Scharenberg et al.v.Duchateau et al. V. Scharenberg et al.

Patent Trial and Appeal Board

Aug 30, 2018

13405183 (P.T.A.B. Aug. 30, 2018)

BoxInterferences@uspto.gov Filed: 30 August 2018
Tel: 571-272-9797

UNITED STATES PATENT AND TRADEMARK OFFICE
_______________

BEFORE THE PATENT TRIAL AND APPEAL BOARD
_______________

Cellectis
(Inventors: Philippe Duchateau, Alexandre Juillerat,
George H. Silva, and Jean-Charles Epinat)

Junior Party
(Patent Application 13/880,860),

v.

Seattle Children’s Research Institute
(Inventors: Andrew M. Scharenberg, Michael T. Certo,
and Kamila S. Gwiazda)

Senior Party
(Patent 8,673,557 and Application 14/173,705),

Patent Interference No. 106,052 (DK)
(Technology Center 1600)

JUDGMENT
37 C.F.R. § 41.127(a)

Before SALLY GARDNER LANE, JAMES T. MOORE, and
DEBORAH KATZ, Administrative Patent Judges.

KATZ, Administrative Patent Judge.

Interference No. 106,052

-2-
1
We enter judgment against both Junior Party, Cellectis, and Senior Party, 2
Seattle Children’s Research Institute (“SCRI”) following the decisions on the 3
parties’ motions. Specifically, in the prior Decision on Motions, Cellectis Motion 4
2 (Paper 26) was granted, holding that the claims of SCRI’s 8,673,557 patent and 5
14/173,705 application are unpatentable under 35 U.S.C. § 112, first paragraph.1 6
(See Decision on Motions, Paper 150, 15:18–31:12.) In the Decision on Priority, 7
we granted SCRI Motion 4, for judgment on priority (Paper 374), holding that 8
SCRI inventors reduced to practice an embodiment of Count 1 earlier than the date 9
Cellectis asserted for conception in its Motion 4, for judgment on priority (Paper 10
231). (See Decision on Priority, Paper 422.) Because Cellectis did not argue for 11
an earlier date of invention, its claims are unpatentable under 35 U.S.C. § 102(g). 12
Therefore, it is ORDERED that Cellectis application 13/880,860 application 13
claims 104-108 be FINALLY REFUSED; 14
it is further ORDERED that SCRI patent 8,673,557 claims 1-14 be 15
CANCELED; and 16
it is further ORDERED that SCRI application 14/173,705 claims 6-8, 11, 18, 17
and 22-29 be FINALLY REFUSED. 18
It is also ORDERED that a copy of this judgment shall be entered into the 19
administrative record of Patent 8,673,557, application 14/173,705, and application 20
13/880,860; 21

1 1 Patent interferences continue under the relevant statutes in effect on
15 March 2013. See Pub. L. 112-29, § 3(n), 125 Stat. 284, 293 (2011).
Interference No. 106,052

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it is further ORDERED that the parties are directed to 35 U.S.C. § 135(c) 1
and to 37 C.F.R. § 41.205 regarding the filing of settlement agreements; and 2
it is further ORDERED that a party seeking judicial review timely serve 3
notice on the Director of the United States Patent and Trademark Office; 37 C.F.R. 4
§§ 90.1 and 104.2. See also 37 C.F.R. § 41.8(b). Attention is directed to Biogen 5
Idec MA, Inc., v. Japanese Foundation for Cancer Research, 785 F.3d 648, 654–57 6
(Fed. Cir. 2015) (determining that pre-AIA § 146 review was eliminated for 7
interference proceedings declared after September 15, 2012). 8

cc (via e-mail):

Attorney for Junior Party Cellectis:

Salvatore J. Arrigo
Scott M. K. Lee
LAW OFFICE OF SALVATORE ARRIGO AND SCOTT LEE, LLP
sal@arrigo.us
scott.lee@arrigo.us

Attorney for Senior Party SCRI:
E. Anthony Figg
R. Danny Huntington
Sharon E. Crane
Seth E. Cockrum
ROTHWELL, FIGG, ERNST & MANBECK, P.C.
efigg@rfem.com
dhuntington@rfem.com
scrane@rfem.com
scockrum@rfem.com

BoxInterferences@uspto.gov Filed: 30 August 2018
Tel: 571-272-9797

UNITED STATES PATENT AND TRADEMARK OFFICE
_______________

BEFORE THE PATENT TRIAL AND APPEAL BOARD
_______________

Cellectis
(Inventors: Philippe Duchateau, Alexandre Juillerat,
George H. Silva, and Jean-Charles Epinat)

Junior Party
(Patent Application 13/880,860),

v.

