Ex Parte Stoiber

Patent Trial and Appeal Board

Nov 6, 2017

12597422 (P.T.A.B. Nov. 6, 2017)

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.
12/597,422 06/25/2010 Heribert Stoiber VOSS:023US 9905
108197 7590 11/08/2017
Parker Highlander PLLC
1120 South Capital of Texas Highway
Bldg. 1, Suite 200
Austin, TX 78746
EXAMINER
ZEMAN, ROBERT A
ART UNIT PAPER NUMBER
1645
NOTIFICATION DATE DELIVERY MODE
11/08/2017 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):
docket @ phiplaw .com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte HERBERT STOIBER1
Appeal 2016-005750
Application 12/597,422
Technology Center 1600
Before FRANCISCO C. PRATS, JOHN G. NEW, and, RYAN H. FLAX,
Administrative Patent Judges.
FLAX, Administrative Patent Judge.
DECISION ON APPEAL
This is a decision on appeal under 35 U.S.C. § 134(a) involving
claims directed to a short consensus repeat-antibody construct (SCR-Ab).
Claims 1—4, 8, 9, 11, 12, 14—16, 25, and 26 are on appeal and rejected under
35 U.S.C. § 103.2 We have jurisdiction under 35 U.S.C. § 6(b).
We affirm.
1 Appellant identifies the Real Party in Interest as “Lysomab GmbH.” See
Letter dated Nov. 3, 2016 (updating Appeal information).
2 Claims 5—7, 10, 13, 17—24, 27, 28, and 31—42 stand withdrawn from
consideration and claims 29 and 30 are cancelled. App. Br. 13—19.
Appeal 2016-005750
Application 12/597,422
STATEMENT OF THE CASE
The Specification states “[t]he technical problem underlying the
present invention is to provide efficacious means and methods for
prevention, treatment or amelioration of an infection with a pathogen or of a
pathological condition associated with an infection with a pathogen or of a
condition associated with a proliferative disease, like cancer.” Spec. 3 (first
paragraph). Further, the Specification states, “[tjhese inventive constructs
are also useful in the medical intervention of cancer and/or of proliferative
disorders, whereby in these embodiments binding molecules are to be
employed that specifically bind to or recognize a cancer cell, tumour cell or
a malignant cell.” Id. (last paragraph).
Claim 1 is the sole independent claim, is representative, and is
reproduced below (paragraph returns added for clarity):
1. A short consensus repeat-antibody construct (SCR-Ab)
comprising
a complement factor H-derived short consensus repeat (fH-
derived SCR) linked to a binding molecule that specifically
recognizes a pathogen,
wherein said fH-derived SCR comprises a polypeptide that is
capable of binding heparin and to negatively charged host cells,
and wherein said complement factor H-derived short consensus
repeat (fH-derived SCR) and said binding molecule are
covalently linked or comprised in a single chain multi-functional
polypeptide.
App. Br. 13 (Claims App’x).
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The following rejections are on appeal:
Claims 1—4, 8, 9, 11, 14—16, 25, and 26 are rejected under 35 U.S.C.
§ 103(a) over Pinter3 and Reiter.4 Answer 2.
Claims 1—4, 8, 9, 11, 12, 14—16, 25, and 26 are rejected under 35
U.S.C. § 103(a) over Pinter, Reiter, and Stiegler.5 Id. at 3^4.
Claims 1—4, 8, 9, 11, 14—16, 25, and 26 are rejected under 35 U.S.C.
§ 103(a) over Pinter and Farries.6 Id. at 5.
Claims 1—4, 8, 9, 11, 12, 14—16, 25, and 26 are rejected under 35
U.S.C. § 103(a) over Pinter, Farries, and Stiegler. Id. at 6.
LAW
Only those arguments made by Appellant in the Briefs have been
considered in this Decision. Arguments not presented in the Briefs are
waived. See 37 C.F.R. § 41.37(c)(l)(iv). Further, an argument raised for the
first time in a Reply Brief can be considered waived if Appellant does not
explain why it could not have been raised previously. See Ex parte
Nakashima, 93 USPQ2d 1834 (BPAI 2010) (informative) (explaining that
arguments and evidence not timely presented in the principal Brief will not
3 Claudia Pinter et al., Interference with Complement Regulatory Molecules
as a Possible Therapeutic Strategy in HIV Infection, 9 Exp. Opin. Invest.
