THE REGENTS OF THE UNIVERSITY OF CALIFORNIA

Patent Trials and Appeals Board

Apr 15, 2020

14900907 - (D) (P.T.A.B. Apr. 15, 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.
14/900,907 12/22/2015 Alcino Silva 034044.108US1 5863
53498 7590 04/15/2020
Suzannah K. Sundby (UC)
Canady + Lortz LLP
1050 30th Street, NW
WASHINGTON, DC 20007
EXAMINER
HUANG, GIGI GEORGIANA
ART UNIT PAPER NUMBER
1613
NOTIFICATION DATE DELIVERY MODE
04/15/2020 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):
suzannah@canadylortz.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte ALCINO SILVA, YONG-SEOK LEE, and DAN EHNINGER1
Appeal 2019-003299
Application 14/900,907
Technology Center 1600
Before ERIC B. GRIMES, DEBORAH KATZ, and
ULRIKE W. JENKS, Administrative Patent Judges.
GRIMES, Administrative Patent Judge.
DECISION ON APPEAL
This is an appeal under 35 U.S.C. § 134(a) involving claims to a
method of treating a cognitive deficit in a subject having Noonan Syndrome,
which have been rejected as anticipated and obvious, and for obviousness-
type double patenting. We have jurisdiction under 35 U.S.C. § 6(b).
We REVERSE.

1 Appellant identifies the real party in interest as The Regents of the
University of California. Appeal Br. 4. We use the word Appellant to refer
to “applicant” as defined in 37 C.F.R. § 1.42(a).
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STATEMENT OF THE CASE
“[T]he present invention is directed to a method of treating a subject
with a cognitive deficit, which comprises administering an effective amount
of one or more hydroxymethylglutaryl CoA (HMG CoA) reductase
inhibitors to a subject afflicted with a cognitive disorder associated with
Noonan Syndrome. Spec. ¶ 12. “An important class of HMG CoA reductase
inhibitors is statins.” Spec. ¶ 37.
“In Noonan Syndrome (NS) 30% to 50% of subjects show cognitive
deficits of unknown etiology and with no known treatment.” Spec. ¶ 34.
“[T]he methods disclosed herein comprise administration of a HMG CoA
reductase inhibitor to improve, enhance, or restore the cognitive function of
subjects suffering from a cognitive deficit. ‘Cognitive function’ as used
herein refers to the performance of some cognitive activity, such as memory,
perception, learning, and reasoning.” Spec. ¶ 40.
“‘[C]ognitive disorder’ refers to a disorder that affects mental
processes, including impairments of memory, learning, awareness, attention,
communication, motor coordination, and/or intellectual capacity.
‘Impairment of cognition,’ or ‘cognitive deficits’ as used herein, are
associated with various disorders, including among others, . . . Noonan
Syndrome.” Spec. ¶ 42. “In the case of cognitive disorders, administration
of the compounds and compositions to a patient suffering from the cognitive
deficit provides a therapeutic benefit where there is improvement,
enhancement, or restoration in the cognitive function.” Spec. ¶ 64.
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Claims 1, 4–13, and 17–20 are on appeal. Claim 1, reproduced below,
is illustrative:
1: A method of treating a cognitive deficit in a subject having
Noonan Syndrome, comprising:
administering an effective amount of one or more
hydroxymethylglutaryl CoA (HMG CoA) reductase inhibitors to a subject
having the cognitive deficit and Noonan Syndrome.

The claims stand rejected as follows:
Claims 1–7, 9, 13, 17, 18, and 20 under 35 U.S.C. § 102(a)(1) as
being anticipated by Bear2 (Ans. 3);
Claims 8, 10–12, and 19 under 35 U.S.C. § 103 as being unpatentable
over Bear2 (Ans. 4);
Claims 1–12 and 20 under 35 U.S.C. § 103 as being unpatentable over
Silva3 in view of Nystrom4 (Ans. 5);
Claims 13 and 17–19 under 35 U.S.C. § 103 as being unpatentable
over Silva3 in view of Nystrom4 further in view of Wu5 further in view of
Smith6 (Ans. 6);

