2-BBB Medicines B.V.

Patent Trials and Appeals Board

May 4, 2020

14692422 - (D) (P.T.A.B. May. 4, 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.
14/692,422 04/21/2015 Pieter Jaap GAILLARD 069818-2970 9245
22428 7590 05/04/2020
FOLEY & LARDNER LLP
3000 K STREET N.W.
SUITE 600
WASHINGTON, DC 20007-5109
EXAMINER
POPA, ILEANA
ART UNIT PAPER NUMBER
1633
NOTIFICATION DATE DELIVERY MODE
05/04/2020 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):
ipdocketing@foley.com
PTOL-90A (Rev. 04/07)

UNITED STATES PATENT AND TRADEMARK OFFICE
____________

BEFORE THE PATENT TRIAL AND APPEAL BOARD
____________

Ex parte PIETER JAAP GAILLARD
____________

Appeal 2019-001991
Application 14/692,4221
Technology Center 1600
____________

Before RYAN H. FLAX, DAVID COTTA, and
CYNTHIA M. HARDMAN, Administrative Patent Judges.

COTTA, Administrative Patent Judge.

DECISION ON APPEAL

This is an appeal under 35 U.S.C. § 134 involving claims to a method
for delivering drugs across the blood-brain-barrier. The Examiner rejected
the claims on appeal as anticipated under 35 U.S.C. § 102(a)(1) and as
obvious under 35 U.S.C. § 103(a). Oral argument was heard on January 30,
2020.
We affirm.

1 We use the word “Appellant” to refer to “applicant” as defined in
37 C.F.R. § 1.42. According to Appellant, the real party in interest is 2-BBB
Medicines B.V. App. Br. 3.
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STATEMENT OF THE CASE
The Specification discloses that the blood brain barrier (“BBB”)
comprises “physical and functional barriers within the blood vessels of the
brain” that “serve to protect neurons.” Spec. ¶ 11. “These barriers . . .
exclud[e], efflux[] and metaboliz[e] potential neurotoxic compounds
(including plasma proteins, cytokines, antibodies, drugs, bacteria and
viruses) from blood and brain.” Id. “For the uptake of essential nutrients,
. . . the blood-brain barrier is equipped with specific carrier systems and
uptake receptors.” Id. “Currently marketed CNS drugs are . . . usually
either very small and potent water soluble compounds (~300 Da) or highly
lipid soluble compounds, so that these compounds can cross the blood-brain
barrier by diffusion.” Id.
According to the Specification, given their size, large molecule
“biopharmaceutical drugs are unlikely candidates for chemical modifications
to enhance their permeability across the blood-brain barrier.” Id. Instead,
biopharmaceutical drugs “rely on invasive and harmful technologies to
patients, like direct and local stereotactic injections, intrathecal infusions and
even (pharmacological) disruption of the blood-brain barrier.” Id. Not
surprisingly, these techniques can have “severe neurological consequences.”
Id. Thus, according to the Specification, “[i]nnovative CNS drug delivery
technologies are . . . highly awaited.” Id.
The Specification discloses, that “[i]t is an object of the invention to
provide for a safe, effective and versatile approach for carrying cargo such
as large proteins and liposomes containing drugs and genes across the cell
membrane and across a blood-tissue barrier such as the blood-brain barrier
for inter alia CNS drug targeting.” Id. ¶ 14.
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Claims 1, 4, 7, 9, 11–14, 17, 18, and 24 are on appeal. Claim 1 is
representative and reads as follows:
1. A method for delivering a drug across the blood-brain
barrier (BBB), comprising administering to a subject in need
thereof an effective amount of a conjugate comprising: a
glutathione conjugated via the thiol group in its cysteine moiety
to a nanocontainer comprising lipid-polyethylene glycol (PEG)
on its surface and an encapsulated drug, wherein the thiol group
is conjugated to the lipid-PEG, such that the drug:
(a) is delivered across the BBB,
(b) accumulates to a lesser extent in at least one of lung,
liver and kidney than does the drug encapsulated in a similarly
administered control nanocontainer (i) which is not conjugated
to a glutathione or (ii) to which the PEG alone is linked, and
(c) accumulates to a greater extent in brain than does the
drug encapsulated in a similarly administered control
nanocontainer (i) which is not conjugated to a glutathione or (ii)
to which the PEG alone is linked.
App. Br. 11.
The claims stand rejected as follows:
Claims 1, 4, 7, 9, 11, 14, 17, and 18 were rejected under 35 U.S.C.
§ 102(b) as anticipated by Wang2 as evidenced by Ananda.3
Claims 1, 4, 7, 9, 11–14, 17, and 18 were rejected under 35 U.S.C.
§ 103(a) as obvious over the combination of Wang, Ananda, and Chong.4

