Deisseroth, Karl A. et al.

Patent Trials and Appeals Board

May 14, 2020

2019003058 (P.T.A.B. May. 14, 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.
14/385,331 09/15/2014 Karl A. Deisseroth STAN-940 1175
77974 7590 05/14/2020
STANFORD UNIVERSITY OFFICE OF TECHNOLOGY LICENSING
BOZICEVIC, FIELD & FRANCIS LLP
201 REDWOOD SHORES PARKWAY
SUITE 200
REDWOOD CITY, CA 94065
EXAMINER
HILL, KEVIN KAI
ART UNIT PAPER NUMBER
1633
NOTIFICATION DATE DELIVERY MODE
05/14/2020 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):
docket@bozpat.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
____________

BEFORE THE PATENT TRIAL AND APPEAL BOARD
____________

Ex parte KARL A. DEISSEROTH, KAY M. TYE,
and MELISSA R. WARDEN
____________

Appeal 2019-003058
Application 14/385,331
Technology Center 1600
____________

Before ULRIKE W. JENKS, RACHEL H. TOWNSEND, and
MICHAEL A. VALEK, Administrative Patent Judges.

VALEK, Administrative Patent Judge.

DECISION ON APPEAL
Appellant submits this appeal under 35 U.S.C. § 134(a) involving
claims to a method for identifying a candidate agent for treating depression
through the use of a rodent animal model.1 We have jurisdiction under
35 U.S.C. § 6(b).
We AFFIRM.
STATEMENT OF THE CASE
According to the Specification, “[c]urrent non-human animal models
of depression are non-specific” and therefore “[t]here is a need in the art for

1 We use the word “Appellant” to refer to “applicant” as defined in
37 C.F.R. § 1.42. Appellant identifies the Board of Trustees of the Leland
Stanford Junior University as the real party in interest. Appeal Br. 3.
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improved non-human animal models of depression.” Spec. ¶ 3. “The
present disclosure provides non-human optogenetic animal models of
depression.” Id. ¶ 4.
The Specification explains that these models “express[] a light-
responsive opsin (e.g., a light-responsive ion channel; a light-responsive ion
pump; etc.) in a neuron of the animal” that, when activated “by exposure of
the light-activated opsin to light[,] modulates the behavior of the animal.”
Id. ¶ 32. According to the Specification,
In some cases, the active optogenetic inhibitor of neuronal
activity (light-responsive opsin) is a halorhodopsin (e.g.,
NpHR) that promotes hyperpolarization of the DA neurons
when activated by light at or near the VTA. Hyperpolarization
of the DA neurons inhibits activity of these neurons. The non-
human animal model exhibits characteristics of depression
when the light-responsive opsin is activated by light. A test
agent is administered to the non-human animal model. When
DA neurons of the VTA are exposed to light of a wavelength
(e.g., amber light) that activates that light-responsive opsin, a
test agent that is a candidate agent for treating depression will
ameliorate at least one symptom of depression in the non-
human animal model.
Id. ¶ 133.
Claims 1–6 and 28–30 are on appeal and can be found in the Claims
Appendix of the Appeal Brief. Claim 1 is representative of the claims on
appeal. It reads as follows:
1. A method for identifying a candidate agent for treating
depression in an individual, comprising:
activating, with a light source, a hyperpolarizing light-
responsive opsin polypeptide expressed in ventral tegmental area
(VTA) dopaminergic neurons in a rodent, wherein the light-
responsive opsin polypeptide hyperpolarizes the VTA
dopaminergic neurons in response to light of an activating
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wavelength from the light source, thereby inhibiting the
dopaminergic neurons and inducing depression in the rodent;
contacting the rodent with a test agent, and
determining the effect of the test agent on a behavior of
the rodent in a depression assay, wherein reduction in a
depressive behavior of the rodent contacted with the test agent,
compared to the behavior of a control rodent that has not been
contacted with the test agent, indicates that the test agent is a
candidate agent for treating depression.
Appeal Br. App. i.
Appellant seeks review of the following rejections:
I. Claims 1–6, 28, and 29 under 35 U.S.C. § 103 as obvious
over Castagné,2 Deisseroth,3 Chuong,4 Zhang,5 Zhao,6
Tsai,7 Friedman,8 Knöpfel,9 and Stuber;10 and

