The Board of Trustees of the Leland Stanford Junior University

Patent Trials and Appeals Board

Dec 30, 2020

2020002908 (P.T.A.B. Dec. 30, 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.
14/590,538 01/06/2015 Mohammad Namavari 221907-1531 9616
166436 7590 12/30/2020
THOMAS | HORSTEMEYER, LLP (Stanford)
3200 WINDY HILL ROAD, SE
SUITE 1600E
ATLANTA, GA 30339
EXAMINER
PERREIRA, MELISSA JEAN
ART UNIT PAPER NUMBER
1618
NOTIFICATION DATE DELIVERY MODE
12/30/2020 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@thomashorstemeyer.com
ozzie.liggins@tkhr.com
uspatents@tkhr.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
________________

BEFORE THE PATENT TRIAL AND APPEAL BOARD
________________

Ex parte MOHAMMAD NAMAVARI,
SANJIV SAM GAMBHIR, and BEVERLY S. MITCHELL1
________________

Appeal 2020-002908
Application 14/590,538
Technology Center 1600
________________

Before FRANCISCO C. PRATS, JOHN G. NEW, and RICHARD J. SMITH
Administrative Patent Judges.

NEW, Administrative Patent Judge.

DECISION ON APPEAL

1 We use the term “Appellant” to refer to the “applicant” as defined in
37 C.F.R. § 1.142. Appellant identifies The Board of Trustees of the
Leland Stanford Junior University as the real party-in-interest. App. Br. 2.
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SUMMARY
Appellant files this appeal under 35 U.S.C. § 134(a) from the
Examiner’s Final Rejection of claims 1 and 7–9 as unpatentable under 35
U.S.C. § 103 as being obvious over the combination of J.A. Montgomery et
al., 9-(2-Deoxy-2-fluoro-/3-D-arabinofuranosyl)guanine: A Metabolically
Stable Cytotoxic Analogue of 2ʹ-Deoxyguanosine, 29 J. MED. CHEM. 29,
2389–92 (1986) (“Montgomery”), Price (US 4,489,052, December 18, 1984)
(“Price”), Lopez et al. (US 4,211,773, July 8, 1980) (“Lopez”), S.L. Berg et
al., Phase II Study of Nelarabine (compound 506U78) in Children and
Young Adults with Refractory T-Cell Malignancies: A Report from the
Children’s Oncology Group, 23 J. CLIN. ONCOL. 3376–82 (2005) (“Berg”),
Radu et al. (US 2009/0105184 A1, April 23, 2009), Halazy et al. (US
4,988,680, January 29, 1991) (“Halazy”) and A. Herrström Sjöberg et al.,
Substrate Specificity of Human Recombinant Mitochondrial
Deoxyguanosine Kinase with Cytostatic and Antiviral Purine and
Pyrimidine Analogs, 53 MOL. PHARMACOL. 270-273 (1998) (“Herrström”).
We have jurisdiction under 35 U.S.C. § 6(b).
We AFFIRM.

NATURE OF THE CLAIMED INVENTION
Appellant’s claimed invention is directed to compounds and methods
of making compounds and uses for the compounds in imaging. Abstr.

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REPRESENTATIVE CLAIM
Claim 1 is representative of the claims on appeal and
recites:
1. A method of imaging an activated T Cell in a subject
comprising:

administering to the subject a compound having formula
3 so that the compound is phosphorylated by deoxyguanosine
kinase present in activated T Cells in the subject; and

imaging the subject, wherein detecting the presence of
the compound corresponds to the presence of the activated T-
cell, wherein formula 3 is represented by the following
structure,

wherein 1st is 18F; and

Rʹ is:

App. Br. Claims App’x 1.

ISSUES AND ANALYSES
We adopt the Examiner’s findings, reasoning, and conclusion that the
claims on appeal are prima facie obvious over the combined cited prior art.
We address the arguments raised by Appellant below.

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Issue 1

Appellant argues that the Examiner erred because the Radu reference
teaches away from the claimed invention. App. Br. 3.