2 Wang et al., US Patent No. 7,446,906, issued Nov. 4, 2008 (“Wang”).
3 Ananda et al., Analysis of Functionalization of Methoxy-PEG as
Maleimide-PEG, 374 Analytical Biochemistry 231–242 (2008) (“Ananda”).
4 Chong et al., Treatment of Acute Nipah Encephalitis with Ribavirin, 49(6)
Ann. Neurol. 810–813 (2001) (“Chong”).
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Claims 1, 4, 7, 9, 11–14, 17, 18, and 24 were rejected under 35 U.S.C.
§ 103 as obvious over the combination of Wang, Ananda, Chong, and
Meyding-Lamadé.5
FINDINGS OF FACT
1. Wang discloses “a delivery system comprising a carrier or an
active compound and a glutathione or a glutathione derivative grafted
thereon.” Wang, 2:48–50. “[T]he active compound can pass through the
blood-brain-barrier (BBB), such as brain endothelial cells, with the targeted
carrier and has a cell penetration rate of about 0.01–100%.” Id. at 3:4–6.
2. Wang’s disclosed compounds comprise “a moiety comprising a
vitamin E derivative or a phospholipid derivative, a polyethylene glycol
(PEG) or a polyethylene glycol derivative bonded thereto, and a glutathione
(GSH) or a glutathione derivative bonded to the polyethylene glycol or the
polyethylene glycol derivative.” Id. at 3:7–13.
3. Wang discloses that the polyethylene glycol derivative in its
genus of disclosed compounds “may comprise carboxylic acid, maleimide,
PDP, amide, or biotin.” Id. at 3:58–59.

5 Meyding-Lamadé et al., Experimental Herpes Simplex Virus Encephalitis:
A Combination Therapy of Acyclovir and Glucocorticoids Reduces Long-
Term Magnetic Resonance Abnormalities, 9 Journal of NeuroVirology 118–
125 (2003) (“Meyding-Lamadé”).
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4. GSH includes four locations available for conjugation. This is
illustrated in the below figure reproduced from Appellant’s Reply Brief.

Reply Br. 2. The above figure shows that GSH includes a thiol group
(“SH”), a primary amino group (“NH2”), and two electrophilic groups that
are available for conjugation. Id. Of these four locations available for
conjugation, two – the thiol group and the primary amino group – may react
with a maleimide. Id.; see also, id. at 7.
5. Example 1 of Wang illustrates a method by which a compound
comprising GSH conjugated to a PEG derivative may be prepared. The
method is illustrated below:

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Wang 4:7–50. The above illustration depicts a method for preparing TPGS-
Glutathione. Id. In the compound produced by the above method
(compound 6), TPGS specifies d-alpha tocopheryl polyethylene glycol. Id.
at 5:20–22.
6. Dr. Swann testifies that Example 1 of Wang “uses a trityl (Trt)
‘protecting’ group that requires a very strong acid – trifluoroacetic acid
(TFA) – in a halogenated solvent for its removal, bypassing more
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conventional protection measures.” Swan Decl. ¶ 11 n. 8.6 Dr. Swann
further testifies that “the sulfhydryl group is only deprotected in the final
step, after the glutathione has been conjugated to the PEG derivative.” Id.
According to Dr. Swann, “the exemplified method by which Wang
conjugated PEG to glutathione demonstrates a significant effort to preserve
the sulfhydryl group.” Id. ¶ 11.
7. Forman7 discloses:
The tripeptide, γ-˪-glutamyl-˪-cysteinyl-glycine known as
glutathione (GSH) . . . is the most important low molecular
weight antioxidant synthesized in cells. It is synthesized by the
sequential addition of cysteine to glutamate followed by the
addition of glycine. The sulfhydryl group (-SH) of the cysteine
is involved in reduction and conjugation reactions that are
usually considered as the most important functions of GSH.
These reactions provide the means for removal of peroxides and
many xenobiotic compounds, however, GSH is also involved in
regulation of the cell cycle.
Forman, 2.
8. Dr. Swann testifies that “Wang’s efforts to protect the
sulfhydryl group when producing a glutathione-PEG conjugate would be
consistent with the efforts of a skilled artisan, who recognizes and
appreciates the significance of protecting the sulfhydryl group to preserve
the biological function of glutathione.” Swann Decl. ¶ 11.

