Ex Parte Katsikis et al

Patent Trial and Appeal Board

Apr 19, 2017

13418045 (P.T.A.B. Apr. 19, 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
www.uspto.gov
APPLICATION NO. FILING DATE FIRST NAMED INVENTOR ATTORNEY DOCKET NO. CONFIRMATION NO.
13/418,045 03/12/2012 Peter D. Katsikis 046528-6006-02-US.601343 1108
78905 7590 04/21/2017
Saul Ewing LLP (Philadelphia)
Attn: Patent Docket Clerk
Centre Square West
1500 Market Street, 38th Floor
Philadelphia, PA 19102-2186
EXAMINER
WANG, SHENGJUN
ART UNIT PAPER NUMBER
1627
NOTIFICATION DATE DELIVERY MODE
04/21/2017 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):
patents@saul.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte PETER D. KATSIKIS, ALINA C. BOESTEANU, and
MARTIN TURNER1
Appeal 2016-004225
Application 13/418,045
Technology Center 1600
Before DONALD E. ADAMS. FRANCISCO C. PRATS, and
RACHEL H. TOWNSEND, Administrative Patent Judges.
TOWNSEND, Administrative Patent Judge.
DECISION ON APPEAL
This is an appeal under 35 U.S.C. § 134 involving claims to a method
of inhibiting influenza virus replication, which have been rejected as
obvious. We have jurisdiction under 35 U.S.C. § 6(b).
We affirm.
STATEMENT OF THE CASE
“PI3K represent a family of enzymes that phosphorylate D-
myophosphatidylinositol (Ptdlns) or its derivatives” and are classified in 3
different classes “depending on their subunit structure, regulation, and
1 Appellants identify the Real Party in Interest as Drexel University and The
Babraham Institute. (Br. 3.)
Appeal 2016-004225
Application 13/418,045
substrate selectivity.” (Spec. 2.) “PI3K belonging to class I are
heterodimers composed of a catalytic subunit of approximately 110 kDa, and
a tightly associated regulatory subunit that modulates the activity and
cellular location of the enzyme.” (Id. at 3.) The class I heterodimers exist in
four isoforms, known as pi 10 alpha, beta, gamma, and delta. (Id.) The
invention is directed to a method “for regulating P13K pi 10 delta kinase in a
cell thereby providing a means for reducing or inhibiting retrovirus infection
or replication in the cell.” (Id. at 7.)
Claims 27, 30-33, 36—39, and 42-44 are on appeal.2 Claim 27 is
representative and reads as follows:
27. A method of inhibiting influenza virus replication in a
mammalian cell, said method comprising contacting said cell with a
therapeutically effective amount of a selective inhibitor of PI3K pi 10 delta,
wherein said inhibitor inhibits influenza virus replication in said
mammalian cell,
wherein said inhibitor is a small molecule compound selected from
the group consisting of INK1197, KAR4000, theophylline, CAL-101, CAL-
263, Compounds (I)-(XXX), a mixture thereof, and a pharmaceutically
acceptable salt thereof:
2 Claims 28, 29, 34, 35, 40, and 41 are also pending, but stand withdrawn
from consideration. (Br. 3.)
2
Appeal 2016-004225
Application 13/418,045
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6
Appeal 2016-004225
Application 13/418,045
The following ground of rejection by the Examiner is before us on
review:
Claims 27, 30-33, 36—39, and 42-44 under 35 U.S.C. § 103(a) as
unpatentable over Diacovo,3 Bengtsson,4 Gruber,5 and Carter.6
In response to a species election requirement, Appellants elected
Compound I as the species of selective inhibitor of PI3K pi 10 delta. (Non-
Final Action July 11, 2013; Response dated Oct. 11, 2013.) Accordingly, as
to the appealed obviousness rejection, we limit our analysis to the
patentability of the elected species and the extent to which the rejected
claims read on it. See Ex parte Ohsaka, 2 USPQ2d 1460, 1461 (BPAI
1987).
