Kite Pharma, Inc. v. Sloan-Kettering Institute

Case: 17-1647 Document: 1-1 Page: 1 Filed: 02/17/2017
UNITED STATES COURT OF APPEALS FOR THE FEDERAL CIRCUIT
NOTICE OF DOCKETING
17-1647 - Kite Pharma, Inc. v. Sloan-Kettering Institute
Date of docketing: February 17, 2017
Appeal from: Patent and Trademark Office - Patent Trial and Appeal Board in Inter Partes Review No. IPR2015-
01719
Appellant(s): Kite Pharma, Inc.
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Peter R. Marksteiner
Clerk of Court
cc: Office of the Solicitor, US Patent and Trademark Office

Eldora Ellison
Michael Richard Fleming
ELDORA L. ELLISON
DIRECTOR
(202) 7728508
EELLISON@SKGF.COM
February 16, 2017
Peter R. Marksteiner Via CM/ECF

Circuit Executive & Clerk of Court
U.S. Court of Appeals for the Federal Circuit
717 Madison Place Northwest, Suite 401
Washington, D.C. 20439
Re: Notice of Appeal; PTAB Case No. IPR2015-01719
Dear Mr. Marksteiner:
Enclosed please find the following documents for filing:
1. The Appellants Notice of Appeal including Appellants Petition for Review (Fed.
Cir. Form 5) pursuant to 35 U.S.C. 141(c), 319; 37 C.F.R. 90.3(a); Fed. R.
App. P. 15; and Fed. Cir. R. 15;
2. The Final Written Decision, dated December 16, 2016 (Paper No. 72) being
appealed;
3. Certificate of Service; and
4. USPTO stamped postcard.
Pursuant to Federal Circuit Rules of Practice and Procedure 46(c) and 52(a) and (c), the
docketing fees for this appeal are being paid to the Court via Pay.gov.
Respectfully submitted,
STERNE, KESSLER, GOLDSTEIN & FOX P.L.L.C.
/s/ Eldora L. Ellison
Eldora L. Ellison
Attorney for Kite Pharma, Inc.
ELE/dbm
Enclosures
Form 5
FORM 5. Petition for Review or Notice of Appeal of an Order or Decision of an AGENCY, BOARD,
COMMISSION, OFFICE OR BUREAU.
United States Court of Appeals for the Federal Circuit
Kite Pharma, Inc.

_________________________, Petitioner or Appellant,
v. PETITION FOR REVIEW

Sloan-Kettering Institute for Cancer Research
_________________________, Respondent or Appellee.
Kite Pharma, Inc. hereby appeals the Court for review of the Final Written
Decision, Paper No. 72, of the USPTO, Patent Trial and Appeal Board in Inter Partes
Review No. IPR2015-01719 entered on December 16, 2016.
/s/ Eldora L. Ellison

_______________________________
Eldora L. Ellison
Sterne, Kessler, Goldstein & Fox P.L.L.C
1100 New York Avenue, NW
Washington, DC 20005
Phone: (202) 772-8508
Fax: (202) 371-2540
*See Fed. R. App. P. 15 for permissible ways of identifying petitioners.
113
UNITED STATES PATENT AND TRADEMARK OFFICE

_____________________
BEFORE THE PATENT TRIAL AND APPEAL BOARD

_____________________
KITE PHARMA, INC.

Petitioner
v.
SLOAN-KETTERING INSTITUTE
FOR CANCER RESEARCH
Patent Owner
_____________________
CASE IPR2015-01719
Patent 7,446,190
_____________________
KITE PHARMA, INC.'S NOTICE OF APPEAL
via PTAB E2E

Patent Trial and Appeal Board
via Hand Carry

Director of the United States Patent and Trademark Office
c/o Office of the General Counsel, 10B20
Madison Building East
600 Dulany Street
Alexandria, VA 22314
via CM/ECF
IPR2015-01719
Patent 7,446,190
Pursuant to 37 C.F.R. 90.2(a), notice is hereby given that Petitioner Kite
Pharma, Inc. ("Kite") hereby appeals to the United States Court of Appeals for the
Federal Circuit from the Final Written Decision of the Patent Trial and Appeal
Board entered on December 16, 2016, in case IPR2015-01719, Paper 72, and from
all underlying findings, orders, decisions, rulings, and opinions. This notice is
timely filed within 63 days of the Board's Final Written Decision. 37 C.F.R.
90.3(a)(l).
In accordance with 37 C.F.R. 90.2(a)(3)(ii), Kite indicates that the issues
on appeal include, but are not limited to, the Board's determinations with respect to
(i) patentability of claims 1-13 of U.S. Patent No. 7,446,190 ("the '190 Patent")
over the art, (ii) dismissal of Kite's Motion to Exclude Evidence, and (iii) its
findings supporting or relating to the aforementioned issues.
Kite also indicates that the issues on appeal include any other issues decided
adversely to Petitioner in any orders, decisions, rulings, or opinions issued in the
IPR proceeding.
A copy of this Notice of Appeal is being filed with the Patent Trial and
Appeal Board as well as with the Director of the United States Patent and
Trademark Office in accordance with 37 C.F.R. 90.2(a)(1). In addition, this
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Patent 7,446,190
Notice of Appeal and the required fee are being submitted to the Clerk's Office for
the United States Court of Appeals for the Federal Circuit.
Respectfully submitted,
/Eldora L. Ellison/
Date: February 16, 2017 Eldora L. Ellison
1100 New York Avenue, N.W. Registration No. 39,967
Washington, D.C. 20005-3934 Lead Attorney for Petitioner Kite Pharma, Inc.
(202) 371-2600
2
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Patent No. 7,446,190
CERTIFICATE OF SERVICE (37 C.F.R. 42.6(e))
The undersigned hereby certifies that on February 16, 2017, a true and
correct copy of the above-captioned "Kite Pharma, Inc.'s Notice of Appeal" was
filed electronically through the Patent Trial and Appeal Boards E2E System and
was filed with the Director of the United States Patent and Trademark office c/o
the Office of General Counsel via hand delivery to the following address:
Director of the United States Patent and Trademark Office

c/o Office of the General Counsel
United States Patent and Trademark Office
Madison Building East, Room 10B20
600 Dulany Street
Alexandria, VA 22314
The undersigned hereby also certify that on February 16, 2017, a true and
correct copy of the above-captioned "Kite Pharma, Inc.'s Notice of Appeal" was
filed electronically with the Clerks Office of the United States Court of Appeals
for the Federal Circuit via CM/ECF.
The undersigned hereby further certifies that the above-captioned "Kite
Pharma, Inc.'s Notice of Appeal" was served in its entirety on February 16, 2017,
upon the following parties via electronic mail upon the following counsel of record
for the Patent Owner:
Andrei Iancu (Lead Counsel)

Michael Fleming (Back-Up Counsel)
Morgan Chu (Back-Up Counsel)
Alan Heinrich (Back-Up Counsel)
IPR2015-01719
Patent 7,446,190
Elizabeth Tuan (Back-Up Counsel)

IRELL & MANELLA LLP
1800 Avenue of the Stars, Suite 900
Los Angeles, CA 90067-4276
KiteMSKIPR@irell.com
/Eldora L. Ellison/
Eldora L. Ellison, Ph.D.
Registration No. 39,967
Lead Attorney for Petitioner
Date: February 16, 2017