Analysis
The Examiner finds that Montgomery teaches the cytotoxicity and
inhibitory effects of 9-(2-deoxy-2-fluoro-β-D-arabinofuranosyl) guanine, a
derivative of 9-β-D arabinofuranosylguanine (“araG”), which is a selective
inhibitor of T-cell malignancies. Final Act. 3 (citing Montgomery 2389–91).
The Examiner finds that Montgomery also teaches that the composition
(Montgomery’s 1b) preferentially inhibits DNA synthesis of T-cells relative
to B-lymphoblasts and is a selective inhibitor of T-lymphoblast growth. Id.
(citing Montgomery 2389). The Examiner finds that Montgomery teaches
that the composition is a potential chemotherapeutic agent against T-cell
malignancies. Id. The Examiner finds that Montgomery teaches that the
composition requires T-cell activation to exert its cytotoxic effects and that it
is initially phosphorylated by deoxycytidine kinase. Id. (citing Montgomery
2391).
The Examiner finds that Lopez teaches, inter alia, 2–fluoro arabinosyl
pyrimidine nucleosides, with the general structure:

Id. (citing Lopez, Abstr., col.14, ll. 24–36, and Table 1).
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The Examiner finds that Price teaches that the pyrimidine nucleoside
compounds taught by Lopez (e.g., 1-(2ʹ-deoxy-2ʹ-substituted-D-
arabinofuranosyl) pyrimidine nucleosides) can be radiolabeled with 18F
(substituted for fluorine), and that these compositions can be used in
positron emission tomography (“PET”). Final Act. 3 (citing Price col. 2, ll.
22–32, claim 5).
The Examiner concludes that it would have been obvious to a person
of ordinarily skill in the art to substitute the fluorine taught by Montgomery
with the isotope 18F, as taught by Price, to permit use of the composition in
PET imaging, because Price teaches the substitution of 18F for the fluorine
on an arabinofuranosyl group, as taught by Lopez. Final Act. 3–4.
The Examiner also finds that, although Montgomery neither teaches
nor suggests methods of imaging an activated T-cell, or identifying a
subject with graft versus host disease (GVHD), Berg teaches that nelarabine
(506U78) a water-soluble prodrug of ara-g (9-β-d-arabinofuranosylguanine)
exhibits activity against T-cell lymphoblastic malignancies in patients. Final
Act. 4 (citing Berg Abstr., 3377, 3380).
The Examiner finds that Radu teaches adenosine analog PET probes,
including:

