the fact that the specification and
claims are limited to specific cancer cell types, i.e., cancer cells
expressing C3aR and C5aR.

(Appeal Br. 16.)
We are not persuaded by this argument because Appellant does not
address the knowledge in the art of the complex role of complement in
tumorigenesis and thus in treating cancer in patients through complement.
Appellant does not address the Examiner’s finding that
[i]n contrast to appellant’s arguments, including reliance . . . upon
mechanisms of action, it is maintained that applicant relies upon
experimental murine tumor models based upon defined conditions
(e.g., administering [antagonist] of at the same time of administering
cancer cell lines), implantation of tumor cell lines and not testing
tumor cells implanted into the organ of origin in models or
spontaneous/ chemically induce tumors that allow for a more suitable
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interaction between tumor cells and the surrounding stroma and
provide more relevant information about the role for complement in
the modulation of the tumor microenvironment, where the complexity
and unpredictability in the context of treating cancer via C3a/C5a
complement inhibitors are addressed by [Rutkowski] et al. and
Darling et al.

(See Ans. 18–19.) In light of the post-filing date teachings of Rutkowski and
Darling, we are not persuaded by Appellant’s argument that Example 3
alone would provide enough information for one of ordinary skill in the art
to make a use a method of treating cancer in a subject, as recited in claim 48.
We note further that the results provided in the figures cited in
Example 3 are ambiguous about the effects of anti-C3a and anti-C5a
antibodies on survival of mice injected with tumor cells. Specifically,
Example 3 refers to experiments using different treatments on melanoma
cells in SCID12 mice. (See Spec. ¶ 106.) The Specification reports that
Figure 13A shows the results of administering C3aR-antagonist along with
C5aR-antagonist, which “prolonged survival.” (Id.) Figure 13A depicts two
survival curves, one showing longer survival times than the other. Although
the two curves use different symbols, there is no legend to indicate which
treatment these symbols represent.
The Specification reports, further, that Figure 13B shows the results of
administering anti-C3a antibody along with anti-C5a antibody, which
“prolonged survival even longer.” (Spec. ¶ 106.) Figure 13B is reproduced
below.

12 SCID refers to severe combined immunodeficient mice, which lack a
potential adaptive immune effects against inoculated tumor cells. (See Spec.
¶ 106.)
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Figure 13B depicts one survival curve and a legend with “PBS cont” and
“RA” indicating the same symbol. The control and “RA” treatments are
both depicted as the same symbol in the legend provided. Appellant fails to
direct us to an explanation, either in the Specification or by one who can
testify to the understanding of an ordinarily skilled artisan, how Figure 13B
demonstrates that the combination of anti-C3a and anti-C5a antibodies
increased survival over control. It is not clear how the treatment survival
curve differs from the control curve or even if both curves are present.
We note further that Figure 13C is reported to depict survival of
tumor-injected SCID mice with a combination of C5aR antagonist/C3a
antagonist and anti-C5a/anti-C3a antibody, which “showed that the
combination prolonged survival markedly most efficiently.” (Spec. ¶ 106.)
The curve indicated to be “RA” in the legend of Figure 13C, though, appears
to be the same as the single curve depicted in Figure 13B. Without further
explanation as to how one of ordinary skill in the art would understand these
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figures, we are not persuaded that the results discussed in Example 3 are
strong enough to present an enabling description of the claimed methods.
Finally, we note that although the Specification reports experiments
with C5aR/C3aR antagonists and anti-C3a/anti-C5a antibodies in wild-type
mice, the results obtained with anti-C3a/anti-C5a antibodies alone are not
discussed. (See Spec. ¶ 107.) Again, we are not persuaded that the Example
3 alone provides an enabling description of the claimed methods because it
is not clear that the results in even two different types of mice are consistent.
In general, we are not persuaded that Appellant’s Specification would
indicate to one of ordinary skill in the art how to make or use a method of
treating cancer in a subject in need thereof by administering amounts of anti-
C3a and anti-C5a antibodies, as required in claim 48. Despite Appellant’s
arguments that the teachings of Rutkowski and Darling are only
“generalized concerns,” (Appeal Br. 17), the lack of clarity in the results of
Appellant’s own studies tends to reinforce rather than refute the complexity
and unknown role of complement in tumorigenesis.
Accordingly, Appellant fails to persuade us that the Examiner erred in
rejecting claim 48 or any other claim as lacking an enabling description
under 35 U.S.C. § 112, first paragraph.
Statutory Double-Patenting
The Examiner rejects claims 41–51, 53–55, and 57–58 under 35
U.S.C. § 101 as claiming the same invention as claims 44–51, 53–55, 57,
and 58of commonly assigned U.S. Patent 8,940,299 (the ’299 patent”). (See
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Final Act. 14.) The Examiner explains that this is a statutory double-
patenting rejection. (See Final Act. 14.)
Claim 1 of the ’299 patent recites:
A method of inducing apoptosis in a cancer cell expressing a C3a
receptor (C3aR) and a C5a receptor (C5aR), the method comprising:
administering amounts of a C3aR antagonist and a C5aR antagonist
directly or locally to the cancer cell; wherein the amounts of the C3aR
antagonist and the C5aR antagonist administered to the cancer cell are
effective to substantially reduce or substantially inhibit the activity of
protein kinase B (PKB) in the cancer cell and induce apoptosis in the
cancer cell, and wherein the C3aR antagonist inhibits C3a mediated
C3aR signaling of the cancer cell and the C5aR antagonist inhibits
C5a mediated C5aR signaling of 60 the cancer cell.

(’299 Patent 23:59–24:3.) The Examiner finds that the only difference
between claim 1 of the ’299 patent and Appellant’s currently pending
claims, for example claim 44, is that claim 1 recites “wherein the amounts of
the C3aR antagonist and the C5aR antagonist administered to the cancer cell
are effective to substantially reduce or substantially inhibit the activity of
protein kinase B (PKB) in the cancer cell” as well as being effective to
induce apoptosis. (See Final Act. 14.) The Examiner finds that the
limitation of claim 1 is inherent to the method of claim 44, pointing to
Appellant’s currently pending claim 57. (See Final Act. 14.)
We disagree that the claims of the ’299 patent and Appellant’s
currently pending claims differ only in the limitation regarding protein
kinase B. Instead, as Appellant argues, claim 1 of the ’299 patent recites
administering a C3aR antagonist and a C5aR antagonist, whereas the
currently pending claims recite administering a C3a antagonist and a C5a
antagonist. (See Appeal Br. 20.) Thus, even if reducing or substantially
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inhibiting the activity of protein kinase B is inherent administering C3aR
and C5aR antagonists, administering antagonists to these receptors is not the
same as administering antagonists to C3a and C5a.
Because the claims of the ’299 patent are not directed to the same
invention as Appellant’s currently pending claims, we do not sustain the
Examiner’s rejection under 35 U.S.C. § 101 for double-patenting.
Conclusion
Upon consideration of the record and for the reasons given, we affirm
the Examiner’s rejection.
In summary:
Claims
Rejected
35 U.S.C. § Basis Affirmed Reversed
44–51, 53–55,
57, 58
112, first
paragraph
Written
description
44–51, 53–55,
57, 58

44–51, 53–55,
57, 58
112, first
paragraph
Enablement 44–51, 53–55,
57, 58

44–51, 53–55,
57, 58
101 Statutory
Double
Patenting
44–51, 53–55,
57, 58
Overall
Outcome
44–51, 53–55,
57, 58

No time period for taking any subsequent action in connection with
this appeal may be extended under 37 C.F.R. § 1.136.

AFFIRMED