Ex Parte Dreyer

Board of Patent Appeals and Interferences

Sep 14, 2010

10885422 (B.P.A.I. Sep. 14, 2010)

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.
10/885,422 07/06/2004 Evan B. Dreyer 17322CON3(AP) 7765
51957 7590 09/14/2010
ALLERGAN, INC.
2525 DUPONT DRIVE, T2-7H
IRVINE, CA 92612-1599
EXAMINER
FAY, ZOHREH A
ART UNIT PAPER NUMBER
1627
MAIL DATE DELIVERY MODE
09/14/2010 PAPER
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.
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
__________

BEFORE THE BOARD OF PATENT APPEALS
AND INTERFERENCES
__________

Ex parte EVAN B. DREYER
__________

Appeal 2010-003780
Application 10/885,422
Technology Center 1600
__________

Before CAROL A. SPIEGEL, FRANCISCO C. PRATS, and
JEFFREY N. FREDMAN, Administrative Patent Judges.

PRATS, Administrative Patent Judge.

DECISION ON APPEAL1
This appeal under 35 U.S.C. § 134 involves claims to methods of
treating conditions involving the retinal pigment epithelium. The Examiner
rejected the claims for obviousness and for lack of enablement.
We have jurisdiction under 35 U.S.C. § 6(b). We reverse.

1 The two-month time period for filing an appeal or commencing a civil
action, as recited in 37 C.F.R. § 1.304, or for filing a request for rehearing,
as recited in 37 C.F.R. § 41.52, begins to run from the “MAIL DATE”
(paper delivery mode) or the “NOTIFICATION DATE” (electronic delivery
mode) shown on the PTOL-90A cover letter attached to this decision.
Appeal 2010-003780
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STATEMENT OF THE CASE
Claims 16-33 stand rejected and appealed (App. Br. 5).2 Claims 16
and 26, the independent claims, are representative and read as follows:
16. A method for treating an ophthalmic condition involving
the retinal pigment epithelium of an eye of an individual,
comprising:
administering an amount of an excitatory amino acid
receptor antagonist to the individual [], the amount being
effective in reducing glutamate-induced effects on the retinal
pigment epithelium of the eye of the individual.

26. A method of treating a retinal pigment epithelium
condition of an eye of an individual, comprising:
administering a therapeutically effective amount of a
glutamate receptor antagonist to the individual.

The Examiner cites the following document as evidence of
unpatentability:
Nobutaka Uchida et al., Glutamate stimulates proliferation of retinal
pigment epithelium and its bFGF expression through NMDA receptor
activation, Department of Pharmacology, Showa University School of
Medicine, Tokyo 142, Japan, Vol. 71, No. Suppl. 1, page 274P
XP008040806 (March 20, 1996) (as cited by Appellant on PTO-1449 Form
entered August 1, 2006) (abstract only).

The following rejections are before us for review:
(1) Claims 16-33, rejected under 35 U.S.C. § 112, first paragraph, as
lacking enablement for the full scope of the subject matter claimed (Ans. 3-
6);3 and

2 Appeal Brief filed July 19, 2007.
3 Examiner’s Answer mailed October 28, 2009.
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(2) Claims 16-33, under 35 U.S.C. § 103(a) as obvious over Uchida
“in view of Applicant’s Admission” (Ans. 6).
ENABLEMENT
ISSUE
The Examiner rejected claims 16-33 under 35 U.S.C. § 112, first
paragraph, because “the specification, while being enabling for treatment of
certain ophthalmic conditions using certain glutamate antagonists, does not
reasonably provide enablement for the treatment of ophthalmic conditions
generally involving the retinal pigment epithelium of the eye using all
glutamate antagonists” (Ans. 3 (bolding removed)).
Applying the oft-cited factors set forth in In re Wands, 858 F.2d 731,
737 (Fed. Cir. 1988), the Examiner found that the “prior art does not
recognize that all compounds having glutamate antagonist activity have the
same pharmacological activity” (Ans. 4). Rather, the Examiner contends,
“[a]ccording to Lance, Basic & Clinical pharmacology, Ninth Edition, the
glutamate receptors are divided to many subtypes. Therefore, to use a
glutamate antagonist and expect to be effective on all receptor subtypes is
not recognized by the state of the art” (id.).4
For example, the Examiner argues, the selective interaction of
“compounds with the polyamine site of NMDA receptor subunit is believed
to be responsible for at least in part for both the neuroprotective activity and
relatively favorable side effects profiles of this class of compounds when

