Ex Parte Landerth et al

Patent Trial and Appeal Board

Jun 9, 2017

12438478 (P.T.A.B. Jun. 9, 2017)

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
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APPLICATION NO. FILING DATE FIRST NAMED INVENTOR ATTORNEY DOCKET NO. CONFIRMATION NO.
12/438,478 08/18/2010 Gary E. Landerth CWR-8116US PCT 6050
68705 7590 06/13/2017
TAROLLI, SUNDHEIM, COVELL & TUMMINO, LLP
1300 EAST NINTH STREET
SUITE 1700
CLEVELAND, OH 44114
EXAMINER
COLEMAN, BRENDA LIBBY
ART UNIT PAPER NUMBER
1624
NOTIFICATION DATE DELIVERY MODE
06/13/2017 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):
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PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte GARY E. LANDRETH,
SOPHIA SUNDARARAJAN, and COLIN COMBS
Appeal 2016-003472
Application 12/43 8,47 s1
Technology Center 1600
Before DEMETRA J. MILLS, FRANCISCO C. PRATS, and
RACHEL H. TOWNSEND, Administrative Patent Judges.
PRATS, Administrative Patent Judge.
DECISION ON APPEAL
This appeal under 35 U.S.C. § 134(a) involves claims to a method of
mitigating reperfusion injury associated with treating a cerebrovascular
accident, such as a stroke. The Examiner rejected the claims for
obviousness.
We have jurisdiction under 35 U.S.C. § 6(b). We affirm.
1 Appellants identify Case Western Reserve University as the real party in
interest. App. Br. 2.
Appeal 2016-003472
Application 12/438,478
STATEMENT OF THE CASE
The Specification discloses that “[cjurrently the only FDA approved
therapy for ischemic stroke is reperfusion mediated by the thrombolytic,
tissue plasminogen activator (tPA). While early reperfusion limits ischemic
injury and is clearly beneficial, it does allow reperfusion injury to occur.”
Spec. 1 5.
The Specification discloses that “[o]ne mechanism implicated in
reperfusion injury is a more robust inflammatory response mediated by
leukocytes, which become activated within 30 minutes of ischemic onset.”
Id. In particular, the Specification discloses, “[njeutrophil infiltrates are
detected as early as one hour after reperfusion and are significant six hours
after reperfusion.” Id.
Claim 1 is representative and reads as follows:
Claim 1: A method of mitigating reperfusion injury
associated with treating a cerebrovascular accident in a subject,
the method comprising:
administering a therapeutically effective amount of at
least one PPARy agonist to the subject within a time frame of
about 3 hours after acute ischemia sufficient to a cause the
cerebrovascular accident and prior to reperfusing the
cerebrovascular ischemic tissue, wherein the therapeutically
effective amount is the amount effective to suppress ICAM
expression in the subject, to suppress leukocyte infiltration to
ischemic tissue of the subject, and to mitigate reperfusion
related ischemic injury; and
reperfusing the cerebrovascular ischemic tissue of the subject.
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The Examiner entered and maintained the following rejections:
(1) Claims 1, 5, and 7—19, under 35 U.S.C. § 103(a), for
obviousness over Landreth,2 Darwin,3 and Villegas4 (Final Act. 2—6 (entered
January 13, 2015); Ans. 4);
(2) Claim 6, under 35 U.S.C. § 103(a), for obviousness over
Landreth, Darwin, Villegas, and Lewis5 (Final Act. 6—7; Ans. 4); and
(3) Claims 1, 5, and 7—19, on the ground of nonstatutory
obviousness-type double patenting, over claims 6—10 of U.S. Patent No.
6,191,154 B1 (Final Act. 7-8; Ans. 4).
OBVIOUSNESS—
LANDRETH, DARWIN, AND VILLEGAS
The Examiner’s Prima Facie Case
In rejecting claims 1,5, and 7—19 over Landreth, Darwin, and
Villegas, the Examiner cited Landreth as disclosing that PPARy agonists, the
active agent recited in Appellants’ claim 1, were “useful for treating
ischemia/reperfusion injury following a cerebrovascular accident.” Final
Act. 2.