1100 New York Avenue, N.W.
Washington, D.C. 20005
(202) 371-2600
4971201
Trials@uspto.gov Paper 72
571-272-7822 Entered: December 16, 2016
UNITED STATES PATENT AND TRADEMARK OFFICE

____________
BEFORE THE PATENT TRIAL AND APPEAL BOARD

____________
KITE PHARMA, INC.,

Petitioner,
v.
SLOAN KETTERING INSTITUTE FOR CANCER RESEARCH,

Patent Owner.
____________
Case IPR2015-01719
Patent 7,446,190 B2
____________
Before RAMA G. ELLURU, TINA E. HULSE, and

ELIZABETH A. LAVIER, Administrative Patent Judges.
LAVIER, Administrative Patent Judge.
FINAL WRITTEN DECISION

35 U.S.C. 318(a) and 37 C.F.R. 42.73
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Patent 7,446,190 B2
I. INTRODUCTION
Petitioner, Kite Pharma, Inc. (Kite), filed a Petition requesting an
inter partes review of claims 113 of U.S. Patent No. 7,446,190 B2 (the
190 patent; Ex. 1001), all the claims in the patent. Paper 2 (Pet.). Patent
Owner, Sloan Kettering Institute for Cancer Research (Sloan), filed a
Preliminary Response. Paper 7 (Prelim. Resp.). We instituted an inter
partes review of the challenged claims, on the three grounds of
unpatentability set forth in the Petition. Paper 8 (Dec. Inst.). Sloan filed a
Response to the Petition. Paper 20 (PO Resp.). Kite filed a Reply to the
Response. Paper 31 (Pet. Reply).
Both parties filed motions to exclude certain exhibits and testimony.
Paper 46 (Kite); Paper 52 (Sloan). Both parties opposed the others motion
to exclude. Paper 56 (Kite); Paper 57 (Sloan). And both parties filed reply
briefs in support of their motions to exclude. Paper 58 (Sloan); Paper 59
(Kite). Sloan also filed Motions for Observation on certain cross-
examination testimony of Kites declarants (Papers 4749), to which Kite
filed Responses (Papers 6062).
An oral hearing occurred on October 20, 2016, a transcript of which
has been entered in the record.1 Paper 71 (Tr.).
1
Kite filed Objections to Sloans Demonstrative Exhibits. Paper 70. In this
Final Written Decision, we rely directly on the arguments presented properly
in the parties briefs and the evidence of record. The demonstrative exhibits
are considered only to the extent they are consistent with those arguments
and evidence.
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We have jurisdiction under 35 U.S.C. 6. This Final Written

Decision is issued pursuant to 35 U.S.C. 318(a) and 37 C.F.R. 42.73.
For the reasons that follow, we determine that Kite has not shown by a
preponderance of the evidence that claims 113 of the 190 patent are
unpatentable.
A. The 190 patent

The 190 patent is titled Nucleic Acids Encoding Chimeric T Cell
Receptors. Ex. 1001, at [54]. The 190 patent explains that genetic
engineering of T lymphocytes to express artificial TCRs [(T cell receptors)]
that direct cytotoxicity toward tumor cells is a promising approach for
enhanc[ing] immune recognition and elimination of cancer cells. Ex.
1001, 1:2933. Specifically, the 190 patent describes engineered (i.e.,
chimeric) TCRs that are formed by combining, in a single molecule, an
activation signaling region (from CD3 (also known as the TCR -chain)), a
costimulatory signaling region (from, e.g., CD28), and a binding element for
specific interaction with a selected target. See id. at 2:1418. The 190
patent identifies P28Z as a chimeric TCR in accordance with the
invention. Id. at 5:2829. P28Z is the second chimeric TCR from the left
depicted in Figure 2 (annotated to highlight P28Z (solid line) and P28
(dotted line)), shown below:
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Annotated Figure 2 of the 190 patent diagrams a series of chimeric

TCRs. 2 Id. at 2:42. P28, a control species, includes the intracellular,
transmembrane and much of the extracellular portions of CD28. Id. at
5:2628. The CD28 portion of P28 can be amplified from nucleotides 336
660 of human CD28 cDNA using primers listed in the 190 patent as SEQ
ID NO: 4 and 5, to produce the full sequence SEQ ID NO: 6. See id. at
4:2128, 7:5156; see also id., Certificate of Correction (correcting SEQ ID
NO: 6). The 190 patent states that its most important finding is that the
expression of P28z enables T cells to undergo repeated rounds of antigen-
dependent stimulation and expansion. Ex. 1001, 5:5861.
2
For reference, each of the four chimeric TCRs depicted in Figure 2
includes an scFV (single-chain variable fragment) specific for PSMA
(prostate-specific membrane antigen). See Ex. 1001, 5:2123, 7:4345.
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B. Illustrative Claim
Claim 1 is the only independent claim of the challenged claims, and is
illustrative of the claimed subject matter:
1. A nucleic acid polymer encoding a chimeric T cell receptor,
said chimeric T cell receptor comprising
(a) a zeta chain portion comprising the intracellular domain of
human CD3 chain,
(b) a costimulatory signaling region, and
(c) a binding element that specifically interacts with a selected
target,
wherein the costimulatory signaling region comprises the amino
acid sequence encoded by SEQ ID NO:6.
Ex. 1001, 25:3038 (some formatting added).
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C. Grounds of Unpatentability Instituted for Trial

We instituted trial based on the following grounds of unpatentability:
Ground Claims Basis References

Krause, 4 Finney, 5 and
1 13, 69, 12, 13 103(a)3
Aruffo 6
Krause, Finney, Aruffo,
2 4, 10 103(a)
and Gong7
Krause, Finney, Aruffo,
3 5, 11 103(a)
and Bejcek8
3
The relevant sections of the Leahy-Smith America Invents Act (AIA),
Pub. L. No. 11229, took effect on March 16, 2013. Because the application
from which the 190 patent issued was filed before that date, our citations to
Title 35 are to its pre-AIA version.
4
Krause et al., Antigen-dependent CD28 Signaling Selectively Enhances
Survival and Proliferation in Genetically Modified Activated Human
Primary T Lymphocytes, 188 J. EXP. MED. 61926 (1998) (Ex. 1002).
5
Finney et al., Chimeric Receptors Providing Both Primary and
Costimulatory Signaling in T Cells from a Single Gene Product, 161 J.
IMMUNOL. 279197 (1998) (Ex. 1003).
6
Aruffo & Seed, Molecular Cloning of a CD28 cDNA by a High-Efficiency
COS Cell Expression System, 84 PNAS USA IMMUNOL. 857388 (1987)
(Ex. 1012).
7
Gong et al., Cancer Patient T Cells Genetically Targeted to Prostate-
Specific Membrane Antigen Specifically Lyse Prostate Cancer Cells and
Release Cytokines in Response to Prostate-Specific Membrane Antigen, 1
NEOPLASIA 12327 (1999) (Ex. 1004).
8
Bejcek et al., Development and Characterization of Three Recombinant
Single Chain Antibody Fragments (scFvs) Directed against the CD19
Antigen, 55 CANCER RES. 234651 (1995) (Ex. 1016).
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II. CLAIM CONSTRUCTION