2 WO 2012/054724 A1; Apr. 26, 2012.
3 US 2007/0299096 A1; Dec. 27, 2007.
4 A. Nystrom et al., Noonan syndrome and neurofibromatosis type I in a
family with a novel mutation in NF1, Clin Genet. 76:524–534 (abstract only)
(2009).
5 X. Wu et al., MEK-ERK pathway modulation ameliorates disease
phenotypes in a mouse model of Noonan syndrome associated with the
Raf1(L613V) mutation, J. Clin. Invest. 121:1009–1025 (abstract only)
(2011).
6 WO 2012/019113 A2; Feb. 9, 2012.
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Claims 1–12 and 20 on the basis of nonstatutory double patenting
based on claims 1–22 of U.S. Patent 8,222,293 and Nystrom (Ans. 8); and
Claims 13 and 17–19 on the basis of nonstatutory double patenting
based on claims 1–22 of U.S. Patent 8,222,293, Nystrom, Wu, and Smith
(Ans. 9–10).
OPINION
Anticipation
Claims 1–7, 9, 13, 17, 18, and 20 stand rejected as being anticipated
by Bear. Ans. 3. The Examiner finds that Bear “teaches the treatment of
seizures (a cognitive deficit) in patients with Noonan syndrome with the
administration of 3-hydroxy-3-methylglytaryl[sic]-Coenzyme A reductase
inhibitors (also known as HMG Coenzyme A reductase inhibitors, or
statins).” Ans. 3–4.
The Examiner also finds that Bear “teaches that intellectual disability
and seizures are associated with Noonan syndrome” and these “are cognitive
disorders/deficits per the specification see [42] i.e. impairment of motor
coordination and/or intellectual capacity.” Ans. 4.
The Examiner reasons that “a cognitive deficit is a cognitive disorder,
which is defined in the specification per [42] is be [sic] a disorder that
affects . . . ‘mental processes, including impairments of memory, learning,
awareness, attention, communication, motor coordination, and/or intellectual
capacity.’” Ans. 12. The Examiner finds that seizures are a cognitive deficit
as defined by the Specification because they impair motor coordination and
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cause memory problems, as evidenced by Epilepsy Action Australia.7 Ans.
12.
Appellant argues that “[t]he instant specification teaches that
cognitive deficits relate to deficits in cognitive function, e.g., deficits in
memory perception, learning, and reasoning.” Appeal Br. 12. Appellant
concludes:
[i]n view of the teachings of the instant specification, [and] the
plain and ordinary meanings of “cognitive” and “deficit”, a
“cognitive deficit” refers to “an amount of conscious, i.e.
deliberate and intentional, intellectual activity, such as thinking,
reasoning, or remembering, that is less than what is expected.”
In view of the fact that a seizure is abnormal electrical activity
in the brain that one lacks conscious control over and is
therefore not a deliberate and intentional intellectual activity, a
seizure itself is not a cognitive deficit.
Appeal Br. 12–13.
Appellant also argues that the rejection “appears to be an anticipation-
by-inherency-rejection,” but “[n]ot all subjects who have seizures and
Noonan Syndrome have cognitive deficits.” Appeal Br. 10. Appellant notes
that the Specification states that “only ‘30% to 50% of subjects who have
Noonan Syndrome have cognitive deficits.’” Appeal Br. 14.
We agree with Appellant that the evidence cited by the Examiner does
not support a case of anticipation. Claim 1 is directed to a method of
treating a cognitive deficit in a subject having Noonan syndrome. The
Specification explains that “the methods disclosed herein comprise