4 The Lance reference does not appear to be of record in this application.
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compared to NMDA antagonists that act at other sites on the NMDA
receptor” (id. (citing Collier,5 col. 2, ll. 22-28)).
The Examiner further contends that, because the Specification does
not provide a representative number of examples of glutamate antagonists
capable of treating the full scope of disorders encompassed by the claims,
adequate guidance has not been provided for practicing the full scope of the
claims (id. at 5-6 (citing In re Dreshfield, 110 F. 2d 235 (CCPA 1940)).
Thus, the Examiner concludes:
Since compound structure and activity for such
pharmaceutical use must be determined from case to case by
painstaking experimental study, one of ordinary skill in the art
would be burdened with undue experimentation to determine all
glutamate antagonist[s] being capable of treating all ophthalmic
conditions involving the retinal pigment epithelium eye disease.

(Id. at 6.)
Appellant contends that it is common knowledge in this art that
“dysfunction of the RPE [retinal pigment epithelium] (including, without
limitation, migration from the retinal layer between the choroid and the
photoreceptor cells) can have mechanical and biochemical effects on the
neural cells of the retina” (App. Br. 10). For example, Appellant points out,
“retinal detachment usually occurs between the RPE and photoreceptor
layers of the retina, and can be caused or aggravated by migration of the
RPE or RPE cell death. Such detachment and migration is very often
associated with macular degeneration” (id.).
Appellant contends that the Specification describes Appellant’s
“discovery that pathological conditions involving, for example, RPE

5 U.S. Patent No. 6,509,355 B1 (issued January 21, 2003).
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migration are caused by glutamate” (id. at 9 (citing Spec. 1:25-26)), and that
“ophthalmic conditions involving the RPE [can be treated] by administering
an amount of an excitatory amino acid receptor antagonist. Preferably the
glutamate antagonist is one that crosses the blood-retina barrier and can be
administered chronically” (id. at 10 (citing Spec. 5:20-24)).
Appellant further contends that the Examiner has not provided any
reasoned justification for doubting the assertions made in the Specification
(id. at 11). Moreover, Appellant argues, the Examiner’s Wands analysis is
flawed because it improperly uses non-prior art as evidence of the state of
the art, and improperly applies a per se rule that the pharmaceutical arts are
unpredictable (id. at 12, 13).
Further, Appellant contends, the Examiner ignores the fact that claims
16 and 26, by their terms, encompass the use of only those receptor
antagonists that reduce glutamate-induced effects in the RPE (id.). In this
regard, Appellant argues, the fact that the claims might encompass
inoperative embodiments does not, in and of itself, demonstrate a lack of
enablement (id. at 14 (citing Atlas Powder Co. v. E.I. DuPont de Nemours &
Co., 750 F2d. 1569 (Fed. Cir. 1984)).
Appellant further points out that the claimed receptor antagonists were
known in the art (id. at 16), that the Specification provides an exemplary list
of agents suitable in the claimed methods, and that methods of testing for the
claimed receptor antagonist activity were known in the art (id. at 18-19).
Thus, Appellant concludes “the invention of claims 16-33 are respectfully
submitted to be in compliance with the enablement requirement of 35 U.S.C.
§112(1)” (id. at 20).
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In view of the positions advanced by Appellant and the Examiner, the
issue with respect to this rejection is whether the evidence of record supports
the Examiner’s position that the Specification fails to provide an adequate
disclosure that enables the full scope of the claimed invention.

FINDINGS OF FACT (“FF”)
1. The Specification states:
This application relates to preventing, controlling
reducing and/or treating proliferative vitreoretinopathy.
Proliferative vitreoretinopathy (including epiretinal membrane
formation) is a potentially devastating ophthalmic condition
that can lead to blindness. It can develop after any penetration
of the eye -- surgical or traumatic. Predisposing conditions
therefore include, but are not limited to, penetrating trauma,
retinal tears, traction detachments, vitrectomy, and intraocular
surgery. Any ophthalmic condition that precipitates or permits
migration of retinal pigment is epithelium or glial cells can lead
to the development of proliferative vitreoretinopathy. See
Machamer (1978) British J. Ophthal. 62:737; Hilton et al.
(1983) Ophthalmology 90:121.