In our decision instituting inter partes review, we determined it was
not necessary to construe expressly any of the claim terms. Dec. Inst. 6.
Upon consideration of the full record, express construction remains
unnecessary. See Vivid Techs., Inc. v. Am. Sci. & Engg, Inc., 200 F.3d 795,
803 (Fed. Cir. 1999) (noting claim terms require construction only to the
extent necessary to resolve the controversy). Indeed, neither the Response
nor the Reply directly addresses claim construction, and the parties did not
focus on claim construction issues during the oral hearing.
III. OBVIOUSNESS
A claim is unpatentable for obviousness if, to one of ordinary skill in
the pertinent art, the differences between the subject matter sought to be
patented and the prior art are such that the subject matter as a whole would
have been obvious at the time the invention was made. 35 U.S.C. 103(a)
(2006); see also KSR Intl Co. v. Teleflex Inc., 550 U.S. 398, 40607 (2007).
The question of obviousness is resolved on the basis of underlying factual
determinations including: (1) the scope and content of the prior art; (2) any
differences between the claimed subject matter and the prior art; (3) the level
of ordinary skill in the art; and (4) objective evidence of nonobviousness.
Graham v. John Deere Co., 383 U.S. 1, 1718 (1966).
If all the claimed elements are present in the prior art references, the
obviousness inquiry turns to the combination of those references:
[P]roper analysis under 103 requires, inter alia, consideration
of two factors: (1) whether the prior art would have suggested to
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those of ordinary skill in the art that they should make the
claimed composition or device, or carry out the claimed process;
and (2) whether the prior art would also have revealed that in so
making or carrying out, those of ordinary skill would have a
reasonable expectation of success.
Par Pharm., Inc. v. TWI Pharms., Inc., 773 F.3d 1186, 1196 (Fed. Cir. 2014)
(quoting Medichem, S.A. v. Rolabo, S.L., 437 F.3d 1157, 1164 (Fed. Cir.
2006)).
A. Level of Ordinary Skill in the Art

The parties generally agree9 that one of ordinary skill in the art at the
time of the invention 10 would have had an advanced degree in immunology,
cell biology, biochemistry, molecular biology, or a related discipline, along
with knowledge and experience in the field of T cell research, including
laboratory techniques. See Pet. 3334 (citing Ex. 1008 11 12); PO Resp. 9
(citing Ex. 202212 25; Ex. 1008 12). In light of the parties general
agreement on this point, we adopt that description of the level of ordinary
9
However, Sloan disputes (see PO Resp. 9) Kites assertion that one of
ordinary skill in the art would have taken advantage of certain specialized
skills while working as part of a team (Pet. 34). As these specialties (see
Pet. 34 ([f]or example, an immunologist, a cell biologist, and a clinical
oncologist)) are in disciplines within the ambit of the relevant art of T cell
research, we discern no meaningful distinction in the parties positions on
this issue.
10
The application leading to the 190 patent was filed on May 28, 2003. Ex.
1001, at [22].
11
Declaration of Professor Hinrich Abken, M.D. (Ex. 1008).
12
Declaration of Professor Thomas Brocker, Ph.D. (Ex. 2022).
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skill in the art. In our analysis, we consider the applied prior art as
representative of the level of ordinary skill. See Okajima v. Bourdeau,
261 F.3d 1350, 1355 (Fed. Cir. 2001).
B. Overview of Cited Art

Each of the three grounds of unpatentability upon which we instituted
this review relies on a combination of Krause, Finney, and Aruffo. See Pet.
16. Kite adds Gong and Bejcek for Grounds 2 and 3, respectively. See id.
1. Krause
Krause describes a chimeric CD28 construct specific for GD2, a
molecule overexpressed on the surface neuroblastoma and other human
tumor cells. Ex. 1002, 619. Krause shows that this construct, called 3G6-
CD28, provides CD28 signaling upon specific recognition of the GD2
antigen on tumor cells, and further demonstrates selective expansion of
CD8+ lymphocytes expressing 3G6-CD28 when cultured with cells
expressing allogeneic major histocompatibility complex [(MHC)] class I
together with GD2. Id. Thus, Krause focuses on inducing the CD28-
mediated costimulatory signal. See id. at 619620, 624. Krause does not
indicate that the 3G6-CD28 construct contains CD3 specifically, or any
other TCR complex-related sequence. Rather, for the primary T-cell
activation signal, Krause relies on co-culturing its 3G6-CD28-expressing
cells with cells expressing MHC class I together with GD2. Id. at 620.
For its construct, Krause uses the portion of the CD28 comprising
part of the extracellular, the transmembrane, and the cytoplasmic domains.
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Id. at 620. More specifically, Krause provides primers for amplifying the
CD28 coding sequence from isolated RNA using reverse transcription PCR,
and states that the amplified region runs from nucleotides 336 to 663 of
human CD28. See id. Notably, the 190 patent cites Krause (as well as
another paper with the same primary author) as describing the portion of
CD28 used in the P28 and P28Z constructs. See Ex. 1001, 7:5156.
2. Finney
Finney describes chimeric receptors that feature intracellular
sequences comprising the signaling region of CD28 in series with the
signaling region of the -chain[13] from the TCR complex. Ex. 1003, 2792.
Finney states that [t]hese constructs represent the first of a new generation
of single gene multidomain chimeric receptors capable of mediating both
primary and costimulatory signaling specifically from a single extracellular
recognition event. Id. at 2791. Finneys experimental constructs feature
sequences derived from an scFv extracellular antibody binding site, followed
by one of two spacer sequences (h.28 and G1), followed by a linker,
followed by sequences derived from the intracellular domain of CD3 and
the intracellular and transmembrane domains of CD28. Id. at 2792. In some
constructs, the CD28 sequence is proximal to the cell membrane; in others,
the CD3 sequence is proximal. See id.
13
Unless quoting from Finney or another source, we use the CD3
nomenclature for consistency. The terms are interchangeable, as noted
above.
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Finney further reports that constructs containing the h.28 spacer are
more efficient than constructs with the G1 spacer in mediating IL-2
production in the same assays. See id. at 2791 (Abstract), 279495
(discussing Figure 3). Both spacers include sequences from human IgG1
hinge, but h.28 also includes part of the extracellular region of human
CD28. Id. at 2793. In contrast, G1 includes human IgG1 as well as CH2
and CH3 sequences (but not any sequence from CD28). 14 Id.
3. Aruffo
Aruffo reports the successful cloning of human CD28 cDNA, and
provides the nucleotide sequence. Ex. 1012 (see especially Fig. 2).
4. Gong
Gong discloses a chimeric TCR with a binding region specific for
prostate-specific membrane antigen (PSMA), a glycoprotein expressed on
prostate cancer cells and other tumor cells. Ex. 1004, 123 (Abstract). Gong
reports that T cells transduced with Gongs construct successfully lyse
prostate cancer cells. Id.
5. Bejcek
Bejcek demonstrates cloning, expression, and binding of anti-CD19
single chain antibody fragments. Ex. 1016, 2346 (Abstract).
14
Immunoglobulin G1 (IgG1) is a subclass of antibodies found in humans.
CH2 and CH3 are constant domains of the heavy chain of the antibody.
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C. Ground 1
Kite asserts that claims 13, 69, 12, and 13 are unpatentable because
they would have been obvious over the combination of Krause, Finney, and
Aruffo. Pet. 3451. Sloan does not appear to dispute that the combination
of cited references teaches each of the claim elements. Rather, Sloan argues
Kite has not sufficiently established a rationale for combining the references,
or that one of ordinary skill in the art would have had a reasonable
expectation of success in doing so. See PO Resp. 943. Sloan also argues
that the objective evidence of nonobviousness in this case is
overwhelming. See id. at 4861.
Kite offers three alternative rationales for combining Krause, Finney,
and Aruffo: (1) starting with Krauses construct (with the CD28 sequence as
provided in Aruffo), and adding Finneys CD3 to it (see Pet. 3840); (2)
starting with Finneys chimeric TCR, and replacing its CD28 region with
Krauses CD28 region (with the CD28 sequence as provided in Aruffo) (see
id. at 4045); and (3) routine optimization of Finney, with guidance from
Krause and Aruffo (see id. at 4546).
As explained below, we find none of these rationales to be persuasive.
Accordingly, we conclude that Kite has not carried its burden to prove, by a
preponderance of the evidence, that claims 13, 69, 12, and 13 are
unpatentable as obvious over Krause, Finney, and Aruffo.
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1. Rationale 1: Add Finneys CD3 to Krauses Chimeric T Cell