6 Declaration of Peter W. Swann under 37 C.F.R. § 1.132, dated January 7,
2018 (“Swann Decl.”).
7 Forman et al., Glutathione: Overview of its Protective Roles, Measurement,
and Biosynthesis, 30 Molecular Aspects of Medicine 1–12 (2009)
(“Forman”). Forman was cited by Appellant as evidence that the sulfhydryl
group (–SH) of the cysteine in the reduced form of GSH is involved in
reactions that are usually considered the most important functions of GSH.
App. Br. 7–8.
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9. Dr. Swann testifies that “a skilled person would be wary of
conjugating a biologically inactive molecule such as lipid-PEG to that
sulfhydryl group in the reduced form, as such a modification would be
expected to significantly impair or extinguish the biological function of the
glutathione.” Id. ¶ 10.
10. Ananda discloses:
The reaction of maleimides with thiols is one of the best known
site-specific, simple, and quantitative protein chemical
modification reactions. Accordingly, maleimide-PEG reagents
have evolved as the most desirable protein PEGylation
reagents.
Ananda, 231.
11. Ananda discloses:
Proteins generally have a very limited number of reactive thiols
from their cysteine residues, and accordingly these have been
used for site specific PEGylation of proteins. If and when
maleimide-PEG-reactive thiols are absent, the introduction of
cysteine residues as the target sites by site-directed mutagenesis
has also been advanced as a strategy for site-specific
PEGylation reaction.
Id. (internal citations omitted).
12. Wang II8 discloses: “a delivery system comprising a carrier or
an active compound, and a glutathione ligand or a glutathione derivative
ligand. The glutathione ligand or the glutathione derivative ligand is
covalently bound to the carrier or the active compound.” Wang II 2:59–63.
13. Wang II discloses: “The sulfhydryl group (–SH) of the

8 Wang et al., US Patent No. 8,067,380, issued Nov. 29, 2011 (“Wang II”).
Wang II was cited by Appellant for its disclosure of glutathione derivatives
“in which ‘[t]he sulfhydryl group (–SH) of the glutathione is replaced’ with
sulfonic acid (–SOOOH) or an –SR group, wherein R may comprise C1–C10
alkyl or lactoyl (-CO-CH(OH)-CH3).” App. Br. 6.
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glutathione ligand may be modified to form the glutathione derivative
ligand.” Id. at 3:17–18. In one exemplary glutathione derivative ligand,
“the original sulfhydryl group (–SH) of the glutathione ligand is replaced by
–SR,” where “R may comprise C1-10 alkyl or lactoyl (-CO-CH(OH)-CH3).”
Id. at 3:33–35. In another exemplary glutathione derivative ligand, “the
original sulfhydryl group (–SH) of the glutathione ligand is replaced by
sulfonic acid (–SOOOH).” Id. at 3:50–52.
14. Wang II discloses that “the active compound may pass through
the blood brain barrier, such as brain endothelial cells, with a cell
penetration rate of about 0.01-l00%.” Id. at 3:55–58.
15. The Examiner finds, and Appellant does not dispute, that
“Wang II teaches that liposomes carrying on their surface S-derivatives of
GSH are capable of binding to and cross[ing] the BBB.” Ans. 8.
16. Kannan9 discloses that “S-GSSG [S-labeled glutathione
disulfide] uptake by the brain is minimal in the presence or absence of γ-
glutamyl transpeptidase. Thus, although shared and specific uptake of
GSSG and GSH do exist in some tissues, BBB transport appears to be
specific for GSH.” Kannan 969.
17. Kannan studied the effect of S-hexyl GSH and S-octyl GSH on
uptake of GSH by injecting these compounds together with tracer GSH into
the intracarotid artery of male Sprague-Dawley rats. Id. at 965. Kannan