(Spec. 1.)
2. The Specification further states:
I have discovered that glutamate causes migration and
proliferation of retinal pigment epithelium and/or glial cells.
The invention features the use of glutamate antagonists to
reduce or control retinal pigment epithelium and/or glial
migration and the subsequent development of proliferative
vitreoretinopathy. Avoidance or management of proliferative
vitreoretinopathy can be achieved by administering to the
patient a compound capable of reducing glutamate-induced
retinal pigment epithelium and/or glial migration in a
concentration effective to reduce such migration.

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(Id.)
3. Regarding therapeutic compounds, the Specification discloses:
Particularly preferred compounds are antagonists of the
NMDA [N-methyl-D-aspartate] receptor-channel complex. The
term “NMDA receptor antagonists” includes several sub-types
of NMDA antagonists including: a) channel blockers -- i.e.,
antagonists that operate uncompetitively to block the NMDA
receptor channel; b) receptor antagonists -- antagonists that
compete with NMDA to act at the NMDA binding site; c)
agents acting at either the glycine co-agonist site or any of
several modulation sites such as the zinc site, the magnesium
site, the redox modulatory site, or the polyamine site; d) agents
which inhibit the downstream effects of NMDA receptor
stimulation, such as agents that inhibit activation of protein
kinase C activation by NMDA stimulation, antioxidants, and
agents that decrease phosphatidylinositol metabolism.

(Id. at 3.)
4. The Specification further discloses:
Preferably, the compounds used cross the blood-retina
barrier and can be administered chronically. Other useful
agents act as antagonists of non-NMDA receptors (glutamate
receptor types other than the NMDA receptor complex
discussed above), and include agents which block inotropic
glutamate receptors or interact with metabotropic glutamate
receptors. Still other agents act to limit (reduce) release of
glutamate from cells, thereby acting upstream from the
glutamate receptors in the excitatory neurotoxicity process.
Still other agents may act by blocking downstream effects of
glutamate receptor stimulation, e.g., the intracellular
consequences of glutamate interaction with a cell membrane
glutamate receptor, such as agents (like dantrolene) that block
the rise in intracellular calcium following stimulation of
membrane glutamate receptors.

(Id. at 4.)
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5. The Specification discloses that “[m]any antagonists of the NMDA
receptor have been identified (Watkins et al., Trends in Pharmacological Sci.
11:25, 1990, hereby incorporated by reference)” (id. at 5).
6. The Specification discloses that “[a]mong the preferred compounds
are amantadine derivatives (e.g., memantine, amantadine, and rimantadine),
nitroglycerin, dextorphan, dextromethorphan, and CGS-19755” (id.).
7. The Specification provides a table listing a number of glutamate
antagonists, identified in a variety of classes, including competitive and non-
competitive NMDA antagonists (Spec. 7-10).
8. The Specification further discloses:
An antagonist may be tested for utility in the method of
the invention by monitoring its effect on proliferative
retinopathy as follows.
Cultured fibroblasts will be injected into the vitreous of
the rabbit eye. After two weeks, the degree of vitreopathy can
be assessed histologically. At the time of the initial insult, the
animals will be treated with the compound under consideration.
Such models are well known. A few examples (hereby
incorporated by reference) included Kiumura et al. Human
Gene Therapy, 7:799-808 (1996); Sakamota et al.,
Ophthalmology 102:1417-1421 (1995); Handa et al.
Experimental Eye Research 62:689-696 (1996); Berger et al.
37: 2318-1325 (1996); de Souza et al. Ophthalmologica 209:
212-216 (1995); Nakagawa et al. Ophthalmology & Visual
Science 36:2388-2395 (1995); Steinhorst et al. Archive for
Clinical & Experimental Ophthalmology 232:347-354 (1994).

(Id. at 13.)
PRINCIPLES OF LAW
When making an enablement rejection, the Examiner must present a
reasonable explanation why “the scope of protection provided by that claim
is not adequately enabled by the description of the invention provided in the
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specification of the application; this includes, of course, providing sufficient
reasons for doubting any assertions in the specification as to the scope of
enablement.” In re Wright, 999 F.2d 1557, 1562 (Fed. Cir. 1993).
While the Specification must enable the skilled artisan to practice the
full scope of the claimed subject matter, “[i]t is well settled that patent
applicants are not required to disclose every species encompassed by their
claims, even in an unpredictable art.” In re Vaeck, 947 F.2d 488, 496 (Fed.
Cir. 1991). Moreover, a claim does not lack enablement merely because it
encompasses inoperative embodiments. Atlas Powder Co. v. E.I. DuPont De
Nemours & Co., 750 F.2d 1569, 1576 (Fed. Cir. 1984).
Enablement is not precluded by the necessity for some
experimentation such as routine screening. However,
experimentation needed to practice the invention must not be
undue experimentation. . . . The test is not merely quantitative,
since a considerable amount of experimentation is permissible,
if it is merely routine, or if the specification in question
provides a reasonable amount of guidance with respect to the
direction in which the experimentation should proceed.