Receptor
Kite first argues that an ordinarily skilled artisan focused on the GD2
cancer target in Krause would have been motivated to make a chimeric
TCR that included the CD3 domain disclosed in Finney together with the
binding element and CD28 region Krause teaches, to achieve a chimeric
TCR with both a primary and a costimulatory domain in a single chimeric
receptor. Pet. 38 (citing Ex. 1008 93102). However, the purported
advantages Kite asserts (see id. at 3840) are all advantages taught by
Finney alone (i.e., the advantages of a dual-signaling chimeric T cell
receptor over using two separate constructs), as applied to a GD2 target. That
is, Kite does not proffer any rationale for using Krauses CD28 sequence
rather than Finneys. Using either CD28 sequence would yield the general
advantages of a dual-signaling chimeric TCR noted in rationale (1) by Kite,
but only the combination including Krauses CD28 sequence, not Finneys,
would be within the scope of the challenged claims of the 190 patent.
Central to any allegation of obviousness is that the proponent must
establish that the prior art renders the invention obvious as claimed. Cf.
KSR, 550 U.S. at 418 (discussing various considerations important in
determining whether there was an apparent reason to combine the known
elements in the fashion claimed by the patent at issue). Here, Kites
rationale (1), as presented in the Petition, does not distinguish expressly
between the advantages of Krauses CD28 sequence versus Finneys, or
explain why one of ordinary skill in the art, in developing a dual-signaling
chimeric TCR to target GD2, would have been motivated to retain Krauses
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CD28 sequence over Finneys when combining the two references.

Accordingly, rationale (1) is deficient on its face. However, if we impute
the alleged advantages of Krauses CD28 sequence as discussed with respect
to rationales (2) and (3) to rationale (1),15 then rationale (1) rises or falls
with rationale (2).16
2. Rationale 2: Replacement of Finneys CD28 Sequence with Krauses

CD28 Sequence
Second, Kite argues that an ordinarily skilled artisan focused on
Finneys CD33 cancer target would have had a reason to replace Finneys
CD28 region[17] in Finneys chimeric TCR with Krauses CD28 region,
which is longer than Finneys, specifically because they would have
expected Krauses CD28 region to offer advantages with respect to signal
transduction and cell surface expression levels. Pet. 40 (citing Ex. 1003,
2793, Fig. 2, 2794, Fig. 3A; Ex. 1008, 103108). And although Kites
proposed combination uses the CD28 region from Krause, not Finney, Kite
15
Kite appears to take this approach in its Reply, discussing these
advantages in the context of rationale (1). See Pet. Reply 1114.
16
As we discuss below, rationale (3) is not meaningfully distinct from
rationale (2).
17
The phrase Finneys CD28 region is somewhat vague absent additional
context because, as discussed above, Finney discloses constructs with one of
two spacer sequences, only one of which (h.28) includes extracellular CD28
sequence. By Finneys CD28 region, we understand Kite to mean the
extracellular CD28 sequence from the h.28 spacer plus the transmembrane
and intracellular CD28 sequence from the CD28 cassette. See Ex. 1002,
2793; Pet. 22; Pet. Reply 18 (Figure 4); Tr. 28:1925.
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argues that Finney itself shows the benefits of including additional

extracellular CD28 sequence in a chimeric TCR, because Finneys
construct with a longer CD28 region resulted in more cell surface
expression and IL-2 production as compared to the construct with less
CD28 sequence. Id. at 42.
Further, Kite asserts (see Pet. 4042; see also Pet. Reply 1520) that
the extracellular CD28 sequence of Krause includes particularly
advantageous features: the MYPPPY motif,18 and the adjacent LDN
motif, 19 neither of which is present in Finneys extracellular CD28 sequence
(see Ex. 1008 7475). Kite cites a study by Kariv et al.20 discussing the
significance of the MYPPPY and LDN motifs to CD28 expression and IL-2
18
MYPPPY is the sequence of single-letter amino acid codes representing
Methionine-Tyrosine-Proline-Proline-Proline-Tyrosine. See Ex. 1010, 390.
As Krause does not include full sequence data, Krause does not expressly
mention the MYPPPY motif. Rather, Dr. Abken deduces the inclusion of
the MYPPPY motif in Krause from Krauses primers and the full CD28
sequence disclosed in Aruffo. See Ex. 1008 74. Sloan does not dispute
that Krauses CD28 region includes the MYPPPY motif.
19
LDN is the sequence of single-letter amino acid codes representing
Leucine-Aspartic acid-Asparagine. Cf. Ex. 1006, 32. As with the MYPPPY
motif, Krause does not expressly mention the LDN motif, but Dr. Abken
deduces its inclusion in Krauses extracellular CD28 sequence from
Krauses primers and Aruffos sequence. See Ex. 1008 74. Sloan does not
dispute that Krauses CD28 region includes the LDN motif adjacent to the
MYPPPY motif.
20
Kariv et al., Analysis of the Site of Interaction of CD28 with Its Counter-
receptors CD80 and CD86 and Correlation with Function, 157 J. IMMUNOL.
2938 (1996) (Ex. 1006).
15
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Patent 7,446,190 B2
production. See Pet. 2930 (citing Ex. 1006); see also id. at 4042 (same).
According to Kite, the MYPPPY motif of CD28 was known to be highly
conserved across many species, i.e., virtually identical when compared
among human, mouse, rat, and even chicken, indicating that it may have an
important role in ligand binding and/or signal transduction. Id. at 29
(quoting Ex. 1010,21 390 (emphasis added in Petition)). Kite notes that
amino acids immediately adjacent to the MYPPPY motif, i.e., the LDN
motif, were thought to be required for full surface-level expression of CD28.
Id. at 30 (citing Ex. 1006, 36, Fig. 6; Ex. 1008 75). Accordingly, Kite
argues that one of ordinary skill in the art would have been motivated to
replace Finneys CD28 region with Krauses (which has a longer
extracellular domain, including the MYPPPY and LDN motifs) to improve
both signal transduction and cell surface expression. Id. at 4041; see also
id. at 42 (discussing the benefit of longer CD28 regions).
We do not find Kites analysis to be persuasive, for the reasons
outlined below.
a. Finney Does Not Teach or Suggest that Longer CD28 Sequences Are
Better than Shorter Ones
Kites thesis that longer CD28 regions would be considered
advantageous over shorter ones is not supported by the cited prior art.
Although Kite is correct that Finneys chimeric TCR containing a longer
21
Greenfield et al., CD28/B7 Costimulation: A Review, 18 CRITICAL
REVIEWS IN IMMUNOLOGY 389, 390 (1998) (Ex. 1010).
16
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Patent 7,446,190 B2
region of CD28 performed better than the chimeric TCR with less CD28
sequence (Pet. 42), this statement ignores other differences between
Finneys constructs. As discussed above, Finney teaches constructs
containing one of two spacers, h.28 or G1. Only the h.28 spacer includes
extracellular CD28 sequence; the G1 spacer itself contains no CD28
sequence at all. See Ex. 1003, 2792. However, the two spacers further
differ from each other insofar as the G1 spacer includes human IgG1, CH2
and CH3 sequences, but the h.28 spacer does not. Id. Ultimately, as Sloan
points out, the G1 spacer is 218 amino acids longer than the h.28 spacer.
PO Resp. 13 (citing Ex. 1003, 2793; Ex. 2022 114, 194; Ex. 2021,
188:1013).
Kite does not acknowledge these other differences between Finneys
spacers in the Petition, and this omission undercuts the persuasiveness of
Kites argument. In its Reply, Kite includes a substantive discussion of the
h.28 and G1 spacers, but relies almost exclusively on its experts analyses to
brush aside the other distinctions, concluding that a POSA would have
viewed Finneys constructs as differing essentially in only one way: the
length of the CD28 sequence. Pet. Reply 19 (citing Ex. 1032 22 56; Ex.
1033 23 46). Also, Kite characterizes Sloan as allegedly conced[ing] that
the G1 spacer was inert, [and] non-signaling. Pet. Reply 18 (quoting PO
Resp. 23). But this misses Sloans point, which is that neither the h.28 nor
22
Second Declaration of Dr. Abken (Ex. 1032).
23
Declaration of Professor Jrgen Bajorath, Ph.D. (Ex. 1033).
17
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Patent 7,446,190 B2
the G1 spacer contains binding domains. Kites incomplete representation