2 Vincent Castagné et al., Rodent Models of Depression: Forced Swim and
Tail Suspension Behavioral Despair Tests in Rats and Mice, Current
Protocols in Pharmacology 5.8.1–5.8.14 (2010) (“Castagné”).
3 US 2009/0099038 A1, published April 16, 2009 (“Deisseroth”).
4 US 2012/0121542 A1, published May 17, 2012 (“Chuong”).
5 US 2010/0190229 A1, published July 29, 2010 (“Zhang”).
6 Shengli Zhao et al., Improved Expression of Halorhodopsin for Light-
Induced Silencing of Neuronal Activity, 36 Brain Cell Biology 141–154
(2008) (“Zhao”).
7 Hsing-Chen Tsai et al., Phasic Firing in Dopaminergic Neurons Is
Sufficient for Behavioral Conditioning, 324 Science 1080–1084 (2009)
(“Tsai”).
8 Alexander Friedman et al., Programmed Acute Electrical Stimulation of
Ventral Tegmental Area Alleviates Depressive-Like Behavior, 34
Neuropsychopharmacology 1057–1066 (2009) (“Friedman”).
9 Thomas Knöpfel et al., Remote Control of Cells, 5 Nature Nanotechnology
560–561 (2010) (“Knöpfel”).
10 Garret D. Stuber, Dissecting the Neural Circuitry of Addiction and
Psychiatric Disease With Optogenetics, 35 Neuropsychopharmacology 341–
342 (2009) (“Stuber”).
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II. Claims 29 and 30 under 35 U.S.C. § 103 as obvious over
Castagné, Deisseroth, Chuong, Zhang, Zhao, Tsai,
Friedman, Knöpfel, Stuber, Gradinaru 2008,11 and
Gradinaru 2010.12
Appeal Br. 4; Reply Br. 2, 15.13
Appellant does not argue any claim separately from independent
claim 1, nor does Appellant present arguments for the rejection of claims 29
and 30 that beyond the arguments it presents for the first obviousness
rejection. Accordingly, we analyze the rejections together, focusing on
claim 1, which is representative for all of Appellant’s arguments. The issue
is whether the preponderance of the evidence supports Examiner’s finding
that claim 1 is obvious over the cited prior art.
Findings of Fact
FF1. Castagné teaches protocols for behavioral despair assays (i.e., forced
swim and tail suspension tests) in rats and mice for screening potential
antidepressant compounds. Castagné, Abstr. In these assays, the animal is
contacted with a test compound and monitored for changes to “the duration
of immobility when rodents are exposed to an inescapable situation.” Id.
According to Castagné, the “[t]esting of new substances in the behavioral

