SAAKIAN, Susanna A.

Patent Trials and Appeals Board

Jan 23, 2020

15919361 - (D) (P.T.A.B. Jan. 23, 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.
15/919,361 03/13/2018 Susanna A. SAAKIAN 7016-0023 5480
93192 7590 01/23/2020
ASE Pharmaceuticals, LLC
5425 Park Central Court
Suite 111
Naples, FL 34109
EXAMINER
RAMACHANDRAN, UMAMAHESWARI
ART UNIT PAPER NUMBER
1627
NOTIFICATION DATE DELIVERY MODE
01/23/2020 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):
sakptomail@iplawpro.com
PTOL-90A (Rev. 04/07)

UNITED STATES PATENT AND TRADEMARK OFFICE
____________

BEFORE THE PATENT TRIAL AND APPEAL BOARD
____________

Ex parte SUSANNA A. SAAKIAN
____________

Appeal 2019-005346
Application 15/919,361
Technology Center 1600
____________

Before DONALD E. ADAMS, ERIC B. GRIMES, and
RICHARD M. LEBOVITZ, Administrative Patent Judges.

ADAMS, Administrative Patent Judge.

DECISION ON APPEAL
Pursuant to 35 U.S.C. § 134(a), Appellant1 appeals2 from Examiner’s
decision to reject claims 1–4 and 6–8.3 We have jurisdiction under
35 U.S.C. § 6(b). We AFFIRM-IN-PART.

1 We use the word “Appellant” to refer to “applicant” as defined in 37
C.F.R. § 1.42. Appellant identifies the real party in interest as “ASE
Pharmaceuticals, LLC” (Appellant’s April 10, 2019 Appeal Brief (Appeal
Br.) 3).
2 Appellant states that “[t]his [A]ppeal is related to Appeal 2014-008576,
[Application 13/140,259,] the [D]ecision of which affirmed the
rejections . . . on appeal” was entered July 20, 2016(Appeal Br. 4).
3 Examiner finds Appellant’s pending claim 5 “allowable if rewritten in
independent form including all of the limitations of the base claim and any
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STATEMENT OF THE CASE
Appellant’s disclosure relates “to the fields of organic chemistry, drug
development, pharmacology, and medicine. More particularly, the invention
relates to modulating human physiology by administration of one or more
[2.2.2] bicyclic derivatives” (Spec.4 3). Appellant’s only independent claim,
claim 1, is reproduced below:
1. A method for reducing the number or strength of seizures in
a human subject suffering from epilepsy, the method
comprising the step of orally administering to the subject 50-
1200 mg of the bicyclo-[2.2.2]-octane-2-carboxylate salt per
day at least until the number or strength of seizures in a human
subject is reduced.
(Appeal Br. 12.)

Grounds of rejection before this Panel for review:
Claims 1–3 stand rejected under 35 U.S.C. § 103(a) as unpatentable
over the combination of Saakian.5
Claim 4 stands rejected under 35 U.S.C. § 103(a) as unpatentable over
the combination of Saakian and Hanshermann.6
Claim 6 stands rejected under 35 U.S.C. § 103(a) as unpatentable over
the combination of Saakian and Ledford.7

intervening claims” (Examiner’s November 27, 2018 Final Office Action
(Final Act.) 19).
4 Appellant’s March 13, 2018 Specification.
5 Saakian et al., WO 99/23056, published Mar. 14, 1999, as machine
translated.
6 Hanshermann et al., US 2005/0202088 A1, published Sept. 15, 2005.
7 Heidi Ledford, Epilepsy drug may help alcoholics, available at
http://www.nature.com/news/2008/080528/full/news.2008.859.html,
published May 28, 2008.
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Claim 7 stands rejected under 35 U.S.C. § 103(a) as unpatentable over
the combination of Saakian and Rao.8
Claim 8 stands rejected under 35 U.S.C. § 103(a) as unpatentable over
the combination of Saakian and Zoons.9
Claims 1–4 stand rejected under 35 U.S.C. § 103(a) as unpatentable
over the combination of Kalimullina10 and Saakian.