DISCUSSION
Claim Construction
The Examiner finds that the preamble of the three independent
claims—namely claims 27, 33, and 39 —reciting, respectively, “inhibiting
influenza virus replication in mammalian cell,” “inhibiting influenza virus
pathogenesis in mammalian cell,” and “treating influenza virus infection in a
mammal,” have not been given patentable weight “because the recitation
occurs in the preamble” and preambles such as those recited are “not
accorded any patentable weight where it merely recites the purpose of a
3 Diacovo et al. W02006/089106 A2, published Aug. 24, 2006.
4 Bengtsson et al., US 2008/0132502 Al, published June 5, 2008.
5 Gruber et al., Avian influenza (H5N1): implications for intensive care, 32
Intensive Care Med. 823—29 (2006).
6 Marissa J. Carter, A rationale for using steroids in the treatment of
severe cases ofH5Nl avian influenza, 56 J. Med. Microbio. 875—83 (2007).
7
Appeal 2016-004225
Application 13/418,045
process or the intended use of a structure, and where the body of the claim
does not depend on the preamble for completeness but, instead, the process
steps or structural limitations are able to stand alone.” (Final Action 6.)
We do not agree with the Examiner’s claim interpretation. Here, the
claim preambles are intimately tied to the method. For example, in claim
27, the method requires contacting a mammalian cell with a selective
inhibitor of P13K pi 10 delta in a therapeutically effective amount “wherein
said inhibitor inhibits influenza virus replication” in the cell. In other words,
the therapeutic amount is such that influenza virus replication inhibition in
the mammalian cell that is contacted with the selective inhibitor must be
achieved, which is also the purpose required by the claim preamble.
Similarly, in claim 33, the method requires contacting a mammalian cell
with a selective inhibitor of P13K pi 10 delta in a therapeutically effective
amount “wherein said inhibitor inhibits influenza virus pathogenesis” in the
cell. In other words, the therapeutic amount is such that influenza virus
pathogenesis inhibition in the cell contacted must be achieved, which is also
the purpose required by the claim preamble.
Claim 39 is slightly different, though the claim preamble is also
intimately tied to the body of that claim. In claim 39, the method requires
contacting a mammalian with a selective inhibitor ofP13Kpll0 delta in a
therapeutically effective amount “wherein said inhibitor interferes with []
PI3K pi 10 delta activation and replication of said influenza virus” in the
mammal, as well as “treats influenza virus.” In other words, the therapeutic
amount is such that not only isP13Kpll0 delta activation in the mammal
interfered with, but interference with replication of the influenza virus in the
mammal and treating the influenza virus infection must also be achieved.
8
Appeal 2016-004225
Application 13/418,045
Thus, while the claim preambles are not a “separate limitation,” see,
e.g., Symantec Corp. v. Computer Assocs. Int’l, Inc., 522 F.3d 1279, 1288—
89 (Fed. Cir. 2008), they serve to indicate that the “wherein” clauses recited
in the body of the claim are tied into the therapeutically effective amounts so
as to achieve the stated purpose in the wherein clauses, which are recited
identically in the preamble. See, e.g., Griffin v. Bertina, 285 F.3d 1029,
1033 (Fed. Cir. 2002) (finding that a “wherein” clause limited a process
claim where the clause gave “meaning and purpose to the manipulative
steps”).
Nevertheless, we do not disagree with the Examiner that the
preamble/wherein recitations “do not materially affect the steps of [the]
claimed invention.” (Ans. 6.) That is the single recited step of the method
of treating influenza virus infection of claims 27 and 33 is “contacting said
[mammalian] cell with a therapeutically effective amount of a selective
inhibitor of P13K pi 10 delta.” Claim 39 similarly recites a single step in the
method of treating influenza virus infection, which is “administering a
therapeutically effective amount of a selective inhibitor of phosphoinositide
3 kinase (PI3K) isoform pi 10 delta to said mammal.” Appellants’
Specification discloses that the “therapeutically effective amount” “may be
in the range of from about 1 pg to about 10,000 mg” (Spec. 53) or that
“suitable dose[s] of a compound of the present invention may be in the range
of from about 0.01 mg to about 5,000 mg per day” and that the “dose may be
administered in a single dosage or in multiple dosages, for example from 1
to 4 or more times per day” (Spec. 58).