Seattle Children’s Research Institute
(Inventors: Andrew M. Scharenberg, Michael T. Certo,
and Kamila S. Gwiazda)

Senior Party
(Patent 8,673,557 and Application 14/173,705),

Patent Interference No. 106,052 (DK)
(Technology Center 1600)

Decision on Priority
37 C.F.R. § 41.125(a)

Before SALLY GARDNER LANE, JAMES T. MOORE, and DEBORAH KATZ,
Administrative Patent Judges.

KATZ, Administrative Patent Judge.

Interference 106,052

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Introduction 1
In the Decision on Motions issued previously in this interference, Seattle 2
Children’s Research Institute (“SCRI”) was accorded the filing date, 3
28 February 2011, of its provisional application 61/447,672 as a constructive 4
reduction to practice of Count 1. (See Paper 150, 40:14–44:14.) Subsequently, in 5
the Decision on Rehearing issued 14 August 2017, Cellectis was accorded the 6
filing date, 8 July 2011, of its provisional application 61/505,783 as a constructive 7
reduction to practice of Count 1. (See Paper 158, 5:22–12:11.) 8
Cellectis asserts that its earliest corroborated conception and reduction to 9
practice took place at least by 27 October 2010. (See Cellectis Priority Statement, 10
Paper 24, 2:4–10.) Because this date is earlier than SCRI’s accorded benefit date, 11
28 February 2011, the interference continued with the filing of the priority motions 12
now before us. (See Decision on Rehearing and Scheduling Order, Paper 158, 13
2:18–5:21.) 14
“[P]riority of invention goes to the first party to reduce an invention to 15
practice unless the other party can show that it was the first to conceive of the 16
invention and that it exercised reasonable diligence in later reducing that invention 17
to practice.” Cooper v. Goldfarb, 154 F.3d 1321, 1327 (Fed. Cir. 1998). SCRI 18
asserts that its inventors reduced to practice of an embodiment of Count 1 at least 19
by 6 May 2010. (See SCRI Motion 4, Paper 374.) In contrast, Cellectis asserts 20
that its earliest evidence of conception is the filing of its provisional application 21
61/407,339 on 27 October 2010. (Cellectis Motion 4, Paper 231). Because the 22
date of conception asserted by Cellectis is later than the dates of reduction to 23
practice asserted by SCRI, if SCRI persuades us that its inventors reduced the 24
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invention to practice by the dates asserted, Cellectis cannot prevail. Thus, we 1
exercise our discretion to review SCRI’s Priority Motion 4 first.1 (See 37 C.F.R. 2
§ 41.125(a).) 3
“In order to establish an actual reduction to practice, the inventor must prove 4
that: (1) he constructed an embodiment or performed a process that met all the 5
limitations of the interference count; and (2) he determined that the invention 6
would work for its intended purpose.” Cooper, 154 F.3d at 1327. If the inventor 7
establishes actual reduction to practice by providing his or her own testimony, the 8
testimony must be corroborated to provide independent confirmation of the 9
inventor's testimony and prevent fraud. (See id. at 1330; see Kridl v. McCormick, 10
105 F.3d 1446, 1450 (Fed. Cir. 1997)). 11
The count in this interference is claim 1 of SCRI’s ’557 patent.2 Count 1 12