2 US 6,191,154 B1 (issued Feb. 20, 2001).
3 Mike Darwin, The Pathophysiology of Ischemic Injury,
http://www.alcor.org/Library/html/ischemic.html (1995) (Last Accessed
Sept. 16, 2014).
4 Isabel Villegas et al., Rosiglitazone, an agonist of peroxisome proliferator-
activated receptor gamma, protects against gastric ischemia-reperfusion
damage in rats: role of oxygen free radicals generation, 505 Eur. J.
Pharmacol. 195-203 (2004).
5 US 6,044,845 (issued Apr. 4, 2000).
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The Examiner conceded that Landreth differs from claim 1 in that
Landreth does not disclose “the consequence of administration (suppression
of ICAM expression, suppression of leukocyte infiltration to ischemic tissue,
and migration of reperfusion related ischemic injury) or the time period for
administration (within about 3 hours of acute ischemia).” Id.
To address those deficiencies, the Examiner first cited Darwin as
teaching that neutrophils were a ‘“major mediator’” of reperfusion injury
following brain ischemia, and reasoned that, “[gjiven the importance of
neutrophils in the pathology of ischemia/reperfusion injury, it would have
been prima facie obvious to inhibit the[ir] activity following a stroke.” Final
Act. 2—3. The Examiner then cited Villegas as teaching that “rosiglitazone,
a known PPARy agonist, . . . reduces neutrophil infiltration and release of
proinflammatory cytokines (e.g. TNF-a) (abstract; pg 202, col 2, para 2).”
Id. at 3.
The Examiner found that, “[tjaken together, the cited combination of
prior art reasonably suggests a method of mitigating reperfusion injury
following a cerebrovascular accident (e.g. an ischemic stroke).” Id. The
Examiner reasoned, however, that “[gjiven that strokes are unpredictable . . .
it would not be possible to administer PPARy agonists, such as those
described in Landreth, et al., prior to the cerebrovascular accident.” Id.
(citing Hahn6).
The Examiner concluded, therefore, that an ordinary artisan would
have considered it obvious to “administer the PPARy agonists as soon as
possible (e.g. within 3 hours) of the cerebrovascular accident to mitigate the
6 Cecil D. Hahn et al., Remote Ischemic Per-Conditioning[:] A Novel
Therapy for Acute Stroke?, 42 Stroke 2960-62 (2011).
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damage caused by the neutrophils” and also would have considered it
obvious “to administer the PPARy agonists prior to reperfusion to ensure
that the PPARy agonist is present upon the arrival of the neutrophils during
reperfusion.” Id. As to the recitations in claim 1 directed to suppression of
ICAM expression and suppression of leukocyte infiltration and migration,
the Examiner further concluded that those recitations ‘“simply express[] the
intended result of a process step positively recited.’” Id. (citing Hoffer v.
Microsoft Corp., 405 F.3d 1326, 1329, (Fed. Cir. 2005); MPEP § 2111.04).
Analysis
As stated in In re Oetiker, 977 F.2d 1443, 1445 (Fed. Cir. 1992):
[T]he examiner bears the initial burden ... of presenting a
prima facie case of unpatentability. . . .
After evidence or argument is submitted by the applicant
in response, patentability is determined on the totality of the
record, by a preponderance of evidence with due consideration
to persuasiveness of argument.
We select claim 1 as representative of the rejected claims, as
Appellants do not provide separate argument for other claims subject to this
rejection. 37 C.F.R. § 41.37(c)(l)(iv). Appellants do not persuade us that a
preponderance of the evidence fails to support the Examiner’s conclusion
that the process recited in claim 1 would have been obvious to an ordinary
artisan.
As the Examiner found, Landreth discloses treating stroke, a
cerebrovascular accident undisputedly encompassed by claim 1, using
PPARy agonists, the therapeutic agent recited in claim 1. See Landreth
2:15—23 (disclosing administration of “a therapeutically effective amount of
a PPARy agonist to the subject, wherein the subject. . . suffer[s] from a
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disease with an inflammatory component. . . selected from the group
consisting of. . . stroke” among others).