ISSUE
Does the preponderance of evidence relied upon by Examiner support
a conclusion of obviousness?
FACTUAL FINDINGS (FF)
FF 1. Saakian discloses
that derivatives of bicyclo [2.2.2] octane-2-carboxylic acid, in
particular its alkali metal and alkaline-earth metals possess
anticonvulsant activity in the absence of any side effects and
may be useful for the prevention and [treatment of] epilepsy
due to their efficient and selective effect on convulsive response
in mammals regardless of the sex of animals.
(Saakian 211; see id. (Saakian “provides a method of arresting a convulsive
state, which comprises administering to the animal an effective amount of a

8 Marie Luise Rao et al., Serum Amino Acids, Liver Status, and Antiepileptic
Drug Therapy in Epilepsy, 33 Epilepsia 347–354 (1993).
9 E. Zoons et al., Seizures in adults with bacterial meningitis, 70 Neurology
2109–2115 (2008).
10 L.B. Kalimullina et al., The piriform cortex and cortical nucleus of the
amygdala in epileptogenesis: The role of the rostro-caudal gradient,” 31
USPEKHI FIZIOLOGICHESKIKH NAUK 63–74 (2000), as translated in
PTO 122278.
11 Saakian is not paginated. Therefore, all reference to a page number of this
machine translation refers to a page number as if the document was
paginated consecutively beginning with the first page.
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bicyclo [2.2.2] octane-2-carboxylic acid”); id. at 5 (Saakian discloses that
the “Na-salt of said acid – Sakritsin – was more preferred for use as an
anticonvulsant compared to known drugs such as phenobarbital, phenytoin
and konvuleks”); see generally Ans.12 4–5.)
FF 2. Saakian discloses dosage forms designed for a single dose, including
orally administrable tablets, capsules or powders, “comprising an effective
amount of a salt of bicyclo [2.2.2] octane-2-carboxylic acid” (Saakian 2; see
id. (Saakian discloses that its dosage forms, i.e. compositions, are formulated
“to produce the desired therapeutic effect”); id. (Saakian discloses
“[p]harmaceutical compositions in the form of tablets or capsules containing
from 50 to 100 mg of active ingredient”); see generally Ans. 5).
FF 3. Saakian discloses that “[t]he term ‘effective amount’ means an
amount of compound required to relieve convulsive state or any of its
symptoms, conducted by a pharmaceutical composition comprising a
compound” within the scope of Saakian’s disclosure (Saakian 2; see id. at 2–
3 (Saakian discloses that “[a]n effective amount is generally determined by
the physician in each case and depends on the severity of the disease, age
and weight of the recipient and route of administration”); see generally Ans.
5).
FF 4. Saakian discloses that “[t]he term ‘relief of convulsive
state’ . . . includes prevention, containment, lessening the severity of a
disease or a symptom or its consequences” (Saakian 2; see generally Ans.
5).