In re Wands, 858 F.2d at 736-37 (citations omitted).
ANALYSIS
We agree with Appellant that the evidence of record does not support
the Examiner’s position that the Specification fails to adequately enable the
full scope of the claimed invention.
Specifically, claim 16 recites a method for treating an ophthalmic
condition involving the retinal pigment epithelium of an individual’s eye.
Claim 16 requires the practitioner to administer an excitatory amino acid
receptor antagonist to the individual. The receptor antagonist must be
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administered in an amount that is effective to reduce glutamate-induced
effects on the retinal pigment epithelium (RPE) of the eye of the individual.
As explained in the Specification, the glutamate-induced effects are
undesired migration and proliferation of cells in the RPE (FF 2). Thus,
claim 16 requires the practitioner to administer, to an individual suffering
from an ophthalmic condition involving undesired migration and
proliferation of the cells of the RPE, an excitatory amino acid receptor
antagonist in an amount sufficient to reduce the degree of migration and
proliferation.
Claim 26 recites a similar method of treating a retinal pigment
epithelium condition in an individual’s eye. Claim 26 requires the
practitioner to administer a therapeutically effective amount of a glutamate
receptor antagonist to the individual.
Thus, similar to claim 16, claim 26 requires the practitioner to
administer, to an individual suffering from an eye condition involving
undesired migration and proliferation of the cells of the RPE, a glutamate
receptor antagonist in an amount sufficient to reduce the degree of migration
and/or proliferation.
The Specification discloses examples of ophthalmic conditions, such
as penetrating trauma, retinal tears, traction detachments, vitrectomy, and
intraocular surgery that predispose individuals to undesired RPE
proliferation and migration (FF 1). The Specification also notes that other
conditions involving RPE proliferation and migration were known in the art
(id. (citing “Machamer (1978) British J. Ophthal. 62:737; Hilton et al.
(1983) Ophthalmology 90:121.”)).
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In contrast, while the Examiner urges that treating only “certain …
conditions” are enabled (Ans. 3 (bolding removed)), the Examiner fails to
point out which conditions resulting in undesired RPE
proliferation/migration would have been considered untreatable by the
described methods, and why they would be untreatable in the disclosed
manner. Even assuming, as the Examiner argues, that not all antagonists of
the different subtypes of glutamate receptors would act to ameliorate RPE
proliferative symptoms in every circumstance, as noted above, a claim does
not lack enablement merely because it encompasses inoperative
embodiments. Atlas Powder v. DuPont, 750 F.2d at 1576.
In this regard, as disclosed in the Specification, and undisputed by the
Examiner, prior art models for screening candidate compounds were known
in the art at the time this application was filed (FF 8). Moreover, the
Specification identifies the general properties of suitable excitatory amino
acid receptor antagonists and glutamate receptor antagonists (FF 2-4), states
that such compounds were known in the art (FF 5), and lists exemplary
compounds suitable in the claimed treatment methods (FF 6-7).
Thus, while the Examiner urges that painstaking experimental study
would have been required to determine which compounds were suitable in
the claimed treatments, the Examiner points to no direct evidence suggesting
that the prior art screening methods entailed anything but routine
experimentation, or that the variety of compounds listed in the Specification
would have failed to provide adequate guidance in choosing compounds
suitable for screening. As noted above, a claim is enabled even if practicing
its full scope requires experimentation, as long as the experimentation is
routine. Wands, 858 F.2d at 736-37.
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In sum, the Specification provides examples of eye conditions
involving the symptomology treated by the claims, and the Examiner does
not dispute that an ordinary artisan would have been able to determine
whether a particular disorder was encompassed by the claims. The
Specification also discloses that an animal model for such disorders was
known in the art, and provides a list of compounds having properties
expected to treat disorders encompassed by the claims.
Given the absence of any clear or direct evidence casting doubt on the
adequacy or veracity of these disclosures, we conclude that Examiner has
not adequately explained why a skilled artisan viewing the instant
Specification would have been unable to practice the full scope of the
claimed subject matter without undue experimentation. Accordingly, we
reverse the Examiner’s enablement rejection of claims 16 and 26, and their
dependent claims.
OBVIOUSNESS
ISSUE
Claims 16-33 also stand rejection under 35 U.S.C. § 103(a) as obvious
over Uchida “in view of Applicant’s Admission” (Ans. 6).
The Examiner cites Uchida as teaching “the effect of glutamate on
proliferation of retinal pigment epithelium by the activation of NMD[A]
receptor” (id. at 7). In particular, the Examiner notes that Uchida “teaches
the effect of glutamate antagonists in abolishing such effect and the role of
glutamate in proliferative vitreoretinopathy” (id.).
The Examiner concedes that Uchida “differs from the claimed
invention in the use of specific NMD[A] receptor antagonists and route of
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administration,” but notes that Appellant’s Specification admits that
memantine and ifenprodil are glutamate antagonists (id.).
Thus, the Examiner reasons, an ordinary artisan would have
considered it obvious to “use the claimed specific compounds memantine
and ifenprodil for the treatment of proliferative vitreoretinopathy, motivated
by the by applicant’s admission that such compounds are glutamate
antagonists. The determination of route of administration is considered to be
within the skill of the artisan in the absence of evidence to the contrary”
(id.). The Examiner further reasons:
One skilled in the art would have been motivated to
combine the teachings of the above reference, since one relates
to effect of glutamate in stimulating proliferation of retinal
pigment epithelium through NMDA activation, and the effect of
glutamate antagonists in abolishing such effect and the other
relates to the claimed specific compounds as glutamate
antagonists. The substitution of one NMD[A] receptor
antagonist for another and the determination of route of
administration is considered to be within the skill of the artisan.