of Sloans position is clear when the quoted passage is considered in
context:
Skilled artisans also used spacer domains derived from CD8,
CD7, and CD4, also found on T cells. See KIT1004, 124; Ex.
2015, 102; Ex. 2030, 183; Ex. 2031, 1669; Ex. 2032, 720; Ex.
2033, 412-413; Ex. 2023, 4319. None of these spacers contained
the ligand-binding domain of the protein from which it derived,
but rather comprised the inert, non-signaling portions of the
proteins constant-like domain. Ex. 2022, 160. Finneys h.28
and G1 spacers likewise contained no portion of the specific
binding domains of CD28 or the IgG1, respectively. Ex. 1003,
2792-93; Ex. 2022, 161. The CH2 and CH3 domains are inert
constant regions within the immunoglobulin. Ex. 2022, 42.
PO Resp. 23. In other words, Sloan argues that Finneys spacers, like other
spacers known in the art, were meant to be non-signaling and otherwise
inert. Accordingly, Sloans argument is consistent with Finneys stated
purpose for its spacer sequences: [s]pacers are used to distance the
extracellular binding domain from the membrane (Ex. 1003, 2792).
To be sure, Finney reports superior results for constructs with the h.28
spacer instead of the G1 spacer. See, e.g., id. at 2793 (The presence of the
CD28 extracellular spacer resulted in greater expression of the CD28-
signaling sequence than did the G1 spacer.), 2795 (Again the h.28 spacer
was more efficient than the G2 spacer at mediating IL-2 production.).
However, as Sloan notes, Finney never compar[es] the relative lengths of
CD28 regions or suggest[s] advantages of longer CD28 regions. PO
Resp. 3. Thus, the ordinarily skilled artisan, reading Finney, would
18
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Patent 7,446,190 B2
appreciate that the h.28 spacer was superior to the G1 spacer, but would not
have attributed that superiority to the presence of extracellular CD28
sequence in the h.28 spacer. Further, we agree with Sloan (see PO Resp.
1516) that even if the ordinarily skilled artisan had attributed some value to
the extracellular CD28 sequence in the h.28 spacer, there would have been
no reason to expect that even more extracellular CD28 sequence would yield
further improvements. As Finney includes only one spacer (h.28)
comprising extracellular CD28 sequence, there is no trend from which one
could extrapolate the relative value of differing extracellular CD28 lengths.
Furthermore, to add more extracellular CD28 sequence would risk adding
binding domains (as discussed further below), contrary to Finneys stated
purpose of the spacer to simply provide distance between the constructs
intended extracellular binding domain and the cell membrane.
b. The Prior Art Does Not Teach or Suggest that Inclusion of the MYPPPY
and/or LDN Motifs Would Have Been Advantageous
We are also not persuaded that one of ordinary skill in the art would
have considered the inclusion of more extracellular CD28 sequence,
particularly the MYPPPY and LDN motifs, to be advantageous in designing
a chimeric TCR.
As discussed above, none of Finneys constructs includes the
MYPPPY or LDN motifs. Krauses construct does, but Krause does not
emphasize (or even acknowledge) this fact. As Sloan points out, [n]either
Krause nor Finney even suggested a signaling role for any extracellular
CD28 portion. PO Resp. 18 (citing Ex. 1003, 2792; Ex. 1002, 623).
19
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Patent 7,446,190 B2
Rather, Krause characterizes its data as strongly suggest[ing] that the