Drugs 199-205 (2000) (“Pinter”).
4 Yoram Reiter & Zvi Fishelson, Targeting of Complement to Tumor Cells
by Heteroconjugates Composed of Antibodies and of the Complement
Component C3b], 142 J. Immunology 2771—77 (1989) (“Reiter”).
5 Gabriela Stiegler et al., Antiviral Activity of the Neutralizing Antibodies
2F5 and 2G12 in Asymptomatic HIV-1-infected Humans: a Phase I
Evaluation, 16 AIDS 2019-25 (2002) (“Stiegler”).
6 US 2002/0068059 Al (published June 6, 2002) (“Farries”).
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be considered when filed in a Reply Brief, absent a showing of good cause
explaining why the argument could not have been presented in the Principal
Brief); Ex parte Borden, 93 USPQ2d 1473, 1477 (BPAI 2010) (informative)
(“Properly interpreted, the Rules do not require the Board to take up a
belated argument that has not been addressed by the Examiner, absent a
showing of good cause.”). “The reply brief is not an opportunity to make
arguments that could have been made during prosecution, but were not. Nor
is the reply brief an opportunity to make arguments that could have been
made in the principal brief on appeal to rebut the Examiner’s rejections, but
were not.” Borden, 93 USPQ2d at 1474; see also MPEP § 1205(c)(l)(iv)
(regarding requirements for separately arguing claims on appeal).
In analyzing patentability and determining obviousness “[t]he
combination of familiar elements according to known methods is likely to be
obvious when it does no more than yield predictable results.” KSR Int’l Co.
v. Teleflex Inc., 550 U.S. 398, 416 (2007). “[W]hen the question is whether
a patent claiming the combination of elements of prior art is obvious,” the
answer depends on “whether the improvement is more than the predictable
use of prior art elements according to their established functions.” Id. at
417. “If a person of ordinary skill can implement a predictable variation [of
a known work], § 103 likely bars its patentability.” Id. “For the same
reason, if a technique has been used to improve one device, and a person of
ordinary skill in the art would recognize that it would improve similar
devices in the same way, using the technique is obvious unless its actual
application is beyond his or her skill.” Id.
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Non-obviousness can be evidenced by unexpected results, but “[t]o be
particularly probative, evidence of unexpected results must establish that
there is a difference between the results obtained and those of the closest
prior art, and that the difference would not have been expected by one of
ordinary skill in the art at the time of the invention.” Bristol-Myers Squibb
Co. v. Teva Pharms. USA, Inc., 752 F.3d 967, 977 (Fed. Cir. 2014).
Consistent with the rule that ah evidence of non­
obviousness must be considered when assessing patentability,
the PTO must consider comparative data in the specification in
determining whether the claimed invention provides unexpected
results. In re Margolis, 785 F.2d 1029, 1031 (Fed. Cir. 1986).
However, “it is well settled that unexpected results must be
established by factual evidence. Mere argument or conclusory
statements in the specification does not suffice.” In re De
Blauwe, 736 F.2d 699, 705 (Fed. Cir. 1984); see also In re Wood,
582 F.2d 638, 642 (CCPA 1978) (“Mere lawyer’s arguments and
conclusory statements in the specification, unsupported by
objective evidence, are insufficient to establish unexpected
results.”); In re Lindner, 457 F.2d 506, 508 (CCPA 1972)
(“[M]ere conclusory statements in the specification ... are
entitled to little weight when the Patent Office questions the
efficacy of those statements.”).
In re Soni, 54 F.3d 746, 750 (Fed. Cir. 1995) (internal cites to USPQ
omitted).
FINDINGS OF FACT
We adopt the Examiner’s findings of fact, reasoning on scope and
content of the claims and prior art, and conclusions set out in the Final
Office Action and Examiner’s Answer. The findings of fact set forth below
are provided to highlight certain evidence.
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FF1. Pinter is directed to interfering with the complement
immune system regulatory controls so as to utilize the complement
immune system to lyse cells and, thus, treat disease. Pinter 199-204;
see also Final Action 4—13 and Answer 2—14 (discussing Pinter).