Landreth explains that its therapeutic strategy is based on the fact that
“[pjroinflammatory cytokines play a critical role in the progressive
neuropathological changes that accompany stroke and other ischemic brain
injuries” and that “[ijschemia in the brain is followed by the induction of
expression of a variety of cytokines (particularly IL-ip, TNF-a, and IL-6),
that have been mechanistically linked to neuropathological changes in the
brain.” Id. at 31:35—43 (citations omitted). Landreth discloses in particular
that “[experimental interventions in which cytokine actions are inhibited
have been reported to ameliorate the clinical and anatomical sequelae of
ischemia.” Landreth 31:43—45.
Although Landreth, thus, describes administering the therapeutic
agent required by claim 1 to a patient population encompassed by claim 1,
based on a strategy of inhibiting inflammation, Landreth does not describe
administering the agent during the period required by claim 1—within about
3 hours of an acute ischemia sufficient to cause the stroke, but prior to
reperfusion.
As the Examiner found, however, Darwin discloses that “neutrophils
are a major mediator of ischemic injury in a variety of organ systems and
that their acute activation is responsible for many of the effects of ischemia
observed in the brain and other body tissues, including the loss of capillary
integrity and the degradation of ultrastructure upon reperfusion.” Darwin 5
(emphasis added).
As the Examiner found, moreover, Villegas discloses that, in a rat
model of gastric ischemia, administration of the PPARy agonist
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rosiglitazone protected against inflammation-related reperfusion injury.
Villegas 195 (“[Rjosiglitazone reduces the damage in ischemia-reperfusion
gastric injury and alleviates the inflammatory response and the oxidative
events.”).
Villegas discloses in particular that the protective effect was
associated with inhibition of neutrophil infiltration. Id. at 201—202
(“[Pjretreatment with the highest dose of rosiglitazone significantly reduced
the myeloperoxidase activity. These data are in agreement with previous
reports which suggest that rosiglitazone and other PPAR-a agonists can
regulate inflammatory responses thorough several mechanisms, including
reduction of the expression ofproinflammatory mediators and neutrophil
infiltration.'”) (citation omitted, emphasis added).
Villegas discloses that its therapeutic effect was similar to that seen in
heart, kidney, and intestinal ischemic injuries. Villegas 200 (“A similar
profile was observed when the beneficial effects of this PPAR-y ligand
against myocardial, renal, and intestinal ischemia-reperfusion injuries were
explored.”) (citations omitted).
Thus, Darwin teaches that reperfusion injury associated with stroke is
mediated by neutrophils, and Villegas teaches the PPARy agonists alleviate
neutrophil-mediated reperfusion gastric injury, a therapeutic effect similar to
that seen in other tissues. Given these teachings, we agree with the
Examiner that an ordinary artisan using a PPARy agonist to treat stroke, as
taught in Landreth, had ample reason for, and a reasonable expectation of
success in, administering the PPARy agonist before reperfusing the stroke
patient, as recited in Appellants’ claim 1, for the purpose of ameliorating
neutrophil-mediated reperfusion damage.
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As Appellants contend, none of Landreth, Darwin, or Villegas appears
to expressly describe claim 1 ’s step of treating stroke patients with
reperfusion. As the Examiner points out, however (Ans. 9), Appellants’
Specification discloses that it was well known in the art to reperfuse stroke
patients by administering tPA soon after the stroke, to remove the ischemia-
causing clot. See Spec. 1 5 (disclosing tPA-mediated reperfusion as only
FDA-approved ischemic stroke therapy). As the Examiner also points out, it
was known in the art that it was desirable to perform reperfusion therapy as
quickly as possible after the ischemic event, but no later than six hours after
the event. Ans. 9 (citing 2004 Press Release).7
Appellants do not persuade us, therefore, that the Examiner erred in
finding that an ordinary artisan, administering a PPARy agonist to a stroke
patient before reperfusion so as to ameliorate neutrophil-mediated
reperfusion damage as discussed above, would have been prompted to
administer the PPARy agonist within 3 hours of the ischemic event. To the
contrary, given the knowledge in the art that reperfusion therapy was most
desirably administered within a few hours of the ischemic event, and given
the suggestion from the combined teachings of Landreth, Darwin, and
Villegas of administering a PPARy agonist to a stroke patient before
reperfusion, we agree with the Examiner that an ordinary artisan would have
had ample reason for, and a reasonable expectation of success in,
7 Early Treatment Confirmed as Key to Stroke Recovery, National Institute
of Neurological Disorders and Stroke (NINDS),
http://www.ninds.nih.gov/news_ and_ events/news_ articles/stroke_pooled_
analysis_ 030404.htm?css=print (2004).