12 Examiner’s May 3, 2019 Answer.
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FF 5. Examiner finds that Saakian does not disclose sustained or delayed
release tablets and relies on Hanshermann to make up for this deficiency in
the Saakian (Ans. 6–7 (citing Hanshermann’s claims 1, 7, 8, 14, 15, and
21)).
FF 6. Examiner finds that although Saakian suggests administering a
bicyclo-[2.2.2]-octane-2-carboxylate salt “generally to all human subjects
with epilepsy, the reference do[es] not explicitly . . . [disclose administration
to,] human subjects suffer[ing] from ethanol addiction” and relies on
Ledford’s disclosure that the “epilepsy drug (e.g. gabapentin) may help
alcoholics; a drug used to treat epilepsy could also ease cravings in
alcoholics” (Ans. 7 (citing Ledford 1); see Ledford 1 (Ledford discloses that
“[p]reliminary small clinical trials have suggested that gabapentin[, a drug
approved for treatment of epileptic seizures and for some conditions that
cause chronic pain,] could . . . be useful in the treatment of drug
addiction”)).
FF 7. Ledford discloses that
Gabapentin is structurally similar to a neurotransmitter called γ-
aminobutyric acid, or GABA, which can slow communication
between neurons in the brain. Although the drug does not
function in precisely the same way as GABA, it can prevent the
chaotic electrical activity in the brain that triggers a seizure.
Alcohol affects the GABA system by mimicking GABA’s
activity in the brain, which contributes to alcohol’s sedative
effect. But chronic drinking can lead to tolerance: a condition
in which more and more alcohol is required to produce the
same GABA response. Without an increasing supply of
alcohol, alcoholics can begin to feel agitated.
There has been a lot of interest in whether epilepsy drugs might
also be useful for treating alcoholism . . . . The drugs could
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help an alcoholic during the early stages of abstinence, until
normal GABA tolerance has been restored.
(Ledford 1–2.)
FF 8. Examiner finds that Saakian does not disclose the treatment of
humans having an “elevated level of liver function markers” and relies on
Rao to make up for this deficiency (Ans. 8 (citing Rao, Abstract and Table
3)).
FF 9. Rao discloses that “[s]timulation of hepatic enzymes by
[antiepileptic drugs (AEDs)] administered in therapeutic dosages has been
observed to vary with respect to the different AEDs” (Rao 347).
FF 10. Rao discloses a study of “serum [amino acid (AA)] profiles and liver
enzymes in 73 epileptic patients and 90 healthy subjects,” and found that
“[s]eventy-two percent of the AED-treated patients and 33%
of the unmedicated patients showed an increase in one or several serum liver
enzymes [alanine aminotransferase (ALT), aspartate amino transferase
(AST), and/or γ-glutamyl transferase (γ-GT)]; particularly γ-GT” (Rao,
Abstract (alteration original)).
FF 11. Rao “observed a significant increase in serum concentrations of
glutamine and glycine and decreased levels of taurine, threonine, serine,
valine, methionine, isoleucine, leucine, phenylalanine, histidine, tryptophan,
and arginine in AED-treated patients but not in unmedicated patients,” and
concludes that “[t]hese results show that the changes in the serum AA
profiles of epileptic patients treated with AEDs occur in patients with
alteration of serum liver enzymes; whether this implies a causal relation is
still uncertain” (Rao, Abstract).