(Id.)

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Appellant contends,6 among other things, that Uchida teaches that
only one of four apparent glutamate antagonists tested was able to inhibit
RPE proliferation in the in vitro test described in Uchida, and that Uchida
therefore teaches away from the claimed methods (App. Br. 22). Moreover,
Appellant argues, rather than teaching specific therapeutic methods, Uchida
describes only basic research suggesting that glutamate might be involved in
retinal wound healing (id.).
Further, Appellant argues, it is improper for the Examiner to rely on
teachings in the Specification as prior art unless there is evidence that the
teachings have been admitted by Appellant as being prior art (id. at 23).
Thus, Appellant concludes, an ordinary artisan “could not have anticipated
the present invention in light of the prior art properly of record, and even if
guessed at, such a person could not have had a reasonable expectation of
success in a method of treating a pathological ophthalmic condition in vitro”
(id. at 25).

6 Appellant appears to have inadvertently supplied a copy of the wrong
Uchida reference with the Appeal Brief. Specifically, the Evidence
Appendix states that it contains a copy of a document with “Ochida” as the
first author, the substance of which appears at page 274P of an unnamed
journal (App. Br. 31 (Evidence Appendix)). However, the actual abstract
supplied by Appellant, while listing N. Uchida as the first author, does not
appear to be from page 274P of the unnamed journal, nor does its title
correspond to the title of the abstract applied by the Examiner (see Ans. 3).
As noted above, in making the obviousness rejection, the Examiner
cited an abstract by N. Uchida et al., entitled “Glutamate stimulates
proliferation of retinal pigment epithelium and Its bFGF through NMDA
receptor activation,” appearing at page 274P of an unnamed journal (see
Ans. 3).
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In view of the positions advanced by Appellant and the Examiner, the
issue with respect to this rejection is whether the evidence of record supports
the Examiner’s position that an ordinary artisan would have considered the
claimed processes of treating conditions involving RPE obvious in view of
the Uchida and Appellant’s admitted prior art.
FINDINGS OF FACT
9. The Uchida abstract reads as follows:
We investigated possible involvement of glutamate in the
proliferation and expression of basic fibroblast growth factor
(bFGF) and its receptor (FGF-R1) of cultured rat retinal
pigment epithelium (RPE) cell. Glutamate (0.2-1.0 mM)
significantly increased proliferation of primary rat RPE cells
after 7-day treatment in concentration-dependent manner
compared with control cells. Glutamate-stimulated cell
proliferation was abolished by addition of MK-801 but not by
addition of CNQX, DNQX and AP-3. NMDA alone
significantly increased proliferation, to the similar extent with
glutamate. NMDA receptor-like immunoreactivity was detected
in most of cultured cells. Expression of bFGF and FGF-R1
mRNA was increased by treatment of glutamate, which was the
highest after 2- and 4-day treatment, respectively, and the
former was inhibited by MK-801. These findings suggested that
glutamate-stimulated proliferation of RPE cells was mediated
by activation of NMDA receptor and bFGF expression and that
glutamate might be involved in retinal wound healing and in
pathogenesis in proliferative vitreoretinopathy.