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administering the PPARy agonist within about 3 hours of the ischemic event,
and before reperfusing the stroke patient, as recited in Appellants’ claim 1.
We, thus, agree with the Examiner that an ordinary artisan would have
considered it obvious to administer a PPARy agonist to a stroke patient
within the time frame required by Appellants’ claim 1. Moreover, given the
teachings in Landreth and Villegas, discussed above, that the PPARy agonist
should be administered in amounts effective to inhibit inflammatory
responses and neutrophil infiltration, Appellants do not persuade us (App.
Br. 18—20) that the Examiner erred in finding that the cited references teach
or suggest administering the therapeutic agent in an amount effective to
suppress ICAM expression and leukocyte infiltration, and to mitigate
reperfusion related ischemic injury, as required by claim 1. Accordingly, for
the reasons discussed, we find that the evidence of record supports the
Examiner’s prima facie case of obviousness as to claim 1.
Appellants’ arguments, that none of Landreth, Darwin, or Villegas
individually teaches or suggests the specific time frame of administering the
PPARy agonist (see App. Br. 14—18; Reply Br. 5), fails to address the
Examiner’s contention that the references, when viewed in combination,
suggest the claimed process. See In re Merck & Co., Inc., 800 F.2d 1091,
1097 (Fed. Cir. 1986). (“Non-obviousness cannot be established by
attacking references individually where the rejection is based upon the
teachings of a combination of references. . . . [The reference] must be read,
not in isolation, but for what it fairly teaches in combination with the prior
art as a whole.”). For similar reasons, the absence in the 2004 Press Release
of a description of administering a PPARy agonist alongside tPA-mediated
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reperfusion (Reply Br. 5) fails to demonstrate the nonobviousness of the
process recited in claim 1.
To that end, although it might be true that none of the references
expressly teach administering a PPARy agonist to a stroke patient within the
time frame specified by Appellants’ claim 1, as the Supreme Court has
explained, “the [obviousness] analysis need not seek out precise teachings
directed to the specific subject matter of the challenged claim, for a court
can take account of the inferences and creative steps that a person of
ordinary skill in the art would employ.” KSR Int’l v. Teleflex Inc., 550 U.S.
398,418 (2007).
In the present case, given the knowledge in the art that reperfusion
therapy was most desirably administered within a few hours of the ischemic
event, and given the suggestion from the combined teachings of Landreth,
Darwin, and Villegas of administering a PPARy agonist to a stroke patient
before reperfusion, we agree with the Examiner that an ordinary artisan
would have reasonably inferred that it would be desirable to administer a
PPARy agonist to a stroke patient within about 3 hours of a stroke-causing
ischemic event, and before reperfusing the stroke patient, as recited in
Appellants’ claim 1.
As to Appellants’ suggestion that the neutrophil-inhibiting effects of
PPARy agonists taught in Villegas would not have been extrapolated to
other tissues (App. Br. 16), as noted above, Villegas teaches that the
therapeutic effect observed therein in gastric tissue was similar to that seen
heart, kidney, and intestinal ischemic injuries. Villegas 200 (“A similar
profile was observed when the beneficial effects of this PPAR-y ligand
against myocardial, renal, and intestinal ischemia-reperfusion injuries were
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explored.”) (citations omitted). We, therefore, discern no error in the
Examiner’s finding that an ordinary artisan would have expected the
therapeutic effects shown in Villegas to extend to other tissues.