1 Both parties requested oral argument. (See Papers 410 and 413.) After reviewing
the parties’ briefs, the panel determined that oral argument is not necessary to
reach a determination of priority. Accordingly, as is the panel’s discretion, no oral
argument was held. (See, e.g., 37 C.F.R. 41.124(c) (“If a request for oral argument
is granted . . . .”).)
2 In the Decision on Motions, the Board determined that the full scope of claim 1
was not described or enabled by the specification of SCRI’s ’557 patent, and that,
therefore, claim 1 is unpatentable under 35 U.S.C. § 112 to SCRI. (See Decision
on Motions, Paper 150, 15:18–31:12.) In contrast, to prove priority of invention, a
party need only show conception and/or reduction to practice of one embodiment
of a count to prevail. See Cooper, 154 F.3d at 1327; see Squires v. Corbett, 560
F.2d 424, 433 (C.C.P.A. 1977) (“The ‘count,’ as distinguished from a party's
‘claim,’ need not be patentable to either party in the sense of being fully supported
by either party's disclosure.”). The count describes the interfering subject matter
that sets the scope of admissible proofs on priority. Here Count 1 is broader than
the description found in at least SCRI’s specification. However we know of no
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recites: 1
A method of increasing mutagenesis of a nucleotide sequence at 2
a selected nucleic acid site in a cell comprising: 3
selecting a sequence for targeted mutagenesis in said cell; 4
selecting an endonuclease that cleaves at said selected nucleic 5
acid site; and 6
coupling the activity of said endonuclease and the activity of 7
one or more end-processing enzymes within said cell so as to increase 8
mutagenesis at said selected nucleic acid site. 9
10
(See Second Redeclaration, Paper 159, at 2.) To actually reduce to practice an 11
embodiment of Count 1, the inventors must show an increase in mutagenesis at a 12
selected site when the activity of an endonuclease and one or more end-processing 13
enzymes are coupled in a cell. 14
After reviewing the parties’ arguments, we determine that a preponderance 15
of the evidence supports SCRI’s motion this its inventors were the first to invent an 16
embodiment of Count 1. 17
18

reason, and neither party has argued, that Count 1 may not include subject matter
not described one of the parties’ specifications. (See 37 CFR § 41.201 (“Count
means the Board’s description of the interfering subject matter that sets the scope
of admissible proofs on priority.”); see Decision on Motions, Paper 150, 39:23–
40:13.) Neither party requested a new count for this priority phase.
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SCRI Priority Motion 1
SCRI argues that its inventors actually reduced to practice an embodiment of 2
Count 1 in April and May 2010. (See SCRI Motion 4, Paper 374, 8:18–16:20.) 3
Evidence of First Actual Reduction to Practice 4
First, SCRI argues that inventor Kamila Gwiadza performed experiments 5
coupling an endonuclease to an end-processing enzyme, specifically an 6
exonuclease, and demonstrating increased mutagenesis at a selected nucleic acid 7
site by 12 April 2010. (SCRI Motion 4, Paper 374, 11:1–16:20.) 8
To support its arguments SCRI presents the testimony of Dr. Kamila 9
Gwiazda and Dr. Michael Certo. They testify they were both graduate students in 10
the laboratory of Dr. Andrew Scharenberg in late March 2010. (See Declaration of 11
Kamila S. Gwiazda, Ph.D. (“Gwiazda Decl.”), Ex. 2150, ¶ 9; and Declaration of 12
Michael T. Certo (“Certo Decl.”), Ex. 2149, ¶ 3.) 13
Dr. Certo testifies that on 29 March 2010 he e-mailed a PowerPoint 14
presentation with suggestions for various rotation projects to Kamila Gwiazda. 15
(See Certo Decl., Ex. 2149, ¶ 18.) Dr. Certo cites to Exhibit 2058, which is a copy 16
of an e-mail dated 29 March 2010 from “Mike Certo” to “kamila@uw.edu.” (See 17
Ex. 2058, 1.) The pages accompanying Exhibit 2058 include a slide entitled 18
“Disrupting Conservative End Joining of Endonuclease Breaks.” (Ex. 2058, 7.) 19
The slide includes the question: “Will expression of Trex2 exonuclease increase 20
mutagenic NHEJ?” and includes an experiment described as “Clone Trex2 21
downstream of Y2 linked by T2A and G4S.” (Id.) We understand “NHEJ” to be 22
an abbreviation for “nonhomologous end-joining” and refers to the incidence of 23
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mutagenesis upon repair of a DNA breakpoint resulting from enzyme cutting.3 1
(See SCRI Motion 4, Paper 374, 9:21–24, quoting Exhibit 2053, 671.) 2
Dr. Gwiazda testifies that on 4–8 April 2010 she cloned the end-processing 3
exonuclease Trex24 downstream of a homing endonuclease, either I-SceI or I-AniI 4
Y25, into a viral vector. (See Gwiazda Decl., Ex. 2150, ¶ 13; see SCRI Motion 4, 5
Paper 374, 12:14–23.) Dr. Gwiazda testifies that Exhibit 2061 is an excerpt from 6
the laboratory notebook she used from March to October 2010 to detail the 7
experiments she conducted. (See Gwiazda Decl., Ex. 2150, ¶ 13.) Dr. Gwiazda 8
cites to page five of this notebook, which we reproduce, in part, below. 9