11 Viviana Gradinaru et al., eNpHR: a Natronomonas Halorhodopsin
Enhanced for Optogenetic Applications, 36 Brain Cell Biol. 129–139 (2008)
(“Gradinaru 2008”).
12 Viviana Gradinaru et al., Molecular and Cellular Approaches for
Diversifying and Extending Optogenetics, 141 Cell 154–165 (2010)
(“Gradinaru 2010”).
13 In the Appeal Brief (at 2), claim 30 is incorrectly identified as included in
Examiner’s first rejection. Appellant correctly identifies Examiner’s
rejections in the Reply Brief. See Reply Br. 2, 15.
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despair and tail suspension tests allows a simple assessment of their potential
antidepressant activity by the measurement of their effect on immobility.”
Id.
FF2. Castagné teaches that the behavioral despair tests it teaches for mice
can “be employed for studies using transgenic animals.” Castagné, 5.8.4–5.
FF3. Stuber teaches that “[w]ith the recent advances in the emerging field
of optogenetics, it is now possible to selectively introduce light-gated ion
channels and pumps into genetically defined populations of neurons to
selectively stimulate or inhibit neuronal circuit elements with light.” Stuber,
341–42. Stuber explains that neurons can be transformed to express
“[c]hannelrhodopsin-2 (ChR2)” for optical excitation and “light-sensitive
chloride pump Halorhodopsin (NpHR)” for “optical inhibition of neural
activity.” Id. at 342. According to Stuber, “[t]ransient inhibition of circuit
components” by introduction of NpHR to select neurons “could potentially
be even more valuable” than introducing ChR2 “for assaying the neural basis
of behavior.” Id. at 342.
FF4. Deisseroth teaches systems for screening drug candidates involving
cell lines “having light responsive membrane ion switches,” such as
“halorhodopsin (NpHR) in which amber light affects chloride (Cl-) ion flow
so as to hyperpolarize neuronal membrane and make it resistant to firing.”
Deisseroth, Abstr., ¶ 20. According to Deisseroth, the “system screens for
ion-channel and ion-pump affecting compounds” by introducing “one or
more drug candidates . . . to cells that were made optically responsive by the
addition of the above mentioned proteins (ChR2 and NpHR).” Id. ¶ 21.
FF5. Chuong teaches that light-activated ion pumps (LAIPs), including
NpHR, can be expressed in “cells, tissues, and organisms.” Chuong ¶¶ 6, 68,
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106. Chuong teaches that such LAIPs can be used to “identify a candidate
therapeutic agent or compound” by
expressing a LAIP in [a] subject, contacting the subject with a
light under suitable conditions to activate the LAIP and
hyperpolarize the cell, and administering to the subject a
candidate compound. The subject is then monitored to
determine whether any change occurs that differs from a control
effect in a subject. Thus, for example, a brain region may be
silenced using a LAIP of the invention and a candidate
compound may be administered to the brain and the effect of
the compound determined by comparing the results with those
of a control.
Id. ¶¶ 114–15.
FF6. Zhang teaches the expression of NpHR in target cells of whole
animals, including C. elegans and mice, for “temporally-precise optical
inhibition of neural activity.” Zhang ¶¶ 49, 58. The transformed cells in
such animals are optically stimulated for “downregulation (e.g., neuronal
hyperpolarization or alternatively chronic depolarization) of activity at the
target.” Id. ¶ 9. For example, Zhang describes experiments involving
“expression of NpHR-ECFP fusion protein in the body wall muscles of the
nematode Caenorhabditis elegans using the muscle-specific myosin
promoter (Pmyo-3).” Id. ¶¶ 142–44. According to Zhang, “photoactivation
of NpHR immediately (within ± 150 ms) and essentially completely arrested
swimming behavior” of the transformed animals. Id. at 142.
FF7. Zhang teaches that “[b]oth NpHR and ChR2 can be functionally
expressed and operate at high speed in the mammalian brain.” Zhang ¶ 146.
Zhang further teaches that expression of these proteins “may be genetically
targeted to specific classes of neurons” by using promotors associated with
those neurons. Id. ¶ 147.
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FF8. Zhang teaches that “applications” of this technology “include those
associated with any population of electrically-excitable cells, including
neurons” and that “depression” is one of several diseases associated “with
altered excitation-effector coupling.” Zhang ¶ 11.
FF9. Zhao describes experiments involving “transgenic mice that express
halorhodopsin (NpHR), a light-driven chloride pump that can be used to
silence neuronal activity via light.” Zhao, Abstr. These mice were
successfully transformed to express high levels of NpHr-YFP in cortical
pyramidal neurons. Id. Zhao teaches that
illumination of NpHR-positive neurons in acute brain slices led
to hyperpolarization of neurons and produced rapid, reversible
inhibition of neuronal firing. Thus, in principle NpHR in
transgenic mice silences neurons in a light-inducible manner,
raising the potential for its targeting to genetically distinct
subpopulations of neurons in order to determine how neuronal
activity in each neuron subtype shapes circuitry function and
behavior.
Id.at 151.
FF10. Zhao reports that “NpHR-YFP expression led to the formation of
numerous intracellular blebs, which may disrupt neuronal function.” Zhao,
Abstr. Zhao teaches that this problem can be overcome “[b]y improving the
signal peptide sequence and adding an ER export signal to NpHR-YFP” to
“eliminate[] the formation of blebs and dramatically increase[] the membrane
expression of NpHR-YFP.” Id. Zhao further teaches that mice expressing
this “improved eNpHR in neurons will likely be a valuable tool for probing
circuitry function.” Id.at 151.
FF11. Tsai describes experiments in which mice were transformed to
express “the light-activated cation channel channelrhodopsin-2 (ChR2)” in
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dopaminergic neurons (DA) of the ventral tegmental area (VTA). Tsai, 1081.
The mice were then tested in “the conditioned place preference (CPP)
paradigm . . . with use of phasic optogenetic stimulation [] of DA neurons as
[the] conditioning stimuli.” Id. Tsai teaches that “phasic stimulation [of
VTA domaminergic neurons transformed to express ChR2] sufficed to
establish place preference in the absence of other reward.” Id. at 1083–84.
According to Tsai, this type of “optogenetic approach . . . opens the door to
exploring the causal, temporally precise, and behaviorally relevant
interactions of DA neurons with other neuromodulatory circuits.” Id. at
1084.
FF12. Friedman describes experiments involving acute electrical stimulation
(AES) of DA neurons in the VTA of “Flinder Sensitive Line (FSL) rats, a
genetic animal model of depression.” See Friedman, 1057–58. Friedman
teaches that stimulation of VTA dopaminergic neurons in FSL rats decreased
immobility and “has an antidepressant, and not stimulant, function.” Id. at
1062. In contrast, “[s]timulation of FSL rat brain in the deep mesencephalic
nucleus (a nonspecific region which is not involved in motivation and
emotion) resulted in no effect on depressive behavior.” Id. at 1063.
FF13. Friedman discusses prior work by the same authors demonstrating that
the “dopaminergic system is important in the depressive symptoms of FSL
rats.” Id. at 1063 (citing Freedman 200814). For example, Freedman 2008
explains that the DA system plays a “key role . . . in depressive behavior” and
that a “lower amount of long bursts in VTA neuronal activity may induce