9
Appeal 2016-004225
Application 13/418,045
II
Obviousness
The Examiner finds that the claims 27, 33, and 39 are obvious from
the teachings of Diacovo, Bengtsson, Gruber, and Carter. The Examiner
finds that Diacovo teaches treating inflammation conditions in the
respiratory system caused by pathogens, including virus, by inhibiting PI3K
pi 10 delta and PI3K pi 10 gamma with compounds of general formula II
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and, in particular,
using the compound having the formula
, also known as IC87114, which is a
compound within the scope of the claims. (Final Action 2—3; Spec. 30
(“Compound (I) (IC87114 or 2-[(6-amino-9H-purin-9-yl)methyl]-5-methyl-
3-(o-tolyl)quinazolin-4(3H)-one)).”) The Examiner notes that while
10
Appeal 2016-004225
Application 13/418,045
Diacovo does not expressly teach treating patients with influenza infection,
it does disclose inflammatory conditions include adult respiratory distress
syndrome (“ARDS”), and Bengtsson teaches treating a human with a
respiratory tract condition caused by influenza virus infection through the
administration of a small molecular compound that inhibits P13K-delta.
(Final Action 3—4.) The Examiner further explains that Gruber teaches that
ARDS is known to result from avian influenza, and Carter “teaches that
imbalance of pro-inflammatory and anti-inflammatory cytokines is believed
to be responsible for the development of ARDS and anti-inflammatory
agents are known to be used for treating inflammatory condition caused by
avian influenza.” (Id. at 3) In short, the Examiner finds that
[t]he prior art as a whole teach the compounds herein known as
inhibitors of PI3K pi 10 delta and/or PI3K pi 10 gamma are
useful for treatment of inflammatory conditions in respiratory
tract, particularly those caused by viral infection, such as
ARDS, an advanced conditions commonly caused by influenza
infection. Therefore, it would have been obvious to use such a
compound for treatment of ARDS caused by influenza
infection.
(Ans. 5—6.) We agree with the Examiner’s findings regarding the teachings
of the prior art and the conclusion that these teachings render the claimed
invention obvious.
Appellants argue that the Examiner has clearly erred in not
considering the preamble/wherein clause. (Br. 8—9.) We are not persuaded
that the Examiner did not consider that limitation. The Examiner
specifically pointed to Example 13 of Diacovo, which discusses
administration of particular amounts of IC87114 to mice (10 pM in Example
13) and which demonstrates that IC87114 reduces “neutrophil attachment to
11
Appeal 2016-004225
Application 13/418,045
and rolling on inflamed venular endothelium.” (Diacovo Tflf 254—256.) The
Examiner noted that Appellants have not established the preamble/wherein
limitations “materially affect the steps of [the] claimed invention,” (Final
Action 6; Ans. 6), i.e., contacting the cells with a therapeutically effective
amount, or administering a therapeutically effective amount.
As we noted above, Appellants’ Specification indicates a large
variation of dosage amounts are effective to achieve the claimed therapeutic
effect, including as low as 1 pg. (Spec. 53.) Appellants do not contend that
administration of equivalent amounts of the dosages described in Diacovo
that reduce “neutrophil attachment to and rolling on inflamed venular
endothelium” (Diacovo 254—256)—and which we find would reasonably
be expected to treat inflammation—to achieve the same result in humans,
which dosing in humans the Examiner finds is suggested by Bengtsson
(Bengtsson 1346), would not achieve the claimed result, just that none of
the references discuss achieving that result. However, just as “a patent on a
composition or machine cannot be predicated on a new use of that machine
or composition,” In re Hack, 245 F.2d 246, 248 (CCPA 1957), “[i]t is a
general rule that merely discovering and claiming a new benefit of an old
process cannot render the process again patentable,” In re Woodruff, 919
F.2d 1575, 1578 (Fed. Cir. 1990).