3 Cellectis does not dispute this understanding of the term “NHEJ.”
4 We understand, and Cellectis does not dispute, that Trex2 is in an end-processing
enzyme within the scope of Count 1
5 We understand, and Cellectis does not dispute, that I-SceI and I-AniI Y2 are
endonucleases within the scope of Count 1.
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1
(Kamila March-Oct. 2010 notebook (“Gwiazda notebook”), Ex. 2061, 5.) 2
Page five is dated 4 April 2010 and includes the statement: “Goal: clone Trex2 3
downstream of I-SceI – to see if it will make their parallel actions more efficient 4
(i.e. to see NHEJ better).” (Gwiazda notebook, Ex. 2061, 5.) Page 5 also includes 5
a diagram with an arrow from a fragment labeled “Trex2” in one construct pointing 6
to a position after labels for I-SceI and G4S in a different construct. 7
Dr. Gwiazda testifies that she conducted a first test of the activity of homing 8
endonuclease I-SceI along with end-processing enzyme Trex2 on different vectors, 9
obtaining results on 12 April 2010. (See Gwiazda Decl., Ex. 2150, ¶¶ 16–19; see 10
SCRI Motion 4, Paper 374, 13:10–20.) Dr. Gwiazda explains that she used HEK 11
cells stably expressing a “TLR” construct with an I-SceI recognition site for 12
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transfection of the endonuclease/exonuclease constructs. (See Gwiazda Decl., 1
Ex. 2150, ¶ 19.) 2
SCRI cites to Certo et al., Nature Methods, 8:671 (2011) (“Nature 3
Methods”) (Exhibit 2053) to explain the “TLR” system. (See SCRI Motion 4, 4
Paper 374, 9:11–10:9.) Exhibit 2053 provides that “TLR” is an acronym for 5
“traffic light report” and that TLR constructs allow a researcher to evaluate the 6
efficiency and outcomes of nuclease-induced genome engineering in human cells. 7
(See Nature Methods, Ex. 2053, 671, abstract.) Specifically, the TLR DNA 8
construct includes a site for a nuclease to cleave the DNA of the construct in a cell 9
and, subsequently, for it to be repaired by the cell. If the site is repaired by 10
homology-directed repair (HDR), wherein the original sequence is restored, Green 11
Fluorescent Protein (GFP) is expressed and a green signal is produced. If, instead, 12
the site is repaired by mutagenic nonhomologous end-joining (mutNHEJ), the GFP 13
is shifted out of frame and the protein mCherry is expressed, producing a red 14
signal. 15
To distinguish these results, the Nature Methods paper demonstrates the use 16
of flow cytometry of the cells (“FACS”). (See id., 671-72, Fig. 1.) We reproduce 17
Figure 1 below, in part, as an example of the results of FACS analysis. 18
Interference 106,052