in the diagnosis and/or treatment of conditions such as leukemia, etc. and
that these probes can distinguish between activated T-cells and non-activated
naive T-cells. Final Act. 4 (citing Radu Abstr., ¶¶ 16, 17, 19, 60, 65).
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The Examiner also finds Halazy teaches guanosine derivative
inhibitors of T-cell leukemia, in which controlled suppression of T-cells is
desirable for treatment of T-cell leukemia, and the suppression of host-vs-
graft responses (“GVHD”) in organ transplant recipients, etc. Final Act. 4
(citing Halazy Abstr., col. 1, ll. 14–38).
The Examiner concluded that it would have been obvious to one
ordinarily skilled in the art to employ 18F-labelled 9-(2-deoxy-2-fluoro-β-D-
arabinofuranosyl) guanine for in vivo imaging of activated T-cells, because
Montgomery teaches that 9-(2-deoxy-2-fluoro-β-D-arabinofuranosyl)
guanine exhibits cytotoxicity and inhibitory effects toward T-cell
malignancies. Final Act. 5. The Examiner also finds that Berg teaches that
ara-G (9-β-D-arabinofuranosyl guanine) and ara-G derivatives exhibit
activity against T-cell lymphoblastic malignancies in vivo in patients and
that Radu teaches adenosine analog PET probes for diagnosing and/or
treatment of a condition, such as leukemia, etc. and can distinguish between
activated T-cells, and non-activated naive T-cells. Id. The Examiner also
concludes that it would have been predictable that the 18F-labelled 9-(2-
deoxy-2-fluoro-β-D-arabinofuranosyl) guanine, an adenosine derivative, will
be capable of providing images via PET and for distinguishing between
activated T-cells and non-activated naive T-cells. Id.
The Examiner further concludes “that it would have been obvious to
one ordinarily skilled in the art to use the 18F-labelled 9-(2-deoxy-2-fluoro-
β-D-arabinofuranosyl) guanine” taught by Montgomery for identifying
GVHD in a subject, because Halazy teaches that guanine derivative
inhibitors of T-cell leukemia are desirable for treatment of T-cell leukemia
and GVHD. Final Act. 5. The Examiner further concludes that a skilled
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artisan would have reasonably expected to be able to identify a subject with
graft versus host disease, because “18F-labelled 9-(2-deoxy-2-fluoro-β-D-
arabinofuranosyl) guanine” PET probes can be used for diagnosing subjects
with activated T-cells, not excluding those with GVHD. Id.
The Examiner further finds that Montgomery neither teaches nor
suggests that 9-(2-deoxy-2-fluoro-β-D-arabinofuranosyl) guanine is
phosphorylated by deoxyguanosine kinase present in activated T-cells. Final
Act. 5. However, the Examiner finds that Herrström teaches that
deoxyguanosine kinase is responsible for phosphorylation of purine
deoxynucleosides and their analogs. Id. at 6 (citing Herrström Abstr., 270).
The Examiner finds that Herrström teaches that the enzyme exhibits a broad
substrate specificity toward natural purines and pyrimidines. Id. (citing
Herrström Abstr.). The Examiner also finds that Herrström teaches that ara-
G is a good substrate for the enzyme. Id. (citing Herrström 270). The
Examiner further finds that several important antitumor purine nucleoside
analogs, including ara-G, all require activation by the kinase to be toxic to
the target cells. Id. (citing Herrström Table 1, 272). The Examiner finds
that the enzymes deoxyguanosine kinase (“dGK”) and deoxycytosine kinase
(“dCK”) belong to the same enzyme family and have overlapping substrate
sensitivities. Id. (citing Herrström 270).
The Examiner therefore concludes that it would have been obvious to
one ordinarily skilled in the art that 9-(2-deoxy-2-fluoro-β-D-
arabinofuranosyl) guanine, as taught by Montgomery, can be phosphorylated
by deoxyguanosine kinase present in activated T-cells, because Montgomery
teaches that its composition requires activation to exert its cytotoxic effects
as a chemotherapeutic agent for T-cell malignancies and that can be
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phosphorylated by deoxycytidine kinase (“dCK”). Final Act. 6. The
Examiner also finds that, because Herrström teaches that dGK and dCK are
in the same enzyme family and that both enzymes can phosphorylate purine
deoxynucleosides and their analogs, a skilled artisan would have predicted
that 9-(2-deoxy-2-fluoro-β-D-arabinofuranosyl) guanine could be
phosphorylated and activated by dGK. Id.
Appellant argues that Radu teaches that a variety of different cellular
processes (e.g., phosphorylation, conversion to metabolites via deamination,
etc.) can influence whether a given analog can be retained in T-cells. App.
Br. 4 (citing, e.g., Radu ¶¶ 87, 88). In this context, argues Appellant, Radu
teaches that some nucleoside analogs (e.g., cytosine nucleoside analogs) can
be used in methods of imaging activated T-cells, whereas other nucleoside
analogs do not work in these methods. Id.
Appellant particularly points to paragraph [0060] of Radu, which
Appellant asserts, conducted a radioactive uptake assay with a variety of
different classes of nucleoside analogs to identify candidates for PET probes
that can distinguish between activated T-cells and non-activated naive T-
cells, the results of which are shown in FIG. 1A. App. Br. 4. Appellant
contends that the data presented in FIG. 1A, and associated paragraph
[0060], teaches the ability of different nucleoside analogs to be retained in