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FF 12. Rao discloses that
Nine of [its] patients who were AED-free for ≥4 weeks had an
AA profile which was not different from that of healthy
subjects. On the other hand, 3 of the 9 patients not receiving
AEDs and 74% of the patients receiving AEDs had increases in
one or more of the serum liver enzyme levels, i.e., mostly
increases (induction) in γ-GT. Thus, the AED-induced hepatic
changes may have been involved in the AA alteration in
epilepsy.
(Rao 353.)
FF 13. Examiner finds that Saakian does not disclose the treatment of
humans having “elevated erythrocyte sedimentation” and relies on Zoons to
make up for this deficiency (Ans. 9 (citing Zoons, Abstract; 2111: col. 2, ll.
10–11; Tables 2–3; and 2112: col. 2, para. 2)).
FF 14. Zoons discloses an evaluation of “the occurrence and prognostic
relevance of seizures in adults with community-acquired bacterial
meningitis” (Zoons, Abstract).
FF 15. Zoons discloses that “[p]atients with in-hospital seizures were more
likely to have . . .[, inter alia,] higher median erythrocyte sedimentation
rate . . . than patients without in-hospital seizures” and that antiepileptic
medications were administered to treat seizures (Zoons, Abstract, see also
id. at 2111 (Zoons discloses that “[p]atients with in-hospital seizures were
more likely to have . . . higher median erythrocyte sedimentation rate
(ESR)”); id. at 2112 (“[a]ntiepileptic medication was administered in 98 of
111 evaluated episodes (85%) with seizures”)).
FF 16. Kalimullina discloses
The amygdaloid complex (AC) of the brain is a
nuclearpaleocortical component of the encephalon inasmuch as
its composition includes, in addition to typical nuclei,
formations whose cytoarchitectonic properties are of the
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paleocortical or transitional kind (Figure 1). This applies
primarily to the cortical nucleus of AC, whose seizure
susceptibility was investigated in . . . [Kalimullina’s] study.
(Kalimullina 3.)
FF 17. Kalimullina discloses that “[e]lectrical kindling of AC in rats is
being successfully used to screen new anticonvulsant drugs, and in the
present study it was used to investigate Sacricin” (Kalimullina 16; see Ans.
17).
FF 18. Kalimullina discloses
A single 200 mg/kg dose of Sacricin was administered
intraabdominally following the formation of a partial kindling.
The drug was injected 30 minutes prior to the stimulation
because pharmacokinetic studies have shown that during that
period its concentration in the blood plasma reaches a
maximum. To detect trace effects, the daily electrostimulation
séances were continued in the following days.
(Kalimullina 17; see Ans. 17.)
FF 19. Kalimullina discloses that “in every rat study, Sacricin was found to
reduce the representation of epileptiform activity, both that arising
spontaneously and that relating to LPT evoked by stimulation” (Kalimullina
19; see id. at 20 (Kalimullina discloses that “[t]he anticonvulsant effect of
Sacricin manifested itself in a decline in the severity of seizures”); id. at 22
(Kalimullina discloses that “[t]he administration of Sacricin resulted in a
statistically significant decrease in the number of 2nd stage seizures and
completely blocked the more severe stages (3rd–5th)”); see also Ans. 17–18).
FF 20. Kalimullina discloses that
a 200 mg/kg dose of Sacricin is effective in blocking PTZ-
induced seizures, as is phenobarbital, but when the dose of
Sacricin is doubled to 400 mg/kg then its anticonvulsant effects
are superior to those of phenobarbital (administered in doses of
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15 and 30 mg/kg). The behavioral changes observed in the
present study in rats following a single injection of Sacricin
were not of a dominant or pathological nature.
(Kalimullina 26–27; see Ans. 18.)
FF 21. Examiner finds that Kalimullina “does not explicitly teach the oral
administration in a human subject or the dosage amount of bicyclo-[2.2.2]-
octane-2-carboxylate salt as claimed [by Appellant]” and relies on Saakian
to make up for this deficiency in Kalimullina (Ans. 11; see FF 1–4).
FF 22. Examiner finds that “the pharmaceutical forms, e.g., sustained