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1
(Nature Methods, Ex. 2053, 672, Fig. 1.) Portion “b” of Figure 1 includes 2
diagrams representing DNA constructs and the resulting transcripts. Portion “c” 3
includes four panels, each labeled “mCherry F1” on the y-axis and “eGFP F1” on 4
the x-axis. The left side of Figure 1c depicts homology-directed repair (“HDR”), 5
which produces no significant red signal along the Y-axis of the two panels. In 6
contrast, the right side of Figure 1c depicts mutagenic nonhomologous end-joining 7
(“mutNHEJ”), which produces red signal along the Y-axis of the two panels. (See 8
id., 672, legend for Fig. 1b and 1c; see Certo Decl., Ex. 2149, ¶ 12.) By comparing 9
the amount of red signal along the Y-axis, often indicated by numbers inside the 10
plots. (See id., 672, legend for Fig. 1b and 1c.) 11
Dr. Gwiazda testifies that page 16 of her notebook provides results from her 12
first experiment testing separate I-SceI and Trex2 constructs in the TLR system. 13
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(See Gwiazda Decl., Ex. 2150, ¶ 20; see SCRI Motion 4, Paper 274, 13:21–16:2.) 1
Page 16 of Dr. Gwiazda’s notebook, rotated to the right, is reproduced below. 2
3
(Gwiazda Notebook, Ex. 2061, 16.) Page 16 depicts eight panels arranged in two 4
rows. The top row of panels is labeled “# cells” on the y-axis and “BFP” on the 5
x-axis. The bottom row of panels are each labeled “mCherry” on the y-axis and 6
“GFP” on the x-axis. 7
According to Dr. Gwiazda, the top row of panels on page 16 shows the 8
amount of I-SceI expressed by the cells, as indicated by the amount of blue 9
fluorescent protein (“BFP”) produced from the same vector. (See Gwiazda Decl., 10
Ex. 2150, ¶ 21; see SCRI Motion 4, Paper 374, 14:3–15:4.) To account for 11
different levels of I-SceI expression, Dr. Gwiazda testifies that she examined an 12
equivalent number of cells in each sample so that each sample produced the same 13
number of BFP. (See Gwiazda Decl., Ex. 2150, ¶ 22.) 14
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Given this normalization to the expression of BFP, Dr. Gwiazda testifies that 1
the increase in mCherry expression in the bottom row of panels on page 16 of her 2
notebook indicates an increase in mutagenesis. (See Gwiazda Decl., Ex. 2150, 3
¶ 23; SCRI Motion 4, Paper 374, 15:5–16:2.) Specifically, Dr. Gwiazda testifies 4
that the bottom row of panels on page 16 of her notebook shows that cells not 5
transfected with Trex2 (“Sce + empty vector” and “Sce-Donor + empty vector”) 6
produced a low amount of mCherry (0.21% and 0.13%, respectively). In contrast, 7
cells transfected with Trex2 in addition to Sce-I showed significant increase in 8
mCherry production: 16.8% for “Sce + Trex2” and 14.6% for “Sce-Donor + Trex 9
2.” According to Dr. Gwiazda, this increase indicates an increase in mutagenesis 10
in cells co-transfected with Trex2. (Gwiazda Decl., Ex. 2150, ¶ 24.) Dr. Gwiazda 11
testifies that based on this date, she understood by 12 April 2010, that when the 12
activity of an endonuclease that cleaves at a selected nucleic acid sequence is 13
coupled with the activity of an end-processing enzyme, an increase in mutagenesis 14
at the recognition site of the endonuclease results. (See id., ¶ 25.) 15
SCRI presents the testimony of Fyodor Urnov, Ph.D.6, to support its 16
argument that Dr. Gwiazda’s experiments are an actual reduction to practice of 17