9 Kannan et al., Transport of Glutathione at Blood-Brain Barrier of the Rat:
Inhibition by Glutathione Analogs and Age-Dependence, 263(3) Journal of
Pharmacology and Experimental Therapeutics 964–790 (“Kannan”).
Kannan was cited by the Examiner as evidence that “S-derivatives of GSH
(i.e., obtained by coupling via the native thiol) retain the ability to bind the
BBB transporter.” Ans. 8.
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discloses that S-hexyl GSH inhibited uptake of GSH by 76% and S-octyl
GSH inhibited uptake of GSH by 79%. Id. at 966.
18. Kannan discloses:
The apparent higher affinity of GSH analogs10 than GSH for
this transport system suggest that it functions as a broad
specificity transport system and not solely for GSH. The exact
kinetic mechanism of inhibition of GSH uptake by GSH
analogs remains to be determined. Although the inhibition of
GSH transport may be competitive through a shared transport
mechanism, an allosteric mechanism(s) has not been ruled out.
Regardless of the mechanism of inhibition, the results provide
strong support for the view that GSH transport across the BBB
is mediated by a specific carrier system.
Id. at 969.
ANTICIPATION
Appellant argues claims 1, 4, 7, 9, 11, 14, 17, and 18 together. App.
Br. 4–7. We designate claim 1 as representative.
In finding that Wang anticipates claim 1, the Examiner found that
Wang disclosed “a conjugate produced by reacting GSH with DSPE-PEG-
maleimide (Mal), wherein the conjugate is further incorporated into
nanoliposomes, wherein the nanoliposomes encapsulate an active
compound, and wherein GSH is capable of targeting the nanoliposomes to
the blood-brain-barrier (BBB) via its ability to bind the GSH transporter
found on the BBB.” Ans. 3–4. The Examiner further found that Wang
disclosed using its composition to “deliver the active compound across the
BBB to the brain.” Id. at 4. While Wang does not expressly disclose where

10 GSH analogs include S-hexyl GSH, S-octyl GSH, GSH-monoethyl ester
and BSP-GSH. Kannan 965. Of these, we understand at least S-hexyl and
S-octyl GSH to be derivatized at the sulfhydryl group.
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conjugation of PEG-Mal to GSH occurs, the Examiner found that the
ordinary artisan would have “at once envisioned that Wang et al. teach GSH
coupling to PEG-Mal via the reaction between the native thiol group of GSH
and Mal group of PEG.” Id.
Appellant does not dispute that Wang discloses all of the elements of
claim 1 with the exception of the requirement that the lipid-PEG be
conjugated to GSH “via the thiol group in [GSH’s] cysteine moiety.” See
generally, App. Br.; see also generally Reply. Br. Instead, Appellant
contends that the ordinary artisan would not have at once envisaged binding
GSH to PEG via its native thiol group because Wang makes a “significant
effort” to maintain the native thiol group and because this was consistent
with the understanding in the art at the time that preservation of the thiol
group was necessary to maintain the biological functioning of GSH. Reply
Br. 3, 5. Accordingly, this case turns on whether the ordinary artisan would
have “at once envisaged” binding GSH to PEG-Mal via GSH’s native thiol
group.
We have reviewed the arguments presented and the evidence of
record. Based on our review, we agree with the Examiner that the ordinary
artisan would have at once envisaged conjugating Wang’s PEG-Mal species
to GSH via GSH’s native thiol.
Wang discloses a delivery system that transports an active compound
across the BBB. FF1. The delivery system comprises compounds in which
GSH or a GSH derivative is conjugated to PEG or a PEG derivative. FF2.
Wang specifically identifies five species of PEG derivatives, including, of
particular relevance here, PEG-Mal. FF3. When PEG-Mal binds to GSH, as
disclosed in Wang (see FF2, FF3), the native thiol group of GSH is one of a
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very limited number of locations where it can bind. FF4. The native thiol
group would have been the natural location for conjugation to PEG-Mal and
the ordinary artisan would have at once envisaged conjugating PEG-Mal to
the native thiol because GSH has a thiol group and the reaction of
maleimides with thiols is one of the “best known site-specific, simple, and
quantitative protein chemical modification reactions.” FF10; see also FF11.
In Wrigley, the Federal Circuit explained that where a “prior art
reference . . . discloses a genus and the claim at issue recites a species of that
genus . . . the issue of anticipation turns on whether the genus was of such a
defined and limited class that one of ordinary skill in the art could ‘at once
envisage’ each member of the genus.” 683 F.3d at 1361; see also
Kennametal, Inc. v. Ingersoll Cutting Tool Company, 780 F.3d 1376, 1381–
1382 (Fed. Cir. 2015) (holding that a prior art reference disclosed five
binding agents (one of which was ruthenium) and three coating techniques
(one of which was PVD) anticipated a claim drawn to the specific
combination of ruthenium and PVD). Here, Wang’s disclosure of PEG-Mal
conjugated to GSH (FF2, FF3) comprises a genus of two species – PEG-Mal
bound to GSH’s thiol group, and PEG-Mal bound to GSH’s primary amino
group.11 FF4. Given the limited size of Wang’s PEG-Mal/GSH genus and