FF2. Pinter teaches that competitively interfering with CFH
(complement Factor H) provides “a new therapeutic approach based
on inhibition of the interaction between CFH and the cell surface of
infected cells, thus releasing the protective mechanism,” which
prevented such cells from being naturally destroyed by lysis;
explaining that “C3b fixation is the critical step of a process, which
leads to the formation of a pore in the target cell membrane, the
membrane attack complex (MAC), which eventually results in cell
lysis (Figure 1).” Pinter 199—200; see also Final Action 4—13 and
Answer 2—14 (discussing Pinter).
FF3. Further to the preceding finding of fact, Pinter discloses,
“[i]n the case of free virus, lysis could be further enhanced through
the addition of a blocking antibody against CD55 [complement decay-
accelerating factor], however, CFH binding was shown to be
responsible for most of the resistance mechanism in both cases.”
Pinter 202; see also Final Action 4—13 and Answer 2—14 (discussing
Pinter).
FF4. Pinter discloses, and illustrates, the “functional domains
of human CFH” at Figure 3, which is reproduced below:
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Figure 3: Localisation of the functroaai domains of human CFH.
Co-factor site
C3b site 1 C3b site 2 • C3b site 3
Hepafin Hepann Heparin
binding binding binding
. sits 1 sits 2 site 3
Pinter’s Figure 3 shows CFH’s short consensus repeats (SCRs) 1—20
and identifies that SCR 1—4, 6—10, and 16—20 constitute C3b binding
sites and that SCR 6—10, 12—14, and 18—20 constitute Heparin binding
sites. Pinter 202; see also Final Action 4—13 and Answer 2—14
(discussing Pinter). Pinter also explains that “SCR 1^4[] is
responsible for the co-factor activity of CFH, namely the binding of
C3b for its proteolytic inactivation,” which “leads to the production of
inactivated C3b (iC3b), a molecule which is unable to participate in
the lytic process.” Id.
FF5. Pinter further discloses “SCR 13 is involved in the
interaction with the transmembrane protein of HIV,” “[i]t was shown
that a peptide reproducing the N-terminal half of SCR 13 was able to
compete with the binding of CFH in the HIV target regions,” and
“[t]he same peptide could induce complement-mediated killing of
HIV-infected cells in the presence of antibodies from AIDS patients
or of a monoclonal antibody (mAb) recognising a native epitope on
the gpl20 molecule.” Pinter 202; see also Final Action 4—13 and
Answer 2—14 (discussing Pinter).
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FF6. Pinter further discloses, however, that “[t]he killing
efficiency was clearly dependent on peptide concentration as well as
peptide conformation. High peptide concentrations had to be used (>
20 jig/ml), as the CFH is highly concentrated in human serum (400 -
700 jig/ ml) to achieve an effective competition.” Pinter 202; see also
Final Action 4—13 and Answer 2—14 (discussing Pinter).
FF7. Reiter is directed to and discloses “targeting of
complement” immune-attack on cancer cells using antibodies (mAb)
that “bind to the human and mouse transferrin receptors,” which
allows the therapy to differentiate between proliferating cancer cells
and normal cells. Reiter 2771—72, 2775 (capitalization omitted); see
also Final Action 4—8 and Answer 2-4, 8—10 (discussing Reiter).
FF8. Reiter discloses covalently cross-linking the mAb to C3b
using the cross-linking agent SPDP to form an mAb-C3b conjugate,
which was shown to actively and efficiently induce lysis in cancer
cells via the complement system. Reiter 2771—2276; see also Final
Action 4—8 and Answer 2—4, 8—10 (discussing Reiter).
FF9. Reiter discloses that “mAb conjugated with various toxic
substances have been largely used to eradicate tumor cells in vitro as
well as in vivo,” thus, identifying antibody conjugation as a well-
known method of targeting cells for eradication using the complement
immune system or otherwise. Reiter 2776; see also Final Action 4—8
and Answer 2-4, 8—10 (discussing Reiter).
FF10. Farries is directed to and discloses “C3 protein” and
“[cjonjugates comprising such proteins and a specific binding moiety,
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for example an antibody . . . [and] uses of such proteins and/or
conjugates in therapy.” Farries Abstr., || 42-47; see also Final
Action 8—13 and Answer 5—7, 11—14 (discussing Farries).