7 Memory, Epilepsy Action Australia, www.epilepsy.org.au/about-
epilepsy/living-with-epilepsy/lifestyle-issues/memory/, downloaded Dec. 20,
2017.
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administration of a HMG CoA reductase inhibitor to improve, enhance, or
restore the cognitive function of subjects suffering from a cognitive deficit.”
Spec. ¶ 40.
The Specification defines “cognitive function” to mean “the
performance of some cognitive activity, such as memory, perception,
learning, and reasoning.” Spec. ¶ 40. The Specification further notes, “[i]n
the case of cognitive disorders, administration of the compounds and
compositions to a patient suffering from the cognitive deficit provides a
therapeutic benefit where there is improvement, enhancement, or restoration
in the cognitive function.” Spec. ¶ 64. Thus, according to the instant
specification “cognitive deficit” is defined in terms of “cognitive function”;
i.e., “performance of some cognitive activity, such as memory, perception,
learning, and reasoning.” Spec. ¶ 40.
Bear explains that “[s]eizure disorders can be associated with
abnormal electrical activity in the brain resulting in temporary loss of
consciousness, body convulsions, unusual movements and staring spells, all
of which affect daily activities and the health of the affected individual.”
Bear 1:12–15. Bear teaches administering an HMG CoA reductase inhibitor
to a subject having a seizure disorder. Bear 2:4–6. Bear also teaches that its
methods “normaliz[e] synaptic signaling in the central nervous system to
thereby treat an underlying cause of the seizure disorder.” Bear 2:7–9.
The evidence therefore does not support the Examiner’s finding that
Bear teaches treating a cognitive deficit; i.e., a deficit in cognitive function.
Rather, Bear teaches treating a seizure disorder by normalizing synaptic
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function in the central nervous system. Bear does not describe its method as
having any effect on cognitive function.
The evidence does not support the Examiner’s suggestion that
seizures are equivalent to a cognitive deficit. The Examiner’s position that
“a cognitive deficit is a cognitive disorder,” Ans. 12, is not supported by the
language of the specification, as “cognitive deficit” is defined by the
specification in terms of “cognitive function,” not “cognitive disorder.”
While “cognitive deficits” are associated with various “cognitive disorders,”
including Noonan syndrome, they are not equivalent to “cognitive
disorders.” Rather, “cognitive deficits” are merely one symptom of an
underlying “cognitive disorder.”
By identifying seizures as a cognitive deficit, the Examiner appears to
rely upon the doctrine of inherency; i.e., that treating a seizure episode will
necessarily result in treating a cognitive deficit. The Examiner relies upon
the Epilepsy Action Australia reference to establish inherency.
The Epilepsy Action Australia reference, however, does not state that
each seizure episode will necessarily result in a cognitive deficit; for
example, a memory problem. The reference states that when seizures
happen in sleep, “[t]his can impact on learning ability, memory and
concentration the following day. Regular seizures during sleep can have a
significant impact on daytime functioning and memory.” Epilepsy Action
Australia 1. The reference also states, “[i]t is usually difficult to recall
information straight after a seizure.” Epilepsy Action Australia 2.
While these statements establish that seizures can affect cognitive
function,
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“[i]nherency . . . may not be established by probabilities or
possibilities. The mere fact that a certain thing may result from
a given set of circumstances is not sufficient [Citations
omitted.] If, however, the disclosure is sufficient to show that
the natural result flowing from the operation as taught would
result in the performance of the questioned function, it seems to
be well settled that the disclosure should be regarded as
sufficient.”
In re Oelrich, 666 F.2d 578, 581 (CCPA 1981) (quoting Hansgirg v.
Kemmer, 102 F.2d 212, 214 (CCPA 1939)) (bracketed material in original).
The evidence therefore does not support the Examiner’s finding that
seizures are a cognitive deficit as defined in the Specification, or that
treating seizures in a patient with Noonan Syndrome necessarily also treats a
cognitive deficit in the same patient. We conclude that the rejection of
claims 1–7, 9, 13, 17, 18, and 20 under 35 U.S.C. § 102(a)(1) as being
anticipated by Bear is not supported by a preponderance of the evidence, and
we therefore reverse it.