6 Dr. Urnov testifies that he received a Ph.D. in Biology from Brown
University and has had 27 years of experience in molecular biology, with 15 years
of experience in gene editing. (Declaration of Fyodor Urnov, Ph.D. (“Urnov
Decl.”), Ex. 2156, ¶¶ 2–6.) Dr. Urnov testifies that he has co-developed human
genome editing methods and has co-authored publications regarding targeted
mammalian endogenous gene disruption via non-homologous end-joining using
engineered nucleases. (Urnov Decl., Ex. 2156, ¶ 6.) Cellectis does not dispute
Dr. Urnov’s qualifications as an expert. From his testimony regarding his
experience, we consider Dr. Urnov to be qualified to testify about the subject
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each element of the Count. (See SCRI Motion 4, Paper 374, 40:21–43:4.) 1
Specifically, Dr. Urnov testifies that the element of selecting a sequence for target 2
mutagenesis is satisfied by choosing a sequence that is known to be a recognition 3
site (or target site) for a homing endonuclease, for example the recognition site for 4
I-SceI or I-AniI present in the TLR construct. (See Urnov Decl., Ex. 2156, ¶¶ 26–5
27.) 6
Dr. Urnov testifies further that the element in Count 1 of “coupling the 7
activity of said endonuclease and the activity of at least one or more end-8
processing enzyme within said cell” can be satisfied by expressing both the 9
endonuclease that cleaves at the recognition site in the TLR and an end-processing 10
enzyme in the same cell. (See id. at ¶ 28.) According to Dr. Urnov, the enzymes 11
can either be encoded on two different vectors, cotransfected into the cell or 12
encoded on the same vector to be expressed either as a fusion protein or as two 13
different proteins. (See id.) 14
Dr. Urnov agrees that the results reported on page 16 of Dr. Gwiazda’s 15
notebook (Exhibit 2061) show an increase in mCherry production, which 16
corresponds to an increase in mutagenesis in cells that express both I-SceI and 17
Trex2. (See id. at ¶¶ 35 and 36; see SCRI Motion 4, Paper 374, 40:21–43:4.) We 18
understand Dr. Urnov’s testimony to confirm that Dr. Gwiazda’s experiment on 19
12 April 2010 includes each limitation of Count 1. 20
To corroborate Dr. Gwiazda’s testimony about her work, SCRI presents the 21
testimony of non-inventor Gabrielle M. Curinga, Ph.D. (See SCRI Motion 4, 22