11 At oral argument, counsel for Appellant argued that PEG-Mal could also
be conjugated to GSH by “functionaliz[ing] one of the electrophilic sites on
it to make it a nucleophilic site.” Tr. 7. This argument was not made in
Appellant’s briefing and is thus waived. Moreover, even if we were to
consider it and credit it, these additional binding sites do not expand the
genus disclosed in Wang sufficiently to change our analysis. In re Petering,
301 F.2d 676, 682 (C.C.P.A. 1962); Bristol-Myers Squibb Co. v. Ben Venue
Labs., Inc., 246 F.3d 1368, 1380 (Fed. Cir. 2001) (“[T]he disclosure of a
small genus may anticipate the species of that genus even if the species are
not themselves recited.”).
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the knowledge in the art regarding maleimide/thiol conjugation (e.g., FF10,
FF11), we agree with the Examiner that the ordinary artisan would have at
once envisaged GSH bound to PEG-Mal via its native thiol from Wang’s
disclosure of PEG-Mal bound to GSH.
Appellant argues that the ordinary artisan would not have at once
envisaged conjugating PEG-Mal to the native thiol of GSH because the
native thiol was understood to be “necessary to maintain the biological
functioning of GSH.” Reply Br. 5; see also, App. Br. 5. As support,
Appellant cites Forman, which teaches that in GSH, “[t]he sulfhydryl group
(–SH) of the cysteine is involved in reduction and conjugation reactions that
are usually considered as the most important functions of GSH.” FF7.
Appellant also provides the testimony of Dr. Peter Swann, who opines that
in view of Forman the ordinary artisan would have been “wary of
conjugating a biologically inactive molecule such as lipid-PEG to that
sulfhydryl group in the reduced form, as such a modification would be
expected to significantly impair or extinguish the biological function of the
glutathione.” FF9. We are not persuaded because the Examiner has
presented evidence that S-derivatives of GSH – i.e., GSH in which the native
thiol has not been preserved – were known to cross the BBB.
In particular, Wang II discloses a delivery system in which
compounds comprising S-derivatives of GSH are used to deliver active
compounds across the BBB. FF12–14. The Examiner finds, and Appellant
does not dispute, that “Wang II teaches that liposomes carrying on their
surface S-derivatives of GSH are capable of binding to and cross[ing] the
BBB.” FF15. This finding is consistent with Kannan, which found that two
S-derivatives of GSH – S-hexyl GSH and S-octyl GSH – inhibited GSH
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uptake across the BBB by 76% and 79%. FF17. From this, Kannan
concluded that “inhibition of GSH transport may be competitive through a
shared transport mechanism.” FF18. Kannan qualified this by stating that
“[t]he exact kinetic mechanism of inhibition of GSH uptake by GSH analogs
remains to be determined” and “an allosteric mechanism(s) has not been
ruled out.” Id. In addition, Kannan discloses that glucothione disulfide
(GSSH), another S-derivative of GSH, does not cross the BBB. FF16; see
also, Swaan Decl. ¶ 23 (testifying that the “conjugation of the lipid-PEG to
the sulfhydryl group of glutathione would be expected to be sterically
similar to the oxidized form (GSSG), in which the sulfur of the glutathione
is hidden and not nucleophilic”). However, considering Kannan and Wang
II together, we find that the ordinary artisan would have understood that
some S-derivatives of GSH were capable of crossing the BBB.
In sum, given that GSH already comprises a thiol (FF4), that thiol was
well known to react with maleimides (FF10, FF11), that there are a limited
number of alternative sites where PEG-Mal could conjugate to GSH (FF4),
and that S-derivatives of GSH were known to cross the BBB (FF12–15,
FF17–18), we agree with the Examiner that, based on Wang’s disclosure, the
ordinary artisan would have at once envisioned conjugating GSH to PEG-