Obviousness based on Bear
Claims 8, 10–12, and 19 stand rejected under 35 U.S.C. § 103 as
obvious based on Bear. Ans. 4. The Examiner found that Bear does not
teach that “the subject has a normal cholesterol level or the administration of
the statin to be before, after, or simultaneous with the administration of the
MEK inhibitor,” as recited in these claims. Ans. 4.
The Examiner found that, however, that “it is implicit if not prima
facie obvious that the patients would have a normal cholesterol level” and “it
would be prima facie obvious . . . to administer the second active either
before, during, or after the first active” since Bear teaches combination
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treatment and administration of actives before, concomitant, or after
administration of a Ras inhibitor. Ans. 5.
Appellant argues “[n]owhere has the Examiner asserted that, as an
alternative to claim 1 being anticipated by Bear, claim 1 is prima facie
obvious in view of Bear.” Appeal Br. 15.
We agree with Appellant that the evidence cited by the Examiner does
not support a case of obviousness. As explained above, Bear teaches
treating a seizure disorder by normalizing synaptic function in the central
nervous system. Bear does not describe its method as having any effect on
cognitive function.
Additionally, the evidence does not establish that a cognitive deficit
will necessarily happen after each seizure episode, or that treating seizures
will necessarily treat a cognitive deficit. The evidence therefore does not
support the Examiner’s finding that seizures are a cognitive deficit as
defined in the Specification, and the Examiner has not pointed to evidence in
Bear showing that it would have been obvious to apply its method to treat
cognitive deficits rather than seizures.
We conclude that the rejection of claims 8, 10–12, and 19 under 35
U.S.C. § 103(a) based on Bear is not supported by a preponderance of the
evidence, and we therefore reverse it.