It is undisputed that IC87114 directly blocks the function of pi 10
delta, and that was known in the prior art. (Diacovo 1255.) Appellants’
Specification teaches that “[t]he invention comprises compositions and
methods for modulating PI3K pi 10 delta in a cell thereby inhibiting the
PI3K pi 10 delta response in the cell.” (Spec. 32.) Appellants’ invention
appears to be the discovery that in addition to the functions disclosed in
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Appeal 2016-004225
Application 13/418,045
Diacovo, i.e., that selective inhibitors of P13K pi 10 delta, such as IC87114,
may be involved in inhibiting leukocyte accumulation by inhibiting
upstream targets in pathways that selectively activate P13Kpll0 delta in
endothelial cells (Br. 10; Diacovo 128), inhibiting leukocyte tethering to
endothelial cells (Diacovo 135), inhibiting leukocyte transmigration by
inhibiting P13K delta in endothelial cells (Diacovo 136), or “inhibiting] or
reducing] AKT-activity of endothelial cells, e.g., as measured by AKT-
phosphorylation . . . [or] PDK1 enzyme activity of endothelial cells”
(Diacovo 137), this compound can also inhibit retroviral infection in the cell
(Spec. 33, 45). That a person of ordinary skill in the art would not have
known of the effect also does not preclude a finding of obviousness. PAR
Pharm. v. TWIPharms., Inc., 773 F.3d 1186, 1197 (Fed. Cir. 2014). That is
because “we are not limited to the same motivation that may have motivated
the inventors.” Id. Thus, we also do not find Appellants’ argument that
“[w]ithout the teachings of the present invention, at the time of the invention
one skilled in the art would not have been able to tell or foresee which pi 10
catalytic subunit in a cell should be inhibited in order to interfere with
influenza virus infection or replication.” (Br. 14.)
As noted above, the claimed process includes one step: administering
one of the recited compounds, which include IC87114 disclosed in Diacovo.
We agree with the Examiner that the prior art relied on provides motivation
to treat patients having respiratory tract inflammation, such as ARDS,
caused by avian flu, with a selective inhibitor ofP13Kpll0 delta, such as
IC87114. That “ARDS is a possible, but not certain, complication” of
individuals infected with avian influenza (Br. 11) is immaterial to whether
the prior art provides the requisite motivation to treat a patient population
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Appeal 2016-004225
Application 13/418,045
that in fact has ARDS. One of ordinary skill in the art would have been
motivated to combine the teachings of the cited reference to use IC87114 for
treating patients with ARDS, or other respiratory inflammatory conditions
caused by influenza.
Furthermore, that Diacovo teaches selective inhibitors of PI 3K pi 10
gamma in addition to selective inhibitors of P13K pi 10 delta (Br. 10) does
not derogate from the fact that it teaches a selective inhibitor of P13K pi 10
delta that would result in selective inhibition ofP13Kpll0 delta. Indeed,
Diacovo teaches the same selective inhibitor of P13K pi 10 delta disclosed
for use that Appellants disclosed and claim, i.e., IC87114. (See, e.g., Spec.
27.)
We also do not find the argument that Bengtsson does not “teach the
inhibition of PI3K delta” (Br. 11, 13, 14) persuasive of nonobviousness.
“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.” In re Merck &
Co., 800 F.2d 1091, 1097 (Fed. Cir. 1986). And, “[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).
That Diacovo also teaches selective inhibition of PI 3K pi 10 gamma
in addition to P13K pi 10 delta, does not teach away from the claimed
invention (Br. 13). “The transition ‘comprising’ in a method claim indicates
that the claim is open-ended and allows for additional steps.” Invitrogen
Corp. v. Biocrest Mfg., L.P., 327 F.3d 1364, 1368 (Fed. Cir. 2003).
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Application 13/418,045
Appellants’ method claims use the open ended transition phrase
“comprising” and thus do not preclude the additional administration of a
selective inhibitor of P13K pi 10 gamma.
As discussed, one of ordinary skill in the art need not have a
reasonable expectation of success of inhibiting viral replication in order to
make the Examiner’s combination. PAR Pharm., 773 F.3d at 1197. For the
reasons discussed above, Appellants’ arguments are unpersuasive to
establish that there would not have been a reasonable expectation of success
of treating inflammation due to avian flu virus with IC87114.
For the foregoing reasons, we are not persuaded that the Examiner
erred in maintaining the obviousness rejection of claims 27, 33, and 39.
Claims 30, 32, 36—38, and 42 44 have not been argued separately (Br.
15—17 (noting that the dependent claims are not obvious “[f]or the same
reasons set forth above regarding” the independent claims 27, 33, and 39)),
and therefore fall with claims 27, 33, and 39. 37 C.F.R. § 41.37(c)(l)(iv).
SUMMARY
We affirm the rejection of claims 27, 30-33, 36—39, and 42 44 under
35 U.S.C. § 103(a) as unpatentable over Diacovo, Bengtsson, Gruber, and
Carter.
TIME PERIOD FOR RESPONSE
No time period for taking any subsequent action in connection with
this appeal may be extended under 37 C.F.R. § 1.136(a).
AFFIRMED
15