costimulatory signal is dependent on the cytoplasmic domain of CD28
(Ex. 1002, 623), i.e., not the extracellular domain.
Kariv, on which Kite relies, calls the MYPPPY motif a key site of
common and selective recognition for CD28. Ex. 1006, Abstract. More
specifically, Kariv reports that the majority of substitutions and deletions in
the MYPPPY motif abrogate binding to both receptors, while retaining cell
surface reception, and also notes that the adjacent LDN residues also
contribute to this site of interaction. Ex. 1006, 35. Kite argues that Kariv
supports the motivation to include the MYPPPY and LDN motifs in a
chimeric TCR construct because Karivs studies show that mutations in the
MYPPPY motif dramatically reduced the CD28 proteins ability to signal
the release of IL-2 by T cells and that mutations in the LDN motif
decreased CD28 expression on the cell surface of T cells, indicating that
this adjacent region is required for full protein expression. Pet. 2930
(citing Ex. 1006, 3637, Figs. 6, 7; Ex. 1008 7475). But these
arguments only serve to support the general importance of the MYPPPY
motif to CD28 function; they do not provide specific support for the
proposition that the MYPPPY motif is important in signal transduction. Put
differently, we agree with Sloan and credit the testimony of Dr. Brocker that
Karivs mutational analyses do not indicate whether the MYPPPY and/or
LDN motifs would have been important for signal transduction decoupled
from binding to a natural ligand, i.e., in the case of a chimeric TCR with an
20
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Patent 7,446,190 B2
artificial binding domain not reliant on natural ligand binding to CD28. See
PO Resp. 20; Ex. 2022 82, 13444.
Kites reliance on Greenfield suffers from the same problem, insofar
as Greenfield addresses the importance of the MYPPPY motif in ligand
binding and/or signal transduction (Pet. 29 (quoting Ex. 1010, 390
(emphasis added in Petition))), and its cross-species conservation (id.). The
and/or in Greenfields sentence indicates that the MYPPPY motif was
thought to have been important for ligand binding or signal transduction or
both. Greenfield thus stands for the proposition that the MYPPPY motif is
important for endogenous CD28 function; it is silent as to the potential role,
if any, of the MYPPPY motif in the absence of natural ligand binding to
CD28.
In sum, the prior art references cited by Kite in the Petition that
expressly address the MYPPPY and/or LDN motifs, i.e., Kariv and
Greenfield, show that these sequences are important to CD28 function
generally. Further, Kariv provides evidence that the MYPPPY and LDN
motifs are important for ligand binding. However, these references shed no
light upon what role the MYPPPY and/or LDN motifs would play if natural
CD28 ligand binding is bypassed, as would be the case in a dual-signaling
chimeric TCR. Accordingly, Kites argument, that one of ordinary skill in
the art would have been motivated to include more extracellular CD28
sequence including the MYPPPY and LDN motifs in designing a chimeric
TCR, is not supported sufficiently by Kariv or Greenfield.
21
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Patent 7,446,190 B2
c. The Prior Art Teaches Away from Inclusion of the MYPPPY Motif in a
Chimeric TCR
The foregoing subsections provide a sufficient basis on which to
conclude that Kite has not carried its burden of persuasion as to Ground 1.
However, there is an additional, related reason that further supports this
conclusion, namely that the prior art teaches away from the claimed
combination. More specifically, not only does the prior art fail to provide a
motivation to include the MYPPPY motif in a dual-signaling chimeric TCR
(as discussed above), we find that the prior art would have discouraged the
ordinarily skilled artisan from doing so.
Sloan argues that adding the MYPPPY motif to Finneys dual-
signaling chimeric T cell receptor would have been expected to add
additional binding specificity for CD28s natural ligands, thus risking so-
called off-target binding and/or activation. See PO Resp. 29 (citing Ex.
1006, Abs.; Ex. 2022 146, 185187; Ex. 2087, 10:2557; Ex. 2016,
1210). Sloan argues that this off-target activation could induc[e] the
engineered T cell to target and kill other activated T cells, or to at least
become distractedin either case, significantly limiting any immune
response initiated by the chimeric TCRs or presenting a safety risk. Id. at
2930 (citing Ex. 2022 144146). Sloan avers that Krause itself would
not have presented this problem, because Krauses construct provides only
the costimulatory (CD28) signal, not the primary (CD3) signal, and thus
could not have activated an engineered T cell on its own. Id. at 30 (citing
Ex. 2036, 217; Ex. 1005, 2:3133; Ex. 2022 61).
22
IPR2015-01719
Patent 7,446,190 B2
Although, as Kite notes, Sloan cites no prior art evidence about off-
target binding concerns specifically in regard to the MYPPPY motif (see Pet.
Reply 11), Sloans teach-away argument is nonetheless persuasive. Sloans
argument is based on a reasonable inference from the understanding in the
art at the time of the invention that (1) the MYPPPY motif of CD28s
extracellular sequence played a key role in ligand binding (as discussed
above), and (2) possible ligand binding other than to the scFv, i.e., off-target
binding, was a known, problematic design concern for chimeric TCRs.
Kite replies that Krauses data contradict Sloans position. Kite
argues that when Krause tested its constructs ability to signal in response to
cross-linking antibodies, including antibody OKT3 (which provided the
primary signal), the results showed no evidence of off-target binding to
endogenous B7. Id. at 1112 (discussing Krause Table 2) (citing Ex. 1032
3740). Further, Kite cites to the opinion of one of its experts, Dr.
Bajorath, for the proposition that while the MYPPPY motif is required for
B7 binding, the binding interaction requires other conserved motifs of
CD28, and they must all be present in a particular conformation for binding
to B7 to occur. Id. at 14 (citing Ex. 1033 4855; Ex. 1032 4142).
Kites attempts to minimize the off-target binding problem are not
persuasive. As to Krause, we disagree with Kite that the data in Krause
conclusively show no evidence of off-target binding to endogenous B7. As
Kites expert Dr. Abken admits, all of Krauses transduced T cells also
express endogenous CD28 molecules. Ex. 2162, 40:1941:1, 43:37. This
endogenous CD28 could bind to B7 on neighboring cells. Id. at 43:2244:6.
23
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Patent 7,446,190 B2
Further, Dr. Abken admits that Krauses T cells could receive the co-
stimulatory signal through endogenous CD28. Id. at 44:1622 (Thats not
proven, but it could be.). Ultimately, then, it is impossible to discern from
Krause whether the costimulatory signaling is from endogenous CD28
alone, or from both endogenous CD28 and the MYPPPY motif from the
construct.
Kite also argues that Sloans concerns about off-target binding to the
MYPPPY motif are speculative, relying solely on the unsubstantiated
opinion of Sloans expert, Dr. Brocker. Pet. Reply 11. However, Dr.
Brockers statement that [s]cientists in the field, both before and after the
filing date, expressed concerns with the potential for this type of off-target
binding is well-supported, as the citing references attest. See Ex. 2022
146 (citing Ex. 2087, 24 10:2527; Ex. 2016, 25 1210; Ex. 2027, 26 11002;
24
Capon et al., US 6,319,494 B1 (issued Nov. 20, 2001) (Ex. 2087). Capon
claims methods for treatment of viral diseases or malignancies using
modified T cells, see Ex. 2087, 51:5052:57, and states that its chimeric
proteins will be designed so as to avoid their interaction with other surface
membrane proteins native to the target host, id. at 10:2527.
25
Hombach et al., Adoptive Immunotherapy with Genetically Engineered T
Cells: Modification of the IgG1 Fc Spacer Domain in the Extracellular
Moiety of Chimeric Antigen Receptors Avoids Off-Target Activation and
Unintended Initiation of an Innate Immune Response, 17 GENE THERAPY
1206 (2010) (Ex. 2016).
26
Kowolik et al., CD28 Costimulation Provided through a CD19-Specific
Chimeric Antigen Receptor Enhances In Vivo Persistence and Antitumor
Efficacy of Adoptively Transferred T Cells, 66 CANCER RES. 10995 (2008)
(Ex. 2027). Kowolik cautions that chimeric T cell receptors including
extracellular CD28 domain that apparently contains the binding site for
24
IPR2015-01719
Patent 7,446,190 B2
Ex. 2025, 27 699). As Dr. Brocker notes (see id. at 147), one of these post-
filing-date references, Hombach (Ex. 2016), was co-authored by one of
Kites experts, Dr. Abken. Hombach reports that the IgG1 CH2CH3
extracellular spacer, which is commonly used for chimeric T cell
receptors, causes an off-target T-cell immune response, i.e., one mediated
independently of scFv-mediated CAR[28] binding to cognate target antigen.
Ex. 2016, 120910. Although not expected to have severe clinical
consequences, Hombach explains that off-target activation of engineered
T cell may result in rapid loss of anti-tumour activity because of activation-
induced cell death. Id. at 1211. Accordingly, Hombach advises that [i]n
the long term, therefore, adoptive immunotherapy with engineered T cells
will substantially benefit from modification of the IgG1 Fc spacer domain
to minimize the risks associated with off-target activation. Id.
As Hombach and the other references cited by Dr. Brocker indicate,
off-target binding was considered problematic, and best avoided, in the
design of chimeric TCRs, both before and after the filing date of the 190
patent.
CD80/CD86, in series with chimeric CD3 , may have the potential for
unwanted CD28 mediated activation of the genetically modified T cells.
Id. at 11002 (citing, inter alia, Kariv (Ex. 1006)). Accordingly, Kowolik
does not include the CD28 ectodomain in its construct. Id.
27
Kochenderfer et al., Construction and Preclinical Evaluation of an Anti-
CD19 Chimeric Antigen Receptor, 32 IMMUNOTHERAPY 689 (2009) (Ex.
2025).
28
Chimeric Antigen Receptor. This term is interchangeable with chimeric
T cell receptor or chimeric TCR. Pet. Reply 3 n.2.
25
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Patent 7,446,190 B2
Further, Kite frames Kochenderfer (Ex. 2025) as supportive of its