Obviousness based on Silva and Nystrom
Claims 1–12 and 20 stand rejected under 35 U.S.C. § 103 as obvious
based on Silva in view of Nystrom. Ans. 5. The Examiner finds that, “Silva
teaches the treatment of learning deficits with HMG CoA reductase
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inhibitors (statins) like lovastatin. . . . The cognitive disorders treated with
the statins include conditions that have dysregulation of the Ras protein and
dysregulation of the MAPK (mitogen activated protein kinase) signaling
pathway.” Ans. 5.
The Examiner finds that “Silva also teaches that although the
identified genes affecting cognitive function have diverse activities, they are
related by their effect on the signaling pathways involved in memory
formation, synaptic development, and synaptic maturation.” Ans. 5–6.
The Examiner finds that “Nystrom et al. teaches that Noonan
syndrome and neurofibromatosis type-1 (NF-1) are both conditions with
dysregulation of the RAS-MAPK pathway.” Ans. 6. The Examiner
concludes that it would have been obvious to “treat patients with Noonan’s;
as Silva teaches that the statins can be used to treat cognitive disorders
associated with the RAS protein and dysregulation of MAPK such as NF-1
. . . and Nystrom teaches that Noonan’s is also a condition with
dysregulation of both RAS and MAPK which are the conditions taught by
Silva.” Ans. 6. The Examiner reasons that “the use of the statins for
learning deficits in Noonan’s is prima facie obvious with a reasonable
expectation of success being a cognitive disorder associated with the RAS
protein and dysregulation of MAPK which is the patient population taught
by Silva.” Ans. 6.
Appellant argues that “[n]owhere does Silva mention anything about
Noonan Syndrome” and “nowhere has does [sic] Silva point to the mutant
genes or genes in the Ras-MAPK Pathway that are common to both Noonan
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Syndrome and NF-1 which are responsible for cognitive deficits in both
Noonan Syndrome and NF-1 subjects.” Appeal Br. 19.
Appellant argues that,
although Noonan Syndrome, NF-1, and NFNS
[Neurofibromatosis-Noonan Syndrome, Appeal Br. 24] are
associated with abnormalities in the Ras-MAPK Pathways,
Noonan Syndrome is a disease that is genetically distinct from
both NF-1 and NFNS. Specifically, the genetic defects that
cause deregulation of RAS signaling in Noonan Syndrome are
different from the NF-1 mutation which causes the deregulation
of RAS signaling in NF-1 and NFNS.
Appeal Br. 26.
Appellant argues that, “a drug that is effective in treating one
cognitive disorder may not be effective in treating another cognitive disorder
even where both cognitive disorders involve abnormalities in the Ras-
MAPK Pathway.” Appeal Br. 26. Appellant concludes, “[s]imply because
Noonan Syndrome is associated with abnormalities in the Ras-MAPK
Pathway and statins are known to . . . show some efficacy in treating other
disorders that involve the Ras-MAPK Pathway does not necessarily mean or
suggest that cognitive deficits associated with Noonan Syndrome can be
effectively treated with a HMG CoA reductase inhibitor.” Appeal Br. 27.
We agree with Appellant that the evidence cited by the Examiner does
not support a prima facie case of obviousness. Silva is directed to “methods
of treating cognitive disorders by administering an effective amount of a
hydroxymethylglutaryl CoA (HMG CoA) reductase inhibitor.” Silva ¶ 9.
Silva explains that “[m]utations in genes encoding members of the
MAPK pathway, such as MEK, Ras-GRF, and H-Ras, may cause defects in
learning.” Silva ¶ 47, emphasis added. Silva explains that “[g]enetic and
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biochemical studies implicate components of the MAPK signaling pathway
in cognitive function.” Silva ¶ 57, emphasis added. Silva explains that a
“MAPK signaling pathway[]” . . . refers to a signaling pathway
that uses a cascade of three types of kinases. . . . These
canonical kinases include a MAP kinase kinase kinase
(MAPKKK), which activates a second kinase, the MAP kinase
kinase (MAPKK). . . . Activated MAPKKs modify MAP
kinases (MAPK). . . . In turn, the MAPKs regulate activity of
other protein kinases and numerous transcription factors to
effect the cellular responses triggered by activation of the
signaling cascade. Three distinct pathways form the
superfamily of MAPK pathways, each designated based on the
MAPK involved.
Silva ¶ 57. Each of the three pathways involves a different set of MAPK/
MAPKK/MAPKKK enzymes. See Silva ¶ 57.
Nystrom states that “Noonan syndrome (NS) and neurofibromatosis
type I (NF1) belong to a group of clinically related disorders that share a
common pathogenesis, dysregulation of the RAS-MAPK pathway.”
Nystrom abstract.
Thus, Silva teaches that cognitive deficits in patients with NF-1 can be
treated using HMG CoA reductase inhibitors, and Nystrom teaches that
NF-1 and Noonan’s syndrome involve dysregulation of the same one of the
three pathways in the superfamily of MAPK pathways. However, even
given that the same MAPK pathway is involved in both disorders, Silva
teaches that “the MAPKs regulate activity of other protein kinases and
numerous transcription factors to effect the cellular responses triggered by
activation of the signaling cascade.” Silva ¶ 57. Thus, even a single MAPK
pathway involves the proper function of numerous different proteins in order
to cause the normal cellular responses.
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The Examiner has not pointed to evidence showing that NF-1 and
Noonan’s syndrome were known to involve dysfunction of the same or
related proteins in the RAS-MAPK pathway, such that a treatment that was
effective to treat cognitive deficits in NF-1 patients would be reasonably
expected to have the same effect in Noonan’s syndrome patients, and
“‘obvious to try’ is not the standard under § 103.” In re O’Farrell, 853 F.2d
894, 903 (Fed. Cir. 1988).
An “obvious-to-try” situation exists when a general disclosure
may pique the scientist’s curiosity, such that further
investigation might be done as a result of the disclosure, but the
disclosure itself does not contain a sufficient teaching of how to
obtain the desired result, or that the claimed result would be
obtained if certain directions were pursued.

In re Eli Lilly & Co., 902 F.2d 943, 945 (Fed. Cir. 1990).
We conclude that the rejection of claims 1–12 and 20 under 35 U.S.C.
§ 103(a) based on Silva in view of Nystrom is not supported by a
preponderance of the evidence, and we therefore reverse it.