activated T-cells. Id. According to Appellant, Radu thus teaches that,
whereas some nucleoside analogs such as 2ʹ, 2ʹ-difluorodeoxycytidine
(“dFdC”) are highly retained in activated T-cells, others, such as 2ʹ,2ʹ-
difluorodeoxythymidine (“2ʹFLT”) are poorly retained in activated T-cells.
Id. (also citing Radu ¶ 91 (allegedly teaching that no detectable 18FFLT
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accumulation was observed at sites of immune activation that can be clearly
visualized by other 18F-labelled nucleoside analogs)).
In this way, Appellant argues, Radu teaches that not all nucleoside
analogs can be used to image activated T-cells. and that the properties of a
first class of molecules taught by Radu (e.g. 2ʹ,2ʹ-difluorodeoxycytidine
retention in activated T-cells) are unpredictable and cannot be extrapolated
to different classes of molecules such as 2ʹ,2ʹ-difluorodeoxythymidine or the
claimed 9-(2-deoxy-2-fluoro-β-D-arabinofuranosyl) guanosine. App. Br. 4.
Appellant asserts that Radu does not discuss any guanosine
analogs/derivatives, much less their use in imaging activated T-cells. App.
Br. 4. Furthermore, argues Appellant, Radu teaches that the data shown in
FIG. 1A guided their design of probes directed to nucleoside analogs other
than guanosine, e.g., 18F-radiolabeled PET probes analogous to 2ʹ
deoxycytidine. Id. According to Appellant, the use of nucleoside analogs
other than guanosine as PET probes is emphasized throughout Radu:
Appellant asserts that cytosine is discussed at least 29 times and adenosine is
discussed at least 18 times, whereas guanosine is not discussed at all. Id.
Appellant argues that a person of ordinary skill, comprehending the Radu
reference, would be led to use nucleoside analogs other than guanosine
analogs (specifically cytosine or adenosine analogs) in activated T-cell
imaging methods: a direction divergent from the path taken by the
Appellant. Id.
Appellant summarizes that Radu teaches that a subset of 18F-labelled
nucleoside analogs can be used to image certain types of cells and also that it
is unpredictable as to whether or not a specific nucleoside analog can image
any specific type of cell, due to differences in the way that different
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nucleosides are metabolized. App. Br. 5. Appellant asserts that the data
presented by Radu also shows that, whereas adenosine and cytosine
nucleoside analogs can be used to image activated T-cells, other nucleoside
analogs (i.e., thymidine nucleoside analogs) cannot be used in these
methods. Id. (citing Radu Fig. 1). Consequently, Appellant asserts a skilled
artisan would agree that the teachings of Radu would motivate them to use
adenosine and cytosine nucleoside analogs to image activated T-cells, rather
than other nucleoside analogs. Id. In this way, argues Appellant, Radu
teaches away from imaging methods that use guanosine analogs, including
the specific guanosine analog recited in the claims. Id.
We disagree. A “teaching away” requires a reference to actually
criticize, discredit, or otherwise discourage the claimed solution. See In re
Fulton, 391 F.3d 1195, 1201 (Fed. Cir. 2004). As Appellant acknowledges,
Radu is silent with respect to the use of guanosine analogs, such as the
composition recited in the claims. We cannot reasonably construe mere
silence upon a subject to constitute a criticism or discrediting of, or
discouragement from, that subject. Nor can we reasonably conclude that a
person of ordinary skill in the art would have been discouraged or diverted
from following a path, about which the reference is silent. See In re Gurley,
27 F.3d 551, 553 (Fed. Cir. 1994) (holding that a reference teaches away
when “a person of ordinary skill, upon reading the reference, would be
discouraged from following the path set out in the reference, or would be led
in a direction divergent from the path that was taken by the applicant”). Put
even more simply still, we can infer nothing more from a reference’s silence
upon a given subject than the fact that the reference is silent upon that
subject. Consequently, Radu’s silence upon the subject of using guanosine
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analogs does not amount to a teaching away from the use of guanosine
analogs.
Moreover, consideration of the other prior art references cited by the
Examiner, of which a skilled artisan would have been aware, suggest
precisely the opposite of Appellant’s contention that Radu teaches away.
Radu expressly teaches that: “For example, the PET probe can be a dCK
substrate…. the PET probe can be used to evaluate the efficacy in the
treatment of cancer of anticancer agents that are taken up into cells via
nucleoside transporters and deoxycytidine kinase (dCK)-mediated
phosphorylation.” Radu ¶¶ 6–7. Similarly, Radu teaches that: “The PET
probe can be used to evaluate the efficacy in the treatment of cancer of an
anticancer agent, e.g., cytarabine or 2ʹ-difluorodeoxycytidine, that is taken
up into cells via nucleoside transporters and deoxycytidine kinase (dCK)-
mediated phosphorylation.” Id. at ¶ 18.
Herrström teaches:
Several important antitumor purine analogs (e.g., Ara[-]G, CdA,
CAFdA and 2-F-AraA) all require activation by kinases to be
toxic to the target cells. These analogs are all promising anti-
leukemic drugs in clinical use or in the advanced clinical testing
stages and they are all considered to be phosphorylated
primarily by dCK.