It is well settled, moreover, that “[ojbviousness 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); accord, In re Kubin, 561 F.3d 1351,
1359-61 (Fed. Cir. 2009). Thus, that an ordinary artisan might not
“necessarily” have predicted that PPARy agonists would inhibit neutrophil-
mediated reperfusion injury (Reply Br. 4) does not demonstrate that the
claimed invention would have been unobvious under the § 103 analysis.
In sum, for the reasons discussed, Appellants do not persuade us that
the evidence of record fails to support the Examiner’s conclusion that the
process recited in claim 1 would have been prima facie obvious to an
ordinary artisan. We are not persuaded, moreover, that Appellants have
advanced objective evidence of nonobviousness sufficient to outweigh the
evidence of prima facie obviousness advanced by the Examiner.
In that regard, Appellants contend that || 92—96 of the Specification
demonstrate that the process recited in claim 1 yields unexpected results.
App. Br. 20-22; Reply Br. 3. In particular, Appellants contend, “the
functional limitations recited in claim 1 of suppressing ICAM expression in
the subject and suppressing leukocyte infiltration to ischemic tissue of the
subject, were unexpectedly observed exclusively within the time frame of
about 3 hours after acute ischemia and prior to reperfusing the ischemic
tissue.” App. Br. 20.
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We acknowledge the disclosure in the Specification of the studies
involving a rat model of ischemic stroke, using middle cerebral artery
occlusion (MCAO) via artery suturing as the ischemia trigger, with
reperfusion being performed by releasing the suture. Spec. 199.
We acknowledge, as disclosed in the Specification, that treatment
with either pioglitazone or rosiglitazone8 as the PPARy agonist before
reperfusion resulted in reduced infarction volumes, whereas treatment with
those agents after perfusion yielded larger infarction volumes comparable to
those seen when treating with vehicle only (control):
Half the rats were reperfused at two hours, while the other rats
were reperfused at three hours and fifteen minutes. Animals
that were reperfused at two hours and treated one hour later
had infarction volumes which were similar to animals injected
with vehicle; these infarctions encompass the majority of the
MCA territory. However, animals that were treated at three
hours and reperfused fifteen minutes later had significantly
smaller infarctions volumes when assayed twenty-four hours
after MCAO (Fig. 3).
Spec. 193 (emphasis added).
We acknowledge that PPARy agonist administration before perfusion
also reduced leukocyte infiltration, measured as myeloperoxidase activity,
significantly more than when the PPARy agonist was administered one hour
after perfusion: “Animals reperfused two hours after MCAO and treated
with either pioglitazone or rosiglitazone at three hours had significantly
increased numbers of myeloperoxidase-IR cells within the ischemic
hemisphere relative to the brains of animals which were treated at three
hours and reperfused fifteen minutes later (Fig. 4).” Id. 194.
8 Pioglitazone and rosiglitazone are in a category compound known as
“thiazolidinediones (TZDs).” Spec. 112.
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We acknowledge that treatment with PPARy agonists before perfusion
also reduced ICAM expression:
Rats were treated with either vehicle, pioglitazone (1.0 mg/kg)
or rosiglitazone (0.1 mg/kg) twenty-four hours before and again
at the time of occlusion. Rats were sacrificed twenty-four hours
[after occlusion (see id. 1 16)] and both ICAM-IR by
immunohistochemistry and relative ICAM mRNA levels by
real time PCR examined. Less ICAM-IR was present in TZD
treated rats compared with vehicle treated rats. Furthermore,
there was a significant reduction in ICAM mRNA with both
TZD treatments relative to the vehicle treatment (Fig. 5). The
degree of reduction by pioglitazone and rosiglitazone was
similar.
Spec. 195.