14 Alexander Friedman et al., VTA Dopamine Neuron Bursting is Altered in
an Animal Model of Depression and Corrected by Desipramine, 34 J. Mol.
Neurosci. 201–209 (2008) (“Friedman 2008”).
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depressive states, as release of dopamine, which is important for reward and a
feeling of well-being, requires many long bursts.” Freedman 2008, 208.
FF14. Winter15 describes a study “test[ing] the differential implication of
dopaminergic systems in depressive-like behavior in rats.” Winter, Abstr. In
this study, the animals were chemically lesioned to degenerate DA neurons in
the substantia nigra pars compacta (SNc) and the VTA and then monitored in
various depression assays. Id. at 134. Winter teaches that “dopaminergic
lesions of either the SNc or the VTA contribute to the manifestation of
depressive-like behavior in rats” (id., Abstr.) and that degenerating DA
neurons in these areas “induces depressive behavior in rats” (id. at 139).
Analysis
Examiner finds that Castagné teaches “a method for identifying a
candidate agent for treating depression” comprising “contacting a rodent
with a test agent” and “determining the effect of the test agent on a behavior
of the rodent in a depression assay.” Ans. 4. Examiner acknowledges that
Castagné does “not teach the rodent expresses an active optogenetic
inhibitor of neuronal activity in [the] ventral tegmental area (VTA)
dopaminergic neurons.” Id. at 5.
Regarding the optogenetic limitations of claim 1, Examiner finds that
Deisseroth, Chuong, and Zhang teach optogenetic systems, comprising cells
modified to express NpHR, i.e., a “hyperpolarizing light-responsive opsin
polypeptide,” to screen candidate agents both in culture and, with respect to