position regarding off-target MYPPPY binding. See Pet. Reply 14.
However, discussing its own chimeric TCR (FMC63 28Z, which includes
the MYPPPY motif in its CD28 sequence), Kochenderfer states:
The CD28 sequence contained in FMC63 28Z includes the
sequence (MYPPPY) that is predicted to form the binding site
for the B7 family molecules. Of course, just because the
sequence is present does not mean that it is folded in a way to
give the 3 dimensional structure necessary for binding to the B7
molecules. We accumulated data that assured us that FMC63
28Z transduced T cells do not recognize B7 molecules.
Ex. 2025, 699 (footnote omitted). We are not persuaded that Kochenderfer,
writing years after the 190 patent was filed, supports Kites position that the
ordinarily skilled artisan, at the time of the invention, would have
appreciated that additional CD28 regions not contained in the Krause
construct are required for B7 binding (Pet. Reply 14). To the contrary,
Kochenderfer indicates that there was a concern in the art that the MYPPPY
motif, when used in a chimeric TCR, could bind to endogenous B7, and that
the authors needed to undertake various experiments (see Ex. 2025, 699
700), to convince themselves that their particular MYPPPY-containing
construct did not do so.
After reviewing the arguments and evidence presented by both sides,
we conclude that, at the time of the invention, the ordinarily skilled artisan
would have been generally concerned about off-target binding as presenting
efficacy and safety risks for chimeric TCRs. Indeed, as Hombach (Ex.
2016) and Kochenderfer (Ex. 2025) attest, off-target binding remained a
26
IPR2015-01719
Patent 7,446,190 B2
concern in the art long after the filing of the 190 patent. To avoid risking
off-target binding, we are persuaded that the ordinarily skilled artisan would
have been dissuaded from including sequences that were known to be
important for ligand binding, such as the MYPPPY motif in CD28, in
designing a dual-signaling chimeric TCR with an artificial binding domain.
See In re Gurley, 27 F.3d 551, 553 (Fed. Cir. 1994) (A reference may be
said to teach away when a person of ordinary skill, upon reading the
reference, would be discouraged from following the path set out in the
reference, or would be led in a direction divergent from the path that was
taken by the applicant.).
3. Rationale 3: Routine Optimization of Finneys CD28 Sequence

Kites third proffered rationale is that one of ordinary skill in the art
would have arrived at the invention by using routine optimization to vary
the length of the extracellular CD28 domain of Finneys chimeric receptor.
Pet. 45 (citing Ex. 1008 113117); see also Reply Br. 2022. As with
rationale (2), rationale (3) relies on the premise that Finney teaches that
different lengths of CD28 domains can affect signaling of the chimeric
receptor (Pet. 45 (citing Ex. 1003, 2794, Fig. 3A; Ex. 1008 6869,
114)), such that the length of the extracellular CD28 domain was known
to be a results-effective variable (id. (citing Ex. 1008 6869, 114)).
Accordingly, rationale (2) and rationale (3) are not truly distinct from
one another. Thus our analysis of rationale (2) forecloses rationale (3),
because we are unpersuaded that Finneys data can bear the weight of Kites
arguments.
27
IPR2015-01719
Patent 7,446,190 B2
4. Conclusion
In considering the arguments and evidence presented for Ground 1,
we do not find persuasive any of Kites three rationales for combining the
references. Accordingly, we find that Kite has not proven, by a
preponderance of the evidence, that claims 13, 69, 12, and 13 are
unpatentable as obvious over Krause, Finney, and Aruffo.
D. Grounds 2 and 3
As Grounds 2 and 3 rely on the same primary combination of Krause,
Finney, and Aruffo as does Ground 1, we find that Sloan has not carried its
burden of persuasion with respect to Grounds 2 and 3 for essentially the
same reasons as with respect to Ground 1.
E. Objective Evidence of Nonobviousness

In light of our determination that Kite has not shown by a
preponderance of the evidence that any of the challenged claims is
unpatentable as obvious, we need not reach the merits of Sloans arguments
regarding objective evidence of nonobviousness.
IV. MOTIONS TO EXCLUDE EVIDENCE

Both parties filed motions to exclude evidence offered by the
opposing side. The party moving to exclude evidence bears the burden of
proving that it is entitled to the relief requestednamely, that the material
sought to be excluded is inadmissible under the Federal Rules of Evidence
(FRE). See 37 C.F.R. 42.20(c), 42.62(a).
28
IPR2015-01719
Patent 7,446,190 B2
A. Kites Motion to Exclude Evidence

Kite moves to exclude Exhibit 2079, a Market Capitalization table,
as inadmissible hearsay not supported by underlying data as required by 37
C.F.R. 42.65(b). Paper 46. Because we did not rely on this exhibit or any
testimony associated with it in reaching our Decision, we dismiss Kites
motion as moot.
B. Sloans Motion to Exclude Evidence

Sloan moves to exclude paragraphs 8497 of Exhibit 1032, Dr.
Abkens Second Declaration, which cover Dr. Abkens opinions as to
certain objective indicia of nonobviousness, as based on erroneous legal
standards and thus irrelevant and unreliable under FRE 402 and 702. Paper
52. Because we did not rely on the testimony contained within these
paragraphs, we dismiss Sloans motion as moot.
V. CONCLUSION
We conclude that Kite has not shown by a preponderance of the
evidence that claims 113 of the 190 patent are unpatentable under 35
U.S.C. 103.
VI. ORDER
In consideration of the foregoing, it is hereby:
ORDERED that claims 113 of the 190 patent are not held
unpatentable;
29
IPR2015-01719
Patent 7,446,190 B2
FURTHER ORDERED that Kites Motion to Exclude Evidence is

dismissed;
FURTHER ORDERED that Sloans Motion to Exclude Evidence is
dismissed; and
FURTHER ORDERED that, because this is a Final Written Decision,
the parties to the proceeding seeking judicial review of the decision must
comply with the notice and service requirements of 37 C.F.R. 90.2.
30
IPR2015-01719
Patent 7,446,190 B2
PETITIONER:
Eldora L. Ellison
eellison-PTAB@skgf.com
Ralph W. Powers III

tpowers-PTAB@skgf.com
PATENT OWNER:
Michael Fleming
mfleming@irell.com
Andrei Iancu
aiancu@irell.com
31
2. Petitioner Kite Pharma, Inc. 's Notice of Appeal being filed with the Patent Trial and Appeal Board;
3. Petitioner Kite Pharma, Inc.'s Notice of Appeal being filed with the~C9iyt,Rf Aroe~l_sJ9r the Federal Circuit (Form
5); ~,,.i;_,_~t.J a~~H:n;J v'Ml
4. The Final Written Decision, dated December 16, 2016 (Paper 72) being a~aJcli?:i sn
5. Certificate of Service; and
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A motion, response or reply including confidential material must be accompanied by a
certificate that the motion, response or reply complies with the word limitation. The form
can be embedded within the brief or filed separately.
2016 Rule Changes Summary P a g e |2