release, immediate release are all deemed obvious since they represent
conventional formulations and modes of administration and are all within
the knowledge of the skilled pharmacologist” (Ans. 12).
ANALYSIS
The rejection over Saakian:
The method of Appellant’s claim 1, reproduced above, comprises the
step of orally administering, to a human subject suffering from epilepsy, 50–
1200 mg of bicyclo-[2.2.2]-octane-2-carboxylate salt per day at least until
the number or strength of seizures in a human subject is reduced (see Appeal
Br. 12).
Saakian discloses the oral administration, to a mammal, which
includes a human, suffering from epilepsy, of a single dose of 50 to 100 mg
of bicyclo-[2.2.2]-octane-2-carboxylate salt to provide relief of a convulsive
state, which includes “lessening the severity of a disease or a symptom or its
consequences” (see FF 1–4). In this regard, Saakian further discloses the
administration of an “effective amount” of bicyclo-[2.2.2]-octane-2-
carboxylate salt to treat epilepsy in a mammal, which includes a human (see
id.). Saakian discloses that the “effective amount is generally determined by
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the physician in each case and depends on the severity of the disease, age
and weight of the recipient and route of administration,” wherein the
“effective amount” is defined as “an amount of compound required to
relieve convulsive state or any of its symptoms, conducted by a
pharmaceutical composition comprising a compound” within the scope of
Saakian’s disclosure, i.e., a bicyclo-[2.2.2]-octane-2-carboxylate salt, such
as the sodium salt–Sakritsin (see id.). “[W]here[, as here,] the general
conditions of a claim are disclosed in the prior art, it is not inventive to
discover the optimum or workable ranges by routine experimentation.” In re
Aller, 220 F.2d 454, 456 (CCPA 1955).
For the foregoing reasons, we find no error in Examiner’s conclusion
that, at the time Appellant’s invention was made, it would have been prima
facie obvious, in view of Saakian, to reduce the number or strength of
seizures in a mammal, which includes a human subject, suffering from
epilepsy by orally administering to the subject 50-1200 mg of the bicyclo-
[2.2.2]-octane-2-carboxylate salt per day at least until the number or strength
of seizures in the human subject is reduced (see Ans. 2–6).
For the foregoing reasons, we are not persuaded by Appellant’s
contention that “[t]here is no clear guidance and direction[, in Saakian,] to
select orally administering 50-1200 mg of the bicycle-[2.2.2]-octane-2-
carboxylate salt per day to a human subject with epilepsy at least until the
number or strength of seizures in a human subject is reduced” (Appeal Br. 8;
see id. at 6–7 (Appellant admits that “Saakian teaches the bicyclo-[2.2.2]-
octane-2-carboxylate salt as recited in [Appellant’s] claim 1”).
A reference disclosure is not limited only to its preferred
embodiments, but is available for all that it discloses and suggests to one of
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ordinary skill in the art. In re Lamberti, 545 F.2d 747, 750 (CCPA 1976);
see also In re Susi, 440 F.2d 442, 446 n.3 (CCPA 1971) (Disclosed
examples and preferred embodiments do not constitute a teaching away from
a broader disclosure or non-preferred embodiments). Therefore, we are not
persuaded by Appellant’s contention that Saakian does not provide an
enabling disclosure of Appellant’s claimed invention, because Saakian does
not disclose human clinical studies (see Appeal Br. 6–7).
“Attorney’s argument in a brief cannot take the place of evidence.” In
re Pearson, 494 F.2d 1399, 1405 (CCPA 1974). Therefore, we are not
persuaded by the unsupported assertions of Appellant’s counsel concerning
Saakian’s disclosure (see Appeal Br. 6–10). In this regard, we recognize the
unsupported assertion by Appellant’s counsel that “Saakian’s rodent models
differ significantly from human epilepsy” (id. at 9). This assertion, however,
fails to provide an evidentiary basis to establish that those of ordinary skill in
this art would have considered Saakian’s experimental models to be
insufficient to support Saakian’s disclosure.