Herrström 272 (emphasis added). Ara-G is 9-(β-D-arabinofuranosyl
guanine) the compound recited in the claims, minus the 18F substitution.
We consequently agree with the Examiner that a skilled artisan,
understanding the teachings of Radu and Herrström, would have reasonably
expected that the compound recited in the claims would likely be a
successful candidate as a marker for PET imaging, because Radu teaches
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that substrates for dCK can act as PET markers, and because Herrström
teaches that Ara-G, a close analog of the claimed composition is a substrate
for dCK.

Issue 2
Appellant argues that the Examiner erred because the Examiner
provided no reasonable expectation that claimed molecule would
successfully image activated T-cells. App. Br. 5.

Analysis
Appellant disputes the Examiner’s conclusion that the combination of
the teachings of Montgomery, Price, Lopez, Berg, Radu, Halazy and
Herrström would have provided a skilled artisan with a reasonable
expectation that the claimed molecules are useful to image activated T-cells.
App. Br. 6. Appellant acknowledges that Montgomery teaches a non-
radioactively-labelled version of the claimed molecule. Id. However,
Appellant argues, the teachings of Montgomery are silent with respect to
deoxyguanosine kinase, and also to imaging methodologies, such as PET.
Id.
Appellant concedes that Price and Lopez together teach that
pyrimidine nucleosides can be radiolabeled with 18F and used in PET
methodologies. App. Br. 6. However, Appellant argues, pyrimidines
nucleosides are very different structurally and metabolically from the
guanosine (i.e., purine) analogs recited in the claims. Id. But, argues
Appellant, Price and Lopez neither teach nor suggest guanosine analogs or
deoxyguanosine kinase. Id.
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With respect to Berg, Appellant argues that the reference teaches that
nelabarine is active as a single agent in recurrent T-cell leukemias. App. Br.
6. However, Appellant asserts, nelabarine has a different molecular
structure from the guanosine analog recited in the claims and is not used in
imaging methodologies. Id. Appellant also argues that the Radu disclosure
does not teach guanosine analogs/derivatives, or their phosphorylation by
guanosine kinase. Id. Furthermore, Appellant contends, paragraphs [0087]
and [0088] of Radu outline a number of the different unpredictable cellular
processes (e.g., conversion to metabolites via deamination, etc.) that
influence whether a given analog will be retained in T-cells and be usable as
an imaging agent. Id.
Appellant next argues that Halazy teaches guanosine analogs that are
different structurally and metabolically from the guanosine analog recited in
the claims on appeal. According to Appellant, Halazy is silent with respect
to imaging methodologies. App. Br. 6. Furthermore, Appellant contends,
Herrström teaches that deoxyguanosine kinase is responsible for
phosphorylation of purine deoxynucleosides and their analogs, contending
that phosphorylation is one of the various different cellular processes that
influence the ability of a nucleoside analog to be retained in cells. Id.
Appellant particularly disputes the Examiner’s finding that, because
Radu teaches that adenosine analogs are useful as PET probes to distinguish
between activated and non-activated T-cells, “it would have been predictable
that the 18F-labelled 9-(2-deoxy-2-fluoro-β-D-arabinofuranosyl) guanosine,
an adenosine derivative, will be capable of providing images via PET and
for distinguishing between activated T-cells and non-activated, naive T-
cells.” App. Br. 6–7 (quoting Non-Final Office Act., October 1, 2018 at 5)).
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Appellant argues in response that a person of skill in the art would disagree
with the Examiner’s analysis of Radu, because, e.g., the Examiner was
mistaken in believing that 9-(2-deoxy-2-fluoro-β-D-arabinofuranosyl)
guanosine is an adenosine derivative. Id. at 7. Rather, argues Appellant, a
skilled artisan would have noted that the claimed molecule is a guanosine
derivative, and that it is well known that adenosine derivatives and
guanosine derivatives are distinct types of molecules, with different
metabolic activities. Id.
Appellant next points to the Final Office Action, in which the