FF11. Farries Figure 9 illustrates the ability of conjugates of
C3i-IgG to lyse sheep erythrocytes as compared to C3i and IgG
individually. Farries Figure 9, ^fl[ 102—12; see also Final Action 8—13
and Answer 5—7, 11—14 (discussing Farries).
FF12. Farries discloses:
To make a specific pathogenic target more susceptible to
complement-mediated immune mechanisms. In this approach,
the aim is not to use the super-active C3 convertase to produce
generalized depletion of C3, but instead to use the convertase
locally to concentrate the C3 conversion at a desired target. The
target may be a pathogenic organism, such as a bacteria, virus or
other parasite, or a deleterious host cell or tissue, such as a
tumour cell or a virally infected cell. The C3 convertase could
be localised to the target either by local administration (e.g. direct
injection, possibly in a medium that retards its dispersion into the
general circulation), or by combining with a targeting moiety,
e.g. an antibody. Thus the modified protein could be linked to a
specific immunoglobulin either by chemical cross-linking of the
proteins, or by joining the DNA coding sequences and expressing
(and purifying) the fusion protein (e.g. in the case of IgG, either
the heavy or the light chain could be attached to C3 and co­
expressed with C3, or both chains could be combined within one
complete fusion polypeptide)....
Farries 1 57; see also Final Action 8—13 and Answer 5—7, 11—14
(discussing Farries).
FF13. Farries discloses that a C3 i-antibody conjugate can be
used “to [tjarget C3 [cjonvertase [ajctivity [ajgainst a [particular
[c]ell,” which “initiate[s] complement-dependent attack of a particular
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cell type,” leading to “lysis of these cells.” Farries Tflf 272—90
(discussing Example 10 and Figure 9); see also Final Action 8—13 and
Answer 5—7, 11—14 (discussing Farries).
FF14. Stiegler discloses using 2G12 antibodies to target HIV-1
infected cells, whereby a “[vigorous complement activation was
observed.” Stiegler 2019; see also Final Action 6—8, 11—12 and
Answer 3—4, 6, 9—10, 13—14 (discussing Stiegler).
DISCUSSION
Obviousness over Pinter and Reiter
In view of the above-identified findings of fact and the above-cited
precedent, the Examiner has set forth a prima facie case that the claims (all
but claim 12) would have been obvious over Pinter and Reiter. See Final
Rejection 4—6 and Answer 2—3 and 7—8. For example, Pinter and Reiter
teach and suggest a covalently bound SCR-Ab conjugation would provide an
effective therapy by targeting and destroying pathogen cells. FF1—FF9.
Pinter teaches and suggests an (or several) SCR derived from factor H that is
capable of binding heparin and binding to negatively charged host cells (e.g.,
SCR 13) and would be useful in causing cell lysis via the complement
immune system. FF1—FF6. Reiter teaches and suggests similar, albeit not
identical, cell-lysis-via-complement-immune-system-action and that such a
therapy can be specifically targeted to pathogen cells by conjugating the
complement immune system component to an antibody. FF7—FF9. It would
have been reasonable for a skilled artisan to have consulted among and also
combined these references because they are directed to a common problem,
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that is, therapy by invoking a complement immune system response to a
specific pathogen. Appellant has not presented persuasive argument or
evidence that the Examiner’s determination is incorrect.
Appellant argues a physical linkage between the claimed SCR and
antibody is required for therapeutic efficacy and its inclusion provides
unexpected and surprising results compared to non-physically-linked
formulations. See, e.g., App. Br. 7. Appellant argues that Pinter, while
teaching “SCR 13 (derived from factor H) binds competitively to HIV-
infected cells and that it leads to lysis of the infected cells,” “does not
describe a construct which is linked to a pathogen binding antibody.” Id.
Appellant argues:
(i) Pinter does not describe a construct in which fH-derived
peptides are covalently linked or comprised in a single chain
multi-functional polypeptide to an antibody moiety binding to a
pathogen and/or pathogen infected cell.
(ii) Moreover, there is no hint in Pinter that the claimed coupled
constructs can be used as a tool to enhance the complement-
mediated lysis of said pathogen and/or pathogen infected cell.