The rejection over the combination of Saakian and Hanshermann:
Appellant’s claim 4 depends from and further limits the method of
Appellant’s claim 1 to require that the bicyclo-[2.2.2]-octane-2-carboxylate
salt is formulated for sustained or delayed release” (see Appeal Br. 12).
Based on the combination of Saakian and Hanshermann, Examiner
concludes that, at the time Appellant’s invention was made, it would have
been prima facie obvious “to formulate a sustained or delayed drug release
comprising an anticonvulsant, sacricin from Hanshermann” (Ans. 7; see FF
1–5).
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For the foregoing reasons, we found no deficiency in Saakian.
Therefore, we are not persuaded by Appellant’s contention that “[t]his
rejection is in error for its reliance on Saakian for the reasons provided
above” and “[b]ecause Hanshermann does not cure Saakian’s lack of
teaching or suggestion, this rejection is in error and should be reversed”
(Appeal Br. 10).

The rejection over the combination of Saakian and Ledford:
The method of Appellant’s claim 6 depends from and further limits
the human subject of Appellant’s claim 1 to a human subject that “also
suffers from ethanol addiction and the bicyclo-[2.2.2]-octane-2-carboxylate
salt is administered at least until the dysphoria and the number of strength of
seizures in the subject is reduced” (see Appeal Br. 12).
Examiner recognizes that Saakian fails to disclose the administration
of bicyclo-[2.2.2]-octane-2-carboxylate salt to individuals suffering from
epilepsy and ethanol addiction (FF 6). Ledford discloses that “[a]lcohol
affects the GABA system by mimicking GABA’s activity in the brain,
which contributes to alcohol’s sedative effect” (FF 7). Ledford discloses
gabapentin, a drug useful for the treatment of epilepsy, “is structurally
similar to GABA” and “[a]lthough the drug does not function in precisely
the same way as GABA, it can prevent the chaotic electrical activity in the
brain that triggers a seizure” (FF 6–7). Ledford discloses that “[t]here has
been a lot of interest in whether epilepsy drugs might . . . be useful for
treating alcoholism” and that “[p]reliminary small clinical trials have
suggested that gabapentin could be useful in the treatment of drug addiction”
(FF 6–7).
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In sum, Ledford discloses that gabapentin could be useful in treating
drug addiction, based upon preliminary small clinical trials of a treatment
that uses an antiepileptic drug that is structurally similar to the GABA
neurotransmitter, which is involved in the same system that alcohol affects
by mimicking GABA’s activity in the brain (FF 6–7). Although Ledford
suggests that there is interest in this art as to “whether epilepsy drugs
might . . . be useful for treating alcoholism,” Ledford, at best, suggests the
exploration of a general approach that seems to be a promising field of
experimentation, but gave only general guidance as to how to achieve
Appellant’s claimed result. Stated differently, the combination of Saakian
and Ledbetter falls into O’Farrell’s second class of impermissible “obvious
to try” situations, where
what was “obvious to try” was to explore a new technology or
general approach that seemed to be a promising field of
experimentation, where the prior art gave only general guidance
as to the particular form of the claimed invention or how to
achieve it. [In re O’Farrell, 853 F.2d 894, 903 (Fed. Cir.
1988)]. . . . KSR affirmed the logical inverse of this statement
by stating that § 103 bars patentability unless “the improvement
is more than the predictable use of prior art elements according
to their established functions.” [Teleflex, Inc. v. KSR Int’l Co.,
550 U.S. 398, 417 (2007)].
In re Kubin, 561 F.3d 1351, 1359–60 (Fed. Cir. 2009).
Therefore, we are not persuaded by Examiner’s conclusion, based on
the combination of Saakian and Ledford, that at the time Appellant’s
invention was made, it would have been prima facie obvious to use
Saakian’s sacricin to treat a human subject suffering from both epilepsy and
alcoholism, i.e. ethanol addiction, wherein Saakian’s sacricin is administered
at least until the dysphoria and the number or strength of seizures in the
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subject is reduced (see Ans. 8; see FF 1–4, 6, and 7). Instead, we agree with
Appellant’s contention that “[n]either Saakian nor Ledford teach that
bicyclo-[2.2.2]-octane-2-carboxylate salt acts the same way in alcohol
craving as does gabapentin . . . [and], therefore, [the rejection] lacks the
rational underpinning to support the legal conclusion of obviousness
required by KSR. Accordingly, the rejection is in error and should be
reversed” (Appeal Br. 10).