We further acknowledge the following assertions in the Specification:
To our knowledge this is the first study to specifically assess
whether the time of reperfusion relative to drug administration
alters outcome. Reperfusion can occur spontaneously at various
times after the onset in human ischemic stroke. Since the advent
of thrombolytic therapy for stroke, time of reperfusion is
increasingly controlled by the administration of thrombolytics.
To date thrombolysis is the only FDA approved therapy for
acute ischemic stroke and the practice since its approval has
been to administer thrombolytics and then consider if patients
might be candidates for neuroprotective trials. These
experiments indicate that this approach may not be effective for
some therapies, especially those likely to target reperfusion
injury.
Id. 196.
Although we, thus, acknowledge the assertion in 196 of the
Specification that the described studies were the first Appellants were aware
of that evaluated whether the timing of drug administration relative to
reperfusion affects the therapeutic outcome, we discern no assertion in 196
that the results observed were unexpected, as opposed to merely being an
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affirmation of a predicted result based solely on prior art knowledge. Nor do
we discern any specific assertion of unexpected results in || 92—95, or
elsewhere in the Specification.
Rather, the only assertions of record, that the results described in the
Specification were unexpected, appear in the Appeal Brief and Reply Brief,
in the form of attorney argument. See App. Br. 20—22; Reply Br. 3. It is
well settled, however, that argument by counsel is not a sufficient substitute
for evidence that the results presented were actually unexpected. See In re
Geisler, 116 F.3d 1465, 1471 (Fed. Cir. 1997).
Moreover, contrary to Appellants’ assertion that the Specification
shows that administration of a PPARy agonist within the time frame recited
in claim 1 (within 3 hours after the ischemic event but before reperfusion)
unexpectedly suppresses ICAM expression, the rats in the ICAM experiment
received PPARy agonists 24 hours before occlusion and at the time of
occlusion. Spec. 195. Thus, at least with respect to the ICAM experiment,
the evidence Appellants rely on to show unexpected results is not
commensurate in scope with the claimed subject matter. See In re Kao, 639
F.3d 1057, 1068 (Fed. Cir. 2011) (“Evidence of secondary considerations
must be reasonably commensurate with the scope of the claims.”).
In addition, as to Appellants’ assertions regarding the reduced
infraction volume and leukocyte infiltration shown in || 93 and 94 of the
Specification, we note Villegas’s disclosure that, in its model of gastric
ischemia, significant reperfusion injury and associated neutrophil-related
effects were seen as soon as one hour after reperfusion, and pre-occlusion
administration of a PPARy agonist significantly diminished those symptoms.
See Villegas 1999 (“Our results show that gastric injury was significantly
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increased after 60 min reperfusion following 30 min of ischemia by
clamping the celiac artery. . . . Treatment with either 1 or 4 mg/kg of
rosiglitazone clearly diminished the number and severity of ulcers.”); see
also id. at 201—202 (“[Pjretreatment with the highest dose of rosiglitazone
significantly reduced the myeloperoxidase activity. These data are in
agreement with previous reports which suggest that rosiglitazone and other
PPAR-a agonists can regulate inflammatory responses thorough several
mechanisms, including reduction of the expression ofproinflammatory
mediators and neutrophil infiltration”) (citation omitted, emphasis added).
Given Villegas’s disclosure that pre-reperfusion administration of a
PPARy agonist significantly alleviated reperfusion-associated tissue damage
and neutrophil-mediated effects that otherwise occurred within one hour
after reperfusion in the absence of such treatments, we agree with the
Examiner that the results seen in H 93 and 94 of the Specification, on this
record, would not have been unexpected. In particular, given the teachings
in Villegas, we agree with the Examiner that, on this record, it was not
unexpected that administering a PPARy agonist before reperfusion reduced
infarction volume and leukocyte infiltration, whereas administering the drug
one hour after reperfusion (see Spec. ]Hf 94) did not have the same beneficial
effect.