Mal via the reaction between GSH’s native thiol and the maleimide group of
PEG. This evidence is counterbalanced, to some extent, by evidence
suggesting that in Wang’s Example 1, Wang made a significant effort to
preserve the native thiol. See FF5–6, FF8. However, weighing all the
evidence, we are not persuaded that Wang’s efforts to preserve the native
thiol group in Example 1, assuming such preservation was an intent of the
Example, would have prevented the ordinary artisan from at once envisaging
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PEG-Mal conjugated to GSH’s thiol group. Wang is not limited to its
specific examples. See In re Mills, 470 F.2d 649, 651 (CCPA 1972) (“[A]
reference is not limited to the disclosure of specific working examples.”);
see also Wang 9:10–12 (“While the invention has been described by way of
example and in terms of preferred embodiment, it is to be understood that
the invention is not limited thereto.”). Accordingly, we affirm the
Examiner’s rejection of claim 1. Because they were not argued separately,
claims 4, 7, 9, 11, 14, 17, and 18 fall with claim 1.
OBVIOUSNESS
In finding claims 1, 4, 7, 9, 11–14, 17, and 18 obvious over the
combination of Wang, Ananda, and Chong, the Examiner applied Wang as
discussed above in connection with the Examiner’s anticipation rejection
and relied upon Chong as teaching limitations recited in dependent claims 12
and 13 relating to the use of ribavirin. Ans. 5–6. Similarly, in finding
claims 1, 4, 7, 9, 11–14, 17, 18, and 24 obvious over the combination of
Wang, Ananda, Chong, and Meyding-Lamadé, the Examiner applied Wang
as discussed above in connection with the Examiner’s anticipation rejection
and relied upon Meyding-Lamadé as teaching that limitation recited in
dependent claim 24 relating to the use of a glucocorticoid. Id. at 6.
Appellant does not challenge the Examiner’s findings that the
additional limitations recited in dependent claims 12, 13, and 24 would have
been obvious over the cited art, instead arguing that it would not have been
obvious to conjugate PEG-Mal to GSH via the native thiol group and that
the ordinary artisan would not have expected that a compound in which a
lipid-PEG was conjugated to the GSH via the native thiol group would cross
the BBB. App. Br. 7–10; Reply Br. 8–9. We do not find these arguments
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persuasive. For the reasons already discussed, we agree with the Examiner
that Wang anticipates the method of claim 1. We have discussed above why
Wang anticipates claim 1 and “[i]t is well settled that ‘anticipation is the
epitome of obviousness.’” In re McDaniel, 293 F.3d 1379, 1385 (Fed. Cir.
2002) (quoting Connell v. Sears, Roebuck & Co., 722 F.2d 1542, 1548 (Fed.
Cir. 1983)).
We also agree with the Examiner that the additional limitations of
claims 12 and 13 would have been obvious over the combination of Wang,
Ananda, and Chong and that the additional limitations of claim 24 would
have been obvious over the combination of Wang, Ananda, Chong, and
Meyding-Lamadé for the reasons provided by the Examiner in the Answer
and Final Office Action. Ans. 5–6; Final Act. 3–5. Accordingly, we affirm
the Examiner’s rejection of claims 1, 4, 7, 9, 11–14, 17, and 18 as obvious
over the combination of Wang, Ananda, and Chong, and the Examiner’s
rejection of claims 1, 4, 7, 9, 11–14, 17, 18, and 24 as obvious over the
combination of Wang, Ananda, Chong, and Meyding-Lamadé

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CONCLUSION
In summary:
Claims
Rejected
35 U.S.C. § Basis Affirmed Reversed
1, 4, 7, 9, 11,
14, 17, 18
102(b) Wang

1, 4, 7, 9,
11, 14, 17,
18

1, 4, 7, 9, 11–
14, 17, 18
103(a) Wang, Ananda,
Chong

1, 4, 7, 9,
11–14, 17,
18

1, 4, 7, 9, 11,
14, 17, 18, 24
103(a) Wang, Ananda,
Chong, Meyding-
Lamadé.

1, 4, 7, 9,
11, 14, 17,
18, 24

Overall
Outcome
1, 4, 7, 9,
11, 14, 17,
18, 24

AFFIRMED