The rejection over the combination of Saakian and Rao:
The method of Appellant’s claim 7 depends from and further limits
the human subject of Appellant’s claim 1 to a human subject that has an
elevated liver function marker selected from the group consisting of AST,
ALT, and bilirubin, and the bicyclo-[2.2.2]-octane-2-carboxylate salt is
administered at least until the liver function marker and the number or
strength of seizures in the subject is reduced (see Appeal Br. 13).
Based on the combination of Saakian and Rao, Examiner concludes
that, at the time Appellant’s invention was made, it would have been prima
facie obvious “to administer [Saakian’s] sacricin at least until the liver
function marker and the number or strength of seizures in the subjects is
reduced . . . to treat the symptoms of epilepsy and provide therapeutic
benefits in patients with elevated liver markers,” because Rao discloses that
liver enzymes such as AST and ALT liver markers may be elevated in
patients with epilepsy (Ans. 8; see FF 1–4 and 8–12). We are not persuaded.
The method of Appellant’s claim 7 requires the administration of
bicyclo-[2.2.2]-octane-2-carboxylate salt at least until, inter alia, the liver
function marker is reduced (see Appeal Br. 13). In contrast, Rao discloses a
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study wherein “[s]eventy-two percent of the AED-treated patients [in the
study] . . . showed an increase in one or several serum liver enzymes
[alanine aminotransferase (ALT), aspartate amino transferase (AST), and/or
γ-glutamyl transferase (γ-GT)]; particularly γ-GT” (FF 9). In addition, Rao
discloses that although “[n]ine of [its] patients who were AED-free for ≥4
weeks had an AA profile which was not different from that of healthy
subjects,” “74% of [its] patients receiving AEDs had increases in one or
more of the serum liver enzyme levels, i.e., mostly increases (induction) in
γ-GT. Thus, [Rao concludes that] the AED-induced hepatic changes may
have been involved in the AA alteration in epilepsy” (FF 12; see also FF
11).
In sum, Examiner failed to establish an evidentiary basis on this
record to support a conclusion that the combination of Saakian and Rao
suggests that treatment, of a patient suffering from epilepsy and an elevated
liver function marker, with an anti-epileptic drug will reduce, inter alia, the
liver function marker in the patient, as required by Appellant’s claimed
invention (see Appeal Br. 13; cf. FF 8–12). Therefore, we agree with
Appellant’s contention that “[t]his rejection is in error because it is not based
on any evidence . . . suggesting that a bicyclo-[2.2.2]-octane-2-carboxylate
salt would have been expected to reduce elevated liver enzymes” (Appeal
Br. 11).

The rejection over the combination of Saakian and Zoons:
The method of Appellant’s claim 8 depends from and further limits
the human subject of Appellant’s claim 1 to a human subject that has an
elevated erythrocyte sedimentation rate, and the bicyclo-[2.2.2]-octane-2-
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carboxylate salt is administered at least until the erythrocyte sedimentation
rate and the number or strength of seizures in the subject is reduced (see
Appeal Br. 13).
Based on the combination of Saakian and Zoons, Examiner concludes
that, at the time Appellant’s invention was made, it would have been prima
facie obvious “to administer [Saakian’s] sacricin at least until the
erythrocyte sedimentation rate and the number or strength of seizures in the
subjects is reduced . . . to treat the symptoms of epilepsy and provide
therapeutic benefits in such patients,” because Zoons discloses that
“erythrocyte sedimentation rate is elevated in patients with seizures and anti-
epileptic medications are provided to treat seizures” (Ans. 9; see FF 1–4 and
13–15). We are not persuaded.
Examiner recognizes that Saakian does not disclose the treatment of
humans having “elevated erythrocyte sedimentation” (FF 13). Zoons
discloses that “seizures in adults with community-acquired bacterial
meningitis” correspond to, inter alia, higher median erythrocyte
sedimentation rate” and that these seizures are treated with antiepileptic
medication (see FF 13–15). Examiner does not identify, nor do we find, a
disclosure in Zoons that establishes that the treatment of seizures in patients
with community-acquired bacterial meningitis necessarily results in a
reduced erythrocyte sedimentation rate in these patients. Thus, we agree
with Appellant’s contention that “[t]his rejection is in error because it is not
based on any evidence . . . suggesting that a bicyclo-[2.2.2]-octane-2-
carboxylate salt would have been expected to reduce elevated erythrocyte
sedimentation rates” (Appeal Br. 11).