Federal Circuit Form 31 is a suggested form of the certificate of compliance with this rule. It
is the responsibility of the filing party to ensure that its certificate of compliance is accurate.
When you file a confidential document in CM/ECF, you will be asked to confirm that
your document is compliant with all confidentiality requirements and/or that you have
simultaneously filed a motion to waive the confidentiality requirements, if applicable
(see Figure 1 below).
To confirm, simply select the check box as indicated in Figure 1 and then select OK.
Figure 1. Confidential Brief Tendered Event
Copies, Number of - The number of copies of briefs, appendices, motions, petitions for
rehearing, and other documents are incorporated by reference Fed. Cir. R. 25.
Appendix, Preparing an Rule 30(a)(5) and 30(h): Appendix required copies count reduced
to 6 from 12.
Briefs Rule 31(b): The number of paper copies of briefs for filing reduced to 6 from 12.
Petitions for Hearing or Rehearing En Banc Rule 35(c)(4) and (f): Original copy is no
longer required to be filed. A copy of the nonconfidential version is no longer required to be
served on each party separately represented.
Email Address: The addition of a contact email address is required pursuant to Rule15(a), Rule
47.3(b), Rule 47.3(c)(1)(2), Rule 46(e) and Rule 8(c).
Entry of Appearance (EOA) Rule 47.3: If an attorneys entry of appearance is first submitted
after a case is assigned to a merits panel, the appearance will be treated as a motion to appear.
Counsel must immediately file an updated EOA if representation changes. This included a change
in contact information. Electronic filers must also report a change in contact information to the
PACER Service Center.
Filing and Service Rule 25: Incorporates the provisions of the May 2012 Administrative Order
regarding electronic filing.
Forms: Review the new forms on the website at: www.cafc.uscourts.gov. Most of the forms have
been updated, specifically forms 8 (Entry of Appearance) and 9 (Certificate of Interest now,
identify the real party in interest and/or parent per represented party, and; now, do not include
the names of firms/ attorneys who are already on the docket).
Oral Argument Rule 34 Practice Notes: Shortens the time to 7 days from notification by the
Clerks Office (via Notice of Docket Activity) that the case is fully briefed in which counsel must
advise the Clerks Office of schedule conflicts; Clarifies argument time per side (not per attorney).
Service Rule 25(e): Three additional days are NOT added to the time to file a responsive document
because the court considers service by email through CM/ECF to be delivered when transmitted.
Statement Concerning Discrimination Rules 15(c), 15(c)(2): When a claim of discrimination is
made in a motion or brief, the respondent must now state, in a responsive motion or brief: whether
the respondent concurs or disagrees with the petitioners statement concerning discrimination and
indicate whether or not the respondent believes that the court has jurisdiction over the petition for
review, with reasons provided as necessary.
U.S. COURT OF APPEALS FOR THE FEDERAL CIRCUIT

Kite Pharma, Inc. v. Sloan-Kettering Institute

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Kite Pharma, Inc. v. Sloan-Kettering Institute

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Case: 17-1647 Document: 1-1 Page: 1 Filed: 02/17/2017

UNITED STATES COURT OF APPEALS FOR THE FEDERAL CIRCUIT

17-1647 - Kite Pharma, Inc. v. Sloan-Kettering Institute

Date of docketing: February 17, 2017

Appellant(s): Kite Pharma, Inc.

Critical dates include:

Date of docketing. See Fed. Cir. R. 12 and 15.

cc: Office of the Solicitor, US Patent and Trademark Office

February 16, 2017

Peter R. Marksteiner Via CM/ECF

Re: Notice of Appeal; PTAB Case No. IPR2015-01719

Dear Mr. Marksteiner:

Enclosed please find the following documents for filing:

STERNE, KESSLER, GOLDSTEIN & FOX P.L.L.C.

/s/ Eldora L. Ellison

United States Court of Appeals for the Federal Circuit

Kite Pharma, Inc.

v. PETITION FOR REVIEW

/s/ Eldora L. Ellison

*See Fed. R. App. P. 15 for permissible ways of identifying petitioners.

UNITED STATES PATENT AND TRADEMARK OFFICE

BEFORE THE PATENT TRIAL AND APPEAL BOARD

KITE PHARMA, INC.

KITE PHARMA, INC.'S NOTICE OF APPEAL

via PTAB E2E

via Hand Carry

Pursuant to 37 C.F.R. 90.2(a), notice is hereby given that Petitioner Kite

In accordance with 37 C.F.R. 90.2(a)(3)(ii), Kite indicates that the issues

findings supporting or relating to the aforementioned issues.

adversely to Petitioner in any orders, decisions, rulings, or opinions issued in the

Trademark Office in accordance with 37 C.F.R. 90.2(a)(1). In addition, this

the United States Court of Appeals for the Federal Circuit.

STERNE, KESSLER, GOLDSTEIN & FOX P.L.L.C.

CERTIFICATE OF SERVICE (37 C.F.R. 42.6(e))

Director of the United States Patent and Trademark Office

for the Federal Circuit via CM/ECF.

The undersigned hereby further certifies that the above-captioned "Kite

for the Patent Owner:

Andrei Iancu (Lead Counsel)

Elizabeth Tuan (Back-Up Counsel)

STERNE, KESSLER, GOLDSTEIN & FOX P.L.L.C.

Date: February 16, 2017

UNITED STATES PATENT AND TRADEMARK OFFICE

BEFORE THE PATENT TRIAL AND APPEAL BOARD

KITE PHARMA, INC.,

SLOAN KETTERING INSTITUTE FOR CANCER RESEARCH,

Before RAMA G. ELLURU, TINA E. HULSE, and

LAVIER, Administrative Patent Judge.

FINAL WRITTEN DECISION

We have jurisdiction under 35 U.S.C. 6. This Final Written

A. The 190 patent

Annotated Figure 2 of the 190 patent diagrams a series of chimeric

C. Grounds of Unpatentability Instituted for Trial

Ground Claims Basis References

II. CLAIM CONSTRUCTION

A. Level of Ordinary Skill in the Art

B. Overview of Cited Art

1. Rationale 1: Add Finneys CD3 to Krauses Chimeric T Cell

CD28 sequence over Finneys when combining the two references.

2. Rationale 2: Replacement of Finneys CD28 Sequence with Krauses

argues that Finney itself shows the benefits of including additional

the G1 spacer contains binding domains. Kites incomplete representation

Rather, Krause characterizes its data as strongly suggest[ing] that the

Further, Kite frames Kochenderfer (Ex. 2025) as supportive of its

I certify that I served a copy on counsel of record on February 1, 2017

(OGRUD/(OOLVRQ /s/ (OGRUD/(OOLVRQ

Telephone Number (202) 772-8