(Uchida 274P (abstract P-861).)

PRINCIPLES OF LAW
In KSR Int' l Co. v. Teleflex Inc., 550 U.S. 398 (2007), the Supreme
Court stated:
When there is a design need or market pressure to solve a
problem and there are a finite number of identified, predictable
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solutions, a person of ordinary skill has good reason to pursue
the known options within his or her technical grasp. If this
leads to the anticipated success, it is likely the product not of
innovation but of ordinary skill and common sense. In that
instance the fact that a combination was obvious to try might
show that is was obvious under § 103.

Id. at 421.

Thus, as our reviewing court has stated, “[o]bviousness does not
require absolute predictability of success. . . . For obviousness under § 103,
all that is required is a reasonable expectation of success.” In re O’Farrell,
853 F.2d 894, 903-04 (Fed. Cir. 1988).
However, “patents are not barred just because it was obvious ‘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.’”
Procter & Gamble Co. v. Teva Pharmaceuticals USA, Inc., 566 F.3d 989,
997 (Fed. Cir. 2009) (quoting In re O’Farrell, 853 F.2d, at 903).
ANALYSIS
We agree with Appellant that the evidence of record does not support
the Examiner’s position that an ordinary artisan would have considered the
claimed processes of treating conditions involving RPE obvious in view of
the Uchida and Appellant’s admitted prior art.
As noted above, independent claims 16 and 26 require the practitioner
to administer, to an individual suffering from an ophthalmic condition
involving undesired migration and proliferation of the cells of the RPE, an
excitatory amino acid receptor antagonist (claim 16), or a glutamate receptor
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antagonist (claim 26), in an amount sufficient to reduce the degree of
migration and/or proliferation.
We acknowledge Uchida’s disclosure that glutamate and NMDA both
stimulated cultured rat primary RPE cells in vitro, and that one of four
apparent glutamate antagonists tested by Uchida abolished the glutamate-
stimulated proliferation (FF 9). However, Uchida does not characterize
these findings as suggesting that patients having undesired RPE proliferation
should be treated with glutamate antagonists.
Rather, Uchida states only that its “findings suggested that glutamate-
stimulated proliferation of RPE cells was mediated by activation of NMDA
receptor and bFGF expression and that glutamate might be involved in
retinal wound healing and in pathogenesis in proliferative vitreoretinopathy”
(id. (emphasis added)). Thus, even if Appellant had admitted, which he
apparently did not, that memantine and ifenprodil were known in the art as
glutamate antagonists, Uchida at best suggests that the NMDA receptor
signaling system is one that should be investigated when studying the
pathogenesis of proliferative vitreoretinopathy.
Thus, given the tentative language used by Uchida when
characterizing the relationship between proliferative retinopathy and the
NMDA receptor, and given that only one of four apparent glutamate
antagonists tested by Uchida actually inhibited glutamate-induced RPE
proliferation in vitro, we do not agree that Uchida would have provided an
ordinary artisan with a reasonable expectation that disorders encompassed
by independent claims 16 and 26 would have been treatable using glutamate
receptor antagonists, as the Examiner posits.
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Accordingly, given the evidence before us, we are not persuaded that
the Examiner has made a prima facie case of obviousness, and are therefore
constrained to reverse the Examiner’s § 103 rejection over claims 16 and 26
and their dependents.

SUMMARY
We reverse the Examiner’s rejection of claims 16-33 under 35 U.S.C.
§ 112, first paragraph, as lacking enablement.
We also reverse the Examiner’s rejection of claims 16-33 under 35
U.S.C. § 103(a) as obvious over Uchida and admitted prior art.

REVERSED

alw

ALLERGAN, INC.
2525 DUPONT DRIVE, T2-7H
IRVINE, CA 92612-1599