Id. Appellant also argues that Reiter is directed to a different mechanism
than the fH-derived SCR because the C3b C component of Reiter (a non-
heparin-binding molecule) operates by activation of C3 where the SCR of
the claimed invention is a negative complement regulator. Id. Appellant
contends Reiter operates via the alternative pathway while the claimed
invention activates the classical pathway. Id. at 8. Appellant contends
Reiter’s disclosed heteroconjugate is “totally unrelated” to the claimed
invention. Id. at 9.
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The Examiner responds to Appellant’s arguments and states that
Pinter “disclose[s] that peptides derived from . . . SCR13[] were able to
induce complement-mediated killing (lysis).” Answer 8. The Examiner
determined that Reiter taught that “increased efficacy of hetero-conjugates in
complement mediated cell lysis” and Reiter’s “different pathway is not
germane” because the reference “provides the skilled artisan with a means of
overcoming the deficiencies of the peptides therapy of Pinter (i.e., the need
for high concentrations of peptides).” Id. The Examiner contends that the
skilled artisan would have recognized that using an antibody for selective
targeting of Pinter’s SCR peptide would increase efficiency. Id.
In the Reply Brief, Appellant does not make any significant new
points, but does state, “Reiter makes the unremarkable observation that if
this enzyme [C3b] is targeted to tumor cells, the complement activation by
the C3b enzyme can be focused specifically on the tumor cells.” Reply Br.
2. We note, Appellant argues, for the first time in the Reply Brief, that claim
2 is separately patentable. Id. at 4.
We conclude, on the balance of the evidence presented, the Examiner
has the better position. Appellant largely argues that each reference, taken
individually, would not teach or suggest the invention; however, “[n]on-
obviousness cannot be established by attacking references individually
where the rejection is based upon the teachings of a combination of
references. . . . [The reference] must be read, not in isolation, but for what it
fairly teaches in combination with the prior art as a whole.” In re Merck &
Co., 800 F.2d 1091, 1097 (Fed. Cir. 1986). Here, the prior art combination,
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as a whole, renders the claimed invention obvious for the reasons set forth
by the Examiner.
As to Appellant’s terse argument that the invention achieves an
unexpected result, we are not persuaded. Appellant merely points to the
Specification’s Tables 5 and 6, which indicate that pairing an SCR and
antibody was successful, as evidence of unexpected results. Mere success is
not sufficient evidence that the results would have been surprising to one of
ordinary skill in the art as of the invention date, as compared with the closest
prior art, and particularly in view of the teachings of the prior art of record
that conjoining a cell- or pathogen-killer compound with a targeting
antibody is an effective form of therapy. See, e.g., FF6—FF9 and FF11—
FF13.
As to Appellant’s argument regarding claim 2’s patentability, we
conclude Appellant has not shown good cause why this argument was not
made in the opening brief and, so, the argument is considered to have been
waived.
For the reasons set forth above, we affirm this rejection.
Obviousness over Pinter, Reiter, and Stiegler
The Examiner determined that all pending claims would have been
obvious over Pinter, Reiter, and Stiegler. As Appellant suggests, this
rejection appears to be directed to claim 12, which depends from
independent claim 1. App. Br. 9. The Examiner added Stiegler to the
previously discussed Pinter-Reiter combination for its disclosure that the
antibody 2G12 is potent in targeting HIV-1, with the implication being that
it would have been obvious to substitute 2G12 antibodies for the antibodies
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used in the Reiter conjugated composition if one were targeting HIV (as is
disclosed in Pinter). Answer 4.
Appellant presents a similar argument over this rejection as was made
concerning the first rejection; that is, like Pinter, Stiegler does not suggest
physically combining antibodies with SCRs. App. Br. 9.
In response to Appellant’s argument, the Examiner pointed out that
Stiegler discloses that 2G12 antibodies are potent targeting antibodies (for
HIV-1) and that they “vigorously induced complement activation and hence
would be effective targeting moieties for HIV-infected cells and would
necessarily increase the effectiveness of the peptides of Pinter.” Answer 10;
see also FF14.
We conclude that, on the record before us, the Examiner has the better
position. The Pinter-Reiter combination taught and suggested physically
pairing an SCR and an antibody to invoke a complement system response to
destroy targeted pathogen cells. Stiegler identifies another useful antibody
for such a purpose and, in fact, one that may be even more appropriate to use
with Pinter’s HIV therapy.