In sum, for the reasons discussed, Appellants do not persuade us that
the Examiner failed to make a prima facie case that the process recited in
claim 1 would have been obvious to an ordinary artisan in view of Landreth,
Darwin, and Villegas. Because, for the reasons discussed, we are not
persuaded that Appellants have advanced objective evidence of
nonobviousness sufficient to outweigh the evidence of prima facie
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obviousness, we affirm the Examiner’s rejection of claim 1 over those
references. Claims 5 and 7—19 fall with claim 1 because they were not
argued separately. 37 C.F.R. § 41.37(c)(l)(iv).
OBVIOUSNESS—
LANDRETH, DARWIN, VILLEGAS, AND LEWIS
Claim 6 recites “[t]he method of claim 1, further comprising
administering a thrombolytic agent after administering the PPARy agonist.”
App. Br. 27. In rejecting claim 6, the Examiner relied on the teachings
discussed above in Landreth, Darwin, and Villegas, and cited Lewis as
evidence that an ordinary artisan would have considered it obvious to
administer a thrombolytic agent to a stroke patient after administering a
PPARy agonist to the patient. Final Act. 6—7.
Appellants reiterate their arguments, discussed above, regarding the
alleged shortcomings of Landreth, Darwin, and Villegas as to claim 1, and
assert that Lewis fails to correct those alleged shortcomings. App. Br. 23—
24: Reply Br. 6—8.
For the reasons discussed above, however, Appellants do not persuade
us that a preponderance of the evidence fails to support the Examiner’s
conclusion of obviousness as to claim 1. Because Appellants, therefore, do
not identify, nor do we discern, error in the Examiner’s conclusion of
obviousness as to claim 6, we affirm the Examiner’s rejection of that claim
as well.
DOUBLE PATENTING
In rejecting claims 1,5, and 7—19 on the ground of nonstatutory
obviousness-type double patenting over claims 6—10 of U.S. Patent No.
6,191,154 B1 (“the ’154 patent”), the Examiner found that, although the
rejected claims are not identical to the claims of the ’154 patent, “they are
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not patentably distinct from each other because both the instant claims and
those of the ’ 154 patent encompass treating a central nervous system injury,
such as a stroke or ischemic damage, comprising administration of a PPARy
agonist.” Final Act. 7.
The Examiner found also that the PPARy agonists in appealed claims
7—19 “are recited as PPARy agonists in the ’154 patent. As noted above, the
intended result is not accorded patentable weight. Finally, it would have
been obvious to administer the PPARy agonists with 3 hours of the
cerebrovascular event to minimize damage.” Id. at 8.
In their Appeal Brief, Appellants did not address this rejection. See
App. Br. generally.
In their Reply Brief, Appellants acknowledge that “a response to this
rejection was inadvertently omitted from [the] Brief on Appeal and
respectfully request that the Appellants[’] previous arguments related to this
rejection included in the Appellants’ response mailed December 19, 2014,
be considered.” Reply Br. 8. In addition, in their Reply Brief, Appellants
advance arguments similar to those discussed above with respect to the
Examiner’s obviousness rejections. Id. at 8—12.
“Any argument raised in the reply brief which was not raised in the
appeal brief, or is not responsive to an argument raised in the examiner’s
answer, including any designated new ground of rejection, will not be
considered by the Board for purposes of the present appeal, unless good
cause is shown.” 37 C.F.R. § 41.41(b)(2) (emphasis added).
Accordingly, by rule, unless good cause is shown, we may not
consider Appellants’ arguments in the Reply Brief traversing the Examiner’s
obviousness-type double patenting rejection, because those arguments were
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not submitted in the Appeal Brief. In the present case, Appellants do not
explain sufficiently why inadvertently failing to include those arguments in
the Appeal Brief constitutes good cause for considering those arguments in
the Reply Brief.
We, therefore, summarily affirm the Examiner’s obviousness-type
double patenting rejection. See MPEP § 1205.02 (“If a ground of rejection
stated by the examiner is not addressed in the appellant’s brief, appellant has
waived any challenge to that ground of rejection and the Board may
summarily sustain it, unless the examiner subsequently withdrew the
rejection in the examiner’s answer.”).
SUMMARY
For the reasons discussed, we affirm each of the Examiner’s
rejections.
TIME PERIOD
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
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