15 Christine Winter et al., Lesions of Dopaminergic Neurons in the
Substantia Nigra Pars Compacta and in the Ventral Tegmental Area
Enhance Depressive-Like Behavior in Rats, 184 Behavioral Brain Research
133–141 (2007).
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Zhang, a “transgenic non-human animal.” Id. at 5–6. In addition, Examiner
determines that both Zhao and Tsai “evidence that the ordinary artisan was
enabled to express optogenetic molecules, either ChR2 or NpHR, in rodent
animals, including the VTA dopaminergic neurons, whereby ChR2
optogenetics is demonstrated to change the rodent’s behavior.” Id. at 6.
According to Examiner, it would have been obvious to modify the
depression assays taught in Castagné to employ “a genetically modified
rodent expressing a NpHR hyperpolarizing light-responsive opsin
polypeptide in a method for identifying a candidate agent for treating
depression” because:
a) the scientific and technical concepts of screening
candidate compounds that modulate the activity of a
hyperpolarizing light-responsive opsin polypeptide, wherein
said hyperpolarizing light-responsive opsin polypeptide is
NpHR, were known to the ordinary artisan (Deisseroth et al,
Chuong et al, Zhang et al);
b) the scientific and technical concepts of creating
transgenic rodents whose genome comprises a hyperpolarizing
light-responsive opsin polypeptide . . . were known to the
ordinary artisan (Zhao et al, Zhang et al);
c) the scientific and technical concepts that altering the
activity of a hyperpolarizing light-responsive opsin polypeptide,
to wit, a NpHR, in an animal will change the behavior of said
animal were known and successfully reduced to practice by the
ordinary artisan (Zhang et al);
d) the involvement of the VTA in the process of
depression and that the optogenetic system of Tsai et al
provides precise in vivo stimulus, e.g., optogenetic stimulation
and/or optogenetic stabilization, of the DA neurons in the VTA,
thereby allowing the artisan to analyze the VTA DA neurons
precisely when assaying candidate drugs for the treatment of
depression [was known] (Tsai et al);
e) Stuber taught that transient inhibition of circuit
components (via NpHR-mediated optogenetics) could be
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potentially even more valuable (than ChR2-mediated
activation) for assaying the neural basis of behavior; and
f) Friedman et al taught that the ordinary artisan
previously recognized the scientific and technical concepts of
monitoring depressive-like behavior in animal models when
modulating neural activity in the VTA.
Ans. 22.
We agree with and adopt Examiner’s findings of fact and reasoning
regarding the scope and content of the prior art (Ans. 4–22; Final Act. 4–7;
FF1–14) and determine that Examiner’s rejection of claims 1–6 and 28–30 is
supported by the preponderance of the evidence. We address Appellant’s
arguments below.
Appellant’s arguments that the “cited art fails to disclose or suggest
all claim elements” because each of the cited references taken individually is
distinct from claim 1 is not persuasive. See Appeal Br. 7–10 (emphasis
omitted). As explained above, Examiner’s rejection is based on the
combination of those references. That combination, as articulated by
Examiner, teaches or reasonably suggests all of the limitations of claim 1.
See FF1–14. Appellant cannot overcome Examiner’s rejection “by attacking
[the cited references] individually” because “the rejection is based upon the
teachings of a combination of references.” See Soft Gel Techs., Inc. v.
Jarrow Formulas, Inc., 864 F.3d 1334, 1341 (Fed. Cir. 2017) (quoting In re
Merck & Co., 800 F.2d 1091, 1097 (Fed. Cir. 1986)).
We are unpersuaded by Appellant’s argument that a skilled artisan
would not be motivated to modify Castagné to incorporate a genetically
modified rodent expressing NpHR. See Appeal Br. 10–12. Castagné
teaches that transgenic animals can be used in its mice depression assays.
FF2. Zhao teaches that transgenic mice expressing NpHR in neurons are a
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valuable tool for research. FF9–10. Thus, the record supports Examiner’s
determination that a skilled artisan would be motivated to use Zhao’s
transgenic mouse in Castagné’s depression assay.
Appellant argues that “[s]ince Zhao disclosed that NpHR was
overexpressed in cortical pyramidal neurons and lead to intracellular blebs,
Zhao teaches away from use of such mice for further experiments.” Appeal.
Br. 11. We disagree. Zhao teaches that these issues are successfully
overcome by “improving the signal peptide sequence and adding an ER
export signal to NpHR-YFP.” FF10. Moreover, Zhao affirmatively states
that future transgenic mice expressing this improved eNpHR will be
valuable research. Id. Thus, it certainly does not teach away from their use
in the articulated combination of references. See Galderma Labs., L.P. v.
Tolmar, Inc., 737 F.3d 731, 738 (Fed. Cir. 2013) (quoting DePuy Spine, Inc.
v. Medtronic Sofamor Danek, Inc., 567 F.3d 1314, 1327 (Fed. Cir. 2009))
(explaining that a reference does not teach away if it “does not criticize,
discredit, or otherwise discourage investigation into the invention claimed”).
Appellant’s argument that the cited art provides no reason to include
NpHR in dopaminergic neurons of the VTA is also unpersuasive. See
Appeal Br. 11–12; Reply Br. 12–14. Friedman teaches that
electrostimulation of VTA DA neurons provides an antidepressant effect in
FSL rats. FF12. We agree with Examiner that it would “be a logical
conclusion [from the teaching in Friedman] that enhancing inhibition of
neuronal activity, in other words blocking stimulation (hyperpolarization as
achieved via NpHR), would promote depression-like behavior.” Ans. 25.
This finding is additionally supported by Friedman 2008 and Winter, which
Examiner cites in the Answer. Ans. 27; FF13–14.
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We are not persuaded by Appellant’s argument that “one of ordinary
skill in the art would not necessarily have chosen this minority population of
neurons” because Cao16 reports “contradictory findings” concerning the role
of VTA DA neurons in mediating depression-like symptoms in rats. Reply
Br. 11–12. Cao states that the role of VTA DA neurons is “controversial”
because some studies had shown that decreased activity of such neurons
“contribute[s] to the pathogenesis of depression,” while others have “found
increased activity of VTA DA neurons in stress-induced depression
models.” Cao, 6. But even if there was some controversy in the art
regarding to the precise role of VTA DA neurons in depression,
“[o]bviousness does not require absolute predictability of success.” In re
O’Farrell, 853 F.2d 894, 903 (Fed. Cir. 1988). Here, the record includes
multiple references each of which independently suggests that inhibiting the
activity of VTA DA neurons would induce depression-like symptoms in
rodents. See FF12–14. Thus, we agree that Examiner’s rejection is
supported by a preponderance of the evidence.
Finally, we are not persuaded by Appellant’s unexpected results
argument. Appellant urges that selective inhibition of VTA DA neurons by
activating a hyperpolarizing-light responsive opsin in those neurons revealed
a “depression-like phenotype” that was “unexpected” over the prior art.
Appeal Br. 12 (citing Tye17). However, as explained above, Examiner has