Examiner finds that: “[Radu] was not used to teach that analogs of Radu et
al. are retained in activated T-cells, but was used to teach that PET probes
that are taken up into T-cells can be used to distinguish between activated T-
cells and non-activated naive T-cells.” App. Br. 7 (quoting Final Act. 9).
Appellant responds that, in determinations of obviousness, a prior art
reference must be considered in its entirety, i.e., including teachings that
would lead away from the claimed invention. Id. (citing W.L. Gore &
Assocs., Inc. v. Gurlock, Inc., 721 F.2d 1540, 1550 (Fed. Cir. 1983), cert.
denied, 469 U.S. 851 (1984); MPEP § 2141.02).
In this context, argues Appellant, Radu’s teachings regarding the
unpredictability in this art, as well as which nucleoside analogs do and do
not function in their methods of imaging activated T-cells cannot be ignored
for the purposes of the instant rejection under 35 U.S.C. § 103. App. Br. 7.
Instead, Appellant contends, all of the teachings of Radu, including what
types of nucleoside analogs can function in their methods are relevant, and
would have been considered by those of skill in the art motivated to make
new inventions. Id.
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Appellant summarizes that the teachings of Radu disclose the
unpredictability of this area of technology and provide no data whatsoever
on the abilities of any guanosine analog's ability to be retained in activated
T-cells, much less the specific guanosine analog recited in Appellant's
claims. App. Br. 7. Appellant contends that the remaining prior art
references cited by the Examiner cannot overcome this unpredictability of
this technology. Id. Appellant contends that, consequently, there a person
of ordinary skill in the art could have had no reasonable expectation of
success in arriving at Appellant’s claimed invention. Id.
We are not persuaded by Appellant’s arguments. As an initial matter,
Appellant cannot show non-obviousness by attacking references individually
where the rejections are based on a combinations of references. In re Keller,
642 F.2d 413, 426 (C.C.P.A. 1981) (citing In re Young, 403 F.2d 754, 757
(C.C.P.A. 1968).
The gravamen of Appellant’s argument seems to be based upon the
alleged unpredictability of the art, as allegedly taught by Radu, and, in
particular, the uncertainty concerning whether a given nucleoside analog can
or cannot function as a marker in PET imaging of activated T-cells. See
App. Br. 7. However, and as we have already explained supra, Radu
teaches that nucleoside analogs that are substrates for the enzyme dCK are
useful as PET imaging markers, and Herrström teaches that a guanosine-
based nucleotide, Ara-G, which is a close analog of the composition recited
in the claims, acts as a substrate for dCK. We consequently agree with the
Examiner that the art, and Radu in particular, are not so unpredictable as
Appellant suggests, and that a skill artisan, understanding the teachings of
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Radu and Herrström, would have had a reasonable expectation of success in
employing the molecule recited in the claims to image activated T-cells.
Furthermore, Montgomery expressly teaches that 9-(2-Deoxy-2-
fluoro-β-D-arabinofuranosyl) guanine is a metabolically stable, T-cell
cytotoxic analogue of ara-G. Montgomery 2389. The compound taught by
Montgomery is identical to the claimed composition with the sole exception
that the fluorine atom at the 2-position of the arabinofuranosyl ring is the
fluorine isotope 18F. Radu and Price both teach that using 18F at this position
in the arabinofuranosyl ring makes such nucleotides useful for PET imaging.
We conclude that a skilled artisan, comprehending the teachings of the
combined prior art cited by the Examiner, would reasonable expect that 18F-
labeled ara-g, would be taken up by activated T-cells and would be usable in
PET imaging. We consequently affirm the Examiner’s rejection of the
claims.

CONCLUSION
The Examiner’s rejection of claims 1 and 7–9 under 35 U.S.C. § 103
is affirmed.
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). See 37 C.F.R. §
1.136(a)(1)(iv).
AFFIRMED

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Claims
Rejected
35 U.S.C. § Reference(s)/Basis Affirmed Reversed
1, 7–9 103 Montgomery,
Price, Lopez,
Berg, Radu,
Halazy,
Herrström

1, 7–9

AFFIRMED