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The rejection over the combination of Kalimullina and Saakian:
Based on the combination of Kalimullina and Saakian, Examiner
concludes that, at the time Appellant’s invention was made, it would have
been prima facie obvious to reduce the number or strength of seizures in a
mammal, which includes a human subject, suffering from epilepsy by orally
administering to the subject 50-1200 mg of the bicyclo-[2.2.2]-octane-2-
carboxylate salt per day at least until the number or strength of seizures in
the human subject is reduced, wherein “the pharmaceutical forms, e.g.,
sustained release, immediate release are all deemed obvious since they
represent conventional formulations and modes of administration and are all
within the knowledge of the skilled pharmacologist (see Ans. 11–12; see FF
1–4 and 16–22).

Claim 1:
For the reasons set forth above, with respect to the rejection of claim 1
over Saakian, we are not persuaded by Appellant’s contention that
This rejection is in error for the same reasons as the 103
rejection over only Saakian (section A above). Because this art
is highly unpredictable, and neither Kalimullina nor Saakian’s
present any data from human subjects with epilepsy, any data
concerning the efficacy of oral administration in any species, or
any data from experiments with a dosage/administration
protocol in any way similar to that in claim 1 in any species, the
only reasonable conclusion that the skilled artisan, balancing
the Wands factors in view of claims 1-3 and Kalimullina and
Saakian, could arrive at that undue experimentation would have
been required to arrive at the subject matter of claims 1-3.
(Appeal Br. 11.)

Appeal 2019-005346
Application 15/919,361

18
Claim 4:
Appellant does not address the rejection of claim 4. We do not find,
and Appellant does not identify, error in Examiner’s rejection of claim 4
over the combination of Kalimullina and Saakian (see Ans. 10–12; see also
FF 1–4 and 16–22). Therefore, affirm the rejection of claim 4 over the
combination of Kalimullina and Saakian (see Ans. 10–12; FF 1–4 and 16–
22).
CONCLUSION
The preponderance of evidence relied upon by Examiner supports a
conclusion of obviousness with respect to Appellant’s claims 1–4.
The rejection of claim 1 under 35 U.S.C. § 103(a) as unpatentable
over Saakian is affirmed. Claims 2 and 3 are not separately argued and,
therefore, fall with claim 1.
The rejection of claim 4 under 35 U.S.C. § 103(a) as unpatentable
over the combination of Saakian and Hanshermann is affirmed.
The rejection of claims 1 and 4 under 35 U.S.C. § 103(a) as
unpatentable over the combination of Kalimullina and Saakian. Claims 2
and 3 are not separately argued and, therefore, fall with claim 1.

The preponderance of evidence relied upon by Examiner fails to
support a conclusion of obviousness with respect to Appellant’s claims 6–8.
The rejection of claim 6 under 35 U.S.C. § 103(a) as unpatentable
over the combination of Saakian and Ledford is reversed.
The rejection of claim 7 under 35 U.S.C. § 103(a) as unpatentable
over the combination of Saakian and Rao is reversed.
Appeal 2019-005346
Application 15/919,361

19
The rejection of claim 8 under 35 U.S.C. § 103(a) as unpatentable
over the combination of Saakian and Zoons is reversed.

DECISION SUMMARY
In summary:
Claims
Rejected
35 U.S.C. § Reference(s)/Basis Affirmed Reversed
1–3 103 Saakian 1–3
4 103 Saakian,
Hanshermann
4
6 103 Saakian, Ledford 6
7 103 Saakian, Rao 7
8 103 Saakian, Zoons 8
1–4 103 Kalimullina,
Saakian
1–4
Overall
Outcome
1–4 6–8

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-IN-PART