16 Jun-Li Cao et al., Mesolimbic Dopamine Neurons in the Brain Reward
Circuit Mediate Susceptibility to Social Defeat and Antidepressant Action,
30 J. Neurosci. 16453–16458 (2010) (“Cao”).
17 Kay M. Tye et al., Dopamine Neurons Modulate Neural Encoding and
Expression of Depression-related Behavior, 493 Nature 537–541 (2013)
(“Tye”).
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identified multiple references evidencing that a skilled artisan would have
expected the inhibition of VTA DA neurons to induce depression-like
symptoms in rodents. FF12–14.
Tye does not provide sufficient evidence of unexpected results.
Indeed, Tye confirms that DA neurons had previously “been hypothesized to
be relevant” to depression. Tye, 537 (citing prior art). While it may have
“not been possible to test this hypothesis directly . . . [using] existing
therapeutic interventions [that were] unable to specifically target dopamine
neurons” (id.), the record demonstrates that the optogenetic techniques
recited in claim 1, and discussed in Tye, were known in the art (FF2–10) and
known to be useful for targeting specific subpopulations of neurons in
rodents (FF6–7, FF9, FF11). Thus, the record supports Examiner’s
determination that Appellant’s “depression-like phenotype” is merely the
expected result of applying known techniques to inhibit the activity of
neurons known to be associated with depression-like symptoms in rodents.
See Ans. 27. Such “[e]xpected beneficial results are evidence of
obviousness” that do not overcome Examiner’s prima facie showing. See In
re Gershon, 372 F.2d 535, 537 (CCPA 1967) (“Expected beneficial results
are evidence of obviousness of a claimed invention, just as unexpected
beneficial results are evidence of unobviousness thereof.”).
For these reasons, we determine the preponderance of the evidence
supports Examiner’s rejections. Accordingly, we affirm the rejections of
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claims 1–6 and 28–3018 under 35 U.S.C. § 103 as obvious over the cited
prior art.
DECISION SUMMARY
In summary:
Claims
Rejected
35 U.S.C. § Reference(s)/Basis Affirmed Reversed
1–6, 28, 29 103 Castagné,
Deisseroth,
Chuong, Zhang,
Zhao, Tsai,
Friedman,
Knöpfel, Stuber
1–6, 28, 29
29, 30 103 Castagné,
Deisseroth,
Chuong, Zhang,
Zhao, Tsai,
Friedman,
Knöpfel, Stuber,
Gradinaru 2008,
Gradinaru 2010
29, 30
Overall
Outcome
1–6, 28–30

No time period for taking any subsequent action in connection with
this appeal may be extended under 37 C.F.R. § 1.136(a). See 37 C.F.R.
§ 1.136(a)(1)(iv).
AFFIRMED

18 Appellant relies on the same arguments for the second obviousness
rejection of claims 29 and 30. See Reply Br. 15–17. We, therefore, affirm
the second obviousness rejection for the same reasons as the first.