Obviousness based on Silva, Nystrom, Wu, and Smith
Claims 13 and 17–19 stand rejected under 35 U.S.C. § 103 as obvious
based on Silva in view of Nystrom, further in view of Wu and Smith. Ans.
6. The Examiner relies on Silva and Nystrom for the teachings discussed
above, and relied on Wu and Smith for the additional limitations of
dependent claims 13 and 17–19. Ans. 7.
Appellant argues that neither Wu nor Smith are directed to treating
cognitive deficits in subjects suffering from Noonan Syndrome. Appeal Br.
31.
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We agree with Appellant that the evidence cited by the Examiner does
not support a case of obviousness. As explained in the analysis above, Silva
and Nystrom do not support a prima facie case of obviousness with respect
to claim 1. The Examiner points to no teachings in Wu or Smith that make
up for the deficiencies of Silva and Nystrom.
We therefore reverse the rejection of claims 13 and 17–19 under 35
U.S.C. § 103(a) based on Silva in view of Nystrom further in view of Wu
and Smith.

Nonstatutory Double Patenting
Claims 1–12 and 20 stand rejected based on nonstatutory double
patenting based on claims 1–22 of U.S. Patent 8,222,293 and Nystrom. Ans.
8. Claims 13 and 17–19 stand rejected based on nonstatutory double
patenting based on claims 1–22 of the ’293 patent, Nystrom, Wu, and Smith.
Ans. 9–10.
The ’293 patent issued from the same application that was published
as the Silva reference discussed above with regard to the obviousness
rejections, and the Examiner relies on the same rationale in concluding that
the instant claims would have been obvious variants of the patented claims
to treating a cognitive deficit in a patient having neurofibromatosis type 1
(NF-1). Ans. 8–11. The rejections for nonstatutory double patenting,
therefore, suffer from the same defects as the rejections for obviousness, and
are reversed for the same reasons.

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Objection to Drawings
Appellant requests that we review the Examiner’s objection to the
drawings. Appellant states, “[t]he Examiner newly asserted in the Advisory
Action that the drawings ‘fail to clearly depict the detail essential for proper
understanding of the invention shown in the drawing and the claims.”
Appeal Br. 13. “Thus, the drawing issue appears to relate to the legal
requirement under 35 U.S.C. 113, which is appealable.” Id.
We disagree. The excerpt from the Advisory Action above omits the
end of the sentence. The full sentence states, “[t]he submitted replacement
drawings are not entered as they still fail to clearly depict the detail essential
for proper understanding of the invention shown in the drawing and the
claims are the same as the prior claims examined in the final rejection;
therein these amendments do not place the application in better form for
appeal or simplify the issues for appeal.” Advisory Action 2.
Thus, when taken in context, Examiner’s reference to the claims is
directed to the prior claims examined in the Final Action. The Examiner did
not indicate that the drawings are required to understand the claims.
Since Examiner’s objection to the drawing is not directed to claim
interpretation, the Examiner’s refusal to enter the proposed drawing is
unrelated to any rejection before the Board. See MPEP 1201:
The line of demarcation between appealable matters for the
Board and petitionable matters for the Director of the U.S.
Patent and Trademark Office (Director) should be carefully
observed. The Board will not ordinarily hear a question that
should be decided by the Director on petition, and the Director
will not ordinarily entertain a petition where the question
presented is a matter appealable to the Board. Ordinarily, an
objection is petitionable, and a rejection is appealable, but when
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the objection is “determinative of the rejection” the matter may
be addressed by the Board.

In the present case, the objection to the drawings is not related to the claim
rejections. The Examiner’s objections to the drawings and refusal to enter
an amendment are reviewable by petition under 37 C.F.R. § 1.181 and are
thus not within the jurisdiction of the Board.
DECISION SUMMARY
In summary:
Claims
Rejected
35 U.S.C. § Reference(s)/Basis Affirmed Reversed
1–7, 9, 13,
17, 18, 20
102(a)(1) Bear 1–7, 9, 13,
17, 18, 20
8, 10–12, 19 103 Bear 8, 10–12,
19
1–12, 20 103 Silva, Nystrom 1–12, 20
13, 17–19 103 Silva, Nystrom, Wu,
Smith
13, 17–19
1–12, 20 Nonstatutory double
patenting
1–12, 20
13, 17–19 Nonstatutory double
patenting
13, 17–19
Overall
Outcome
1, 4–13,
17–20

REVERSED