For the reasons above, we affirm this rejection.
Obviousness over Pinter and Farries
In view of the above-identified findings of fact and the above-cited
precedent, the Examiner has set forth a prima facie case that the claims (all
but claim 12) would have been obvious over Pinter and Farries. See Final
Rejection 4—6 and Answer 2—3 and 7—8. For example, Pinter and Farries,
like Pinter and Reiter as discussed above, teach and suggest a covalently
bound SCR-Ab conjugation would provide an effective therapy by targeting
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and destroying pathogen cells. FF1—FF6, FF10—FF13. Pinter is discussed
above (see, e.g., FF1—FF6), and, like Reiter, Farries teaches and suggests a
similar, but, again, not identical, cell-lysis-via-complement-immune-system-
action and that such a therapy can be specifically targeted to pathogen cells
by conjugating the complement immune system component to an antibody.
FF10—FF13. It would have been reasonable for a skilled artisan to have
consulted among and combined these references because they are directed to
a common problem, again, therapy by invoking a complement immune
system response to a specific pathogen. Appellant has not presented
persuasive argument or evidence that the Examiner’s determination is
incorrect.
Appellant renews the arguments over the Pinter reference made
concerning the above-discussed rejections. App. Br. 10. Appellant also
argues,
Farries does not teach or suggest the conjugation of antibodies
with fH-derived SCR molecules capable of binding heparin. The
only experiment in which lysis is shown by using a conjugate
that targets C3 (Fig 9; Example 10) is performed with purified
complement components in the presence of EDTA, which allows
lysis by the alternative pathway only.
Id. Thus, Appellant contends Farries does not cure the alleged defects of
Pinter and suffers from the same deficiency as Reiter, that is, it relates to the
alternative pathway for lysing cells. However, Appellant does concede
Farries teaches targeting cells using complement immune system regulating
compositions bound to antibodies. Id. Appellant argues it would not have
been obvious to combine the teachings of Farries and Pinter because Farries
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does not suggest physically linking an antibody to the specific SCRs of
Pinter and as claimed. Id.
The Examiner’s response to Appellant’s arguments is essentially the
same here as it was in response to the previously discussed rejections. The
Examiner’s rationale for obviousness is that Pinter discloses the SCR
component claimed and Farries, like Reiter, teaches and suggests the
advantages of physically pairing an antibody with the SCR to increase its
therapeutic effectiveness by targeting certain cells. Answer 11—12. The
Examiner cites Huber,7 Appellant’s evidentiary reference, as supportive of
this proposition in that Huber identifies the well-known reason one would
physically combine an SCR and an antibody, which is to target cells desired
to be lysed. Id. at 12 (citing Huber at 10).
On the record before us, we conclude the Examiner has the better
position. Again, Appellant seeks to discredit the prior art references
individually and contends they would not be combined. Each argument is
unpersuasive for the same reasons as set forth above concerning the first
rejection because Farries teaches and suggest essentially the same concepts
as Reiter and would have been combined with Pinter for the same reasons.
For the reasons above, we affirm this rejection.
Obviousness over Pinter, Farries, and Stiegler
The Examiner determined that all pending claims would have been
obvious over Pinter, Farries, and Stiegler. Appellant reiterates the
7 Huber et al., Novel Bifunctional Single-Chain Variable Antibody
Fragments to Enhance Virolysis by Complement: Generation and Proof-of-
Concept, 2014 BioMed Res. Int’l 1-14 (2014) (“Huber”).
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arguments made concerning the rejection of the claims over Pinter, Reiter,
and Stiegler. App. Br. 11. As we have concluded and discussed above,
neither the rejection over Pinter, Reiter, and Stiegler nor the rejection over
Pinter and Farries is overcome by Appellant’s arguments, we are likewise
unpersuaded by Appellant’s argument here and affirm this rejection for the
same reasons.
SUMMARY
The rejection under 35 U.S.C. § 103(a) over Pinter and Reiter is
affirmed.
The rejection under 35 U.S.C. § 103(a) over Pinter, Reiter, and
Stiegler is affirmed.
The rejection under 35 U.S.C. § 103(a) over Pinter and Farries is
affirmed.
The rejection under 35 U.S.C. § 103(a) over Pinter, Farries, and
Stiegler is affirmed.
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
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