matter of this interference and the Count.
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Paper 374, 29:13–40:7.) Dr. Curinga testifies that from March 2010 – February 1
2011 she worked as a postdoctoral fellow and a research scientist in the laboratory 2
of David Rawlings, which shared space with the Scharenberg laboratory. (See 3
Declaration of Gabrielle M. Curinga, Ph.D. (“Curinga Decl.”), Ex. 2154, ¶ 8.) Dr. 4
Curinga testifies that she interacted daily with the members of the Scharenberg 5
laboratory and attended joint laboratory meetings during which various members 6
of both laboratories would present their most recent data. (See id.) 7
Dr. Curinga testifies that she recalls Dr. Gwiazda presenting the data in 8
Exhibit 2063 at a group meeting. (See Curinga Decl., Ex. 2154, ¶¶ 9–10; see SCRI 9
Motion 4, Paper 374, 29:16–30:10.) Our review of page 2 of Exhibit 2063 10
indicates that it includes the same data as shown on page 16 of Dr. Gwiazda’s 11
notebook (Ex. 2061), reproduced above. Both recite the same values in each 12
experimental panel. 13
Dr. Curinga testifies that she 14
understand[s] that the data on page 2 demonstrates that coupling the 15
activity of a homing endonuclease (I-SceI) and an end-processing 16
enzyme (Trex2) in a cell (HEK293T cell) results in an increase in 17
mutagenesis (measured by an increase in mCherry production) at the 18
endonuclease recognition site in that cell. 19
20
(Curinga Decl., Ex. 2154, ¶ 10.) 21
Dr. Curinga also testifies that she knows Dr. Gwiazda presented the data in 22
Exhibit 2063 on 15 April 2010 because she reviewed the storage archive at SCRI 23
and located a copy of it in a folder labeled “10-04-15,” which under the customary 24
and standard practice in the Rawlings and Scharenberg laboratories is where 25
presentations for a given meeting were stored. (See id. at ¶ 12; see SCRI Motion 4, 26
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Paper 374, 30:11–31:12.) Dr. Curinga cites to Exhibit 2064, which she testifies is 1
a screen shot she made of the contents of a folder labeled “10-04-15.” (See Curinga 2
Decl., Ex. 2154, ¶ 13.) Exhibit 2064 includes a file named “KG 4-15-10,” which 3
Dr. Curinga testifies is Gwiazda’s presentation. (See Curinga Decl., Ex. 2154, 4
¶ 14.) 5
Evidence of Second Actual Reduction to Practice 6
SCRI argues that Dr. Gwiazda again reduced to practice an embodiment of 7
Count 1 on 30 April 2010. (See SCRI Motion 4, Paper 374, 16:21–20:16.) Dr. 8
Gwiazda testifies that page 23 of her laboratory notebook includes the details of an 9
experiment wherein she transfected HEK cells having a TLR construct with a 10
recognition site for the homing endonuclease Y2 (I-AniI) with a vector encoding 11
both the Y2 homing endonuclease and Trex2 exonuclease enzymes. (See Gwiazda 12
Decl., Ex. 2150, ¶ 32.) Specifically, Dr. Gwiazda testifies that she did several 13
transfections of HEK cells with different vectors, including: (1) endonuclease Y2 14
connected by the linker G4S to Trex2 (I-Ani Y2-G4S-Trex2), (2) Y2 connected by 15
the linker T2A to Trex2 (I-Ani Y2-T2A-Trex2), (3) Y2 alone (I-Ani Y2), or (4) 16
Trex2 alone. The experiment also included a transfection with no DNA. (See 17
Gwiazda Decl., Ex. 2150, ¶ 32, citing Gwiazda notebook, Ex. 2061, 23.) 18
Dr. Gwiazda testifies that she included the results of this experiment in her 19
notebook on page 26, which is reproduced below. 20
21
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1
(Gwiazda Notebook, Ex. 2061, 26; see Gwiazda Decl., Ex. 2150, ¶ 33.) The 2
notebook page depicts 10 separate panels, each labeled “mCherry” on the y-axis 3
and “GFP” on the x-axis. The panels labeled “Y2-T2A-Trex2” and “Y2-G4S-4
Trex2” have more signal in the region indicating mCherry expression than the 5
panels labeled “Mock,” Y2 alone,” or “Trex2 alone.” According to Dr. Gwiazda, 6
the results on page 26 show that the combination of the homing endonuclease (Y2) 7
and Trex2 results in an increase in mCherry expressing cells, corresponding to an 8
increase in mutagenesis at the I-AniI recognition site. (See Gwiazda Decl., Ex. 9
2150, ¶ 35.) 10
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Dr. Gwiazda testifies that the computer generated the date on the bottom of 1
the FACS analysis on page 26 of her notebook, “4/23/10 11:54 AM,” when the 2
analysis was done. (See id., ¶ 34.) Dr. Gwiazda also testifies that this date 3
correlates with the file name she gave for the FACS analysis, “04-23-10 analysis,” 4
which was consistent with her usual convention of naming data files to include the 5
date the information was collected. (See id.; see SCRI Motion 4, Paper 374, 18:4–6
9.) 7
Dr. Gwiazda testifies that she included a bar graph with the average of the 8
quantitative results from each experiment on page 27 of her notebook. (See 9
Gwiazda Decl., Ex. 2150, ¶ 35.) We reproduce the bar graph, rotated to the left for 10
easier review, below. 11
12
(Gwiazda Notebook, Ex. 2061, 27.) The bar graph is labeled “Fold change in 13
NHEJ (mCherry) expression” on the y-axis. The x-axis is labeled with treatments, 14
including, from left to right and in increasing height order: “Mock,” “Trex2,” 15
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“Y2,” “Y2 T2A Trex2,” and “Y2 G4S Trex2” on the x-axis. According to Dr. 1
Gwiazda, 2
[t]he bar graph dramatically shows the fold increase in 3
mutagenesis that is observed when the activity of an end-processing 4
enzyme is coupled with that of a homing endonuclease. The results in 5
this experiment were not normalized for expression of the homing 6
endonuclease. However, the important takeaway from this experiment 7
is that relative to homing endonuclease or Trex2 alone, the 8
combination of homing endonuclease and Trex2 results in 9
significantly higher mutagenesis. In particular, the I-Ani(Y2)-T2A-10
Trex2 construct exhibits a nearly 3-fold improvement over the I-11
Ani(Y2) endonuclease alone, whereas the I-Ani(Y2)-G4S-Trex2 12
construct exhibits a nearly 10-fold improvement over the I-Ani(Y2) 13
endonuclease alone. 14
15
(Gwiazda Decl., Ex. 2150, ¶ 36; see SCRI Motion 4, Paper 375, 19:3–9.) 16
Dr. Urnov agrees with Dr. Gwiazda’s analysis of page 26 of her notebook, 17
testifying that the reported results demonstrate the combination of a homing 18
endonuclease and an end-processing enzyme produces in an increase in 19
mutagenesis. (See Urnov Decl., Ex. 2156, ¶¶ 37–41; see SCRI Motion 4, Paper 20
374, 40:21–43:4.) According to Dr. Urnov, this data demonstrates coupling an 21
endonuclease (I-AniI(Y2)) with an end-processing enzyme (Trex2) to increase 22
mutagenesis. (See Urnov Decl., Ex. 2156, ¶ 41.) 23
SCRI presents Dr. Curinga’s testimony to corroborate Dr. Gwiazda’s 24
testimony. (See SCRI Motion 4, Paper 374, 31:13–32:3.) Dr. Curinga refers to a 25
copy of a presentation in Exhibit 2163. (See Curinga Decl., Ex. 2154, ¶ 15.) We 26
find that the bar graph on page 4 of Exhibit 2163 is the same as the bar graph on 27
page 27 of Dr. Gwiazda’s notebook (Ex. 2061), reproduced above. The labeling of 28
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the axes is the same and the heights of the bars appear to be the same in both 1
graphs. 2
Dr. Curinga testifies that she recalls Dr. Gwiazda presenting the data 3
provided in Exhibit 2163 at a laboratory meeting. (See id.) She testifies further 4
that she understands the data on page 4 of Exhibit 2163 to “demonstrate[] that 5
mutagenesis in a cell is increased when the activity of a different homing 6
endonuclease (I-AniI Y2) is coupled with Trex2 as demonstrated by an increase in 7
mCherry production.” (See id.) 8
Dr. Curinga testifies that she reviewed the storage archive at SCRI and 9
found a copy of Exhibit 2163 in a folder labeled “10-04-29,” indicating to her that 10
Gwiazda presented the data in Exhibit 2163 on April 29, 2010. (See id. at ¶ 16; see 11
SCRI Motion 4, Paper 374, 32:4–33:11.) Dr. Curinga also cites to Exhibit 2065, 12
which is a screen shot she made of a file entitled “10-04-29” and includes the file 13
“KG 4-15-29.” (See Curinga Decl., Ex. 2154, ¶ 18.) Dr. Curinga testifies that that 14
name of the file may have been a typo, indicating 2015, instead of 2010. (See id.) 15
Evidence of Third Actual Reduction to Practice 16
SCRI puts forth additional evidence of an actual reduction to practice on 6 17
May 2010. (See SCRI Motion 4, Paper 374, 20:17–24:10.) According to Dr. 18
Gwiazda, page 29 of her laboratory notebook begins the record of an experiment to 19
determine the activity of the homing endonuclease I-SceI with either wild type or 20
variants of the exonuclease Trex2 (called D193N and K59A) in HEK cells 21
containing the TLR construct. (See Gwiazda Decl., Ex. 2150, ¶¶ 42–44.) Dr. 22
Gwiazda testifies that she included the FACS analyses of these transfections on 23
page 33 of her notebook, which we reproduce below, rotated to the right. 24
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1
2
(Gwiazda Notebook, Ex. 2061, 33; see Gwiazda Decl., Ex. 2150, ¶ 45.) Page 33 3
includes eight panels: four top panels that are labeled “BFP” on the x-axis, and 4
four bottom panels labeled “mCherry” on the y-axis and “GFP” on the x-axis. 5
Dr. Gwiazda notes that page 33 also provides the file name “4_30_10 . . . ,” 6
which Dr. Gwiazda testifies indicates the data was collected on 30 April 2010, 7
under her convention of naming data files by the date the data was collected. (See 8
Gwiazda Decl., Ex. 2150, ¶ 46; see SCRI Motion 4, Paper 374, 22:2–9.) Dr. 9
Gwiazda also notes that page 33 of her notebook includes the notation “5/6/10 10
10:55 AM,” which was added by the computer to indicate the data was processed 11
on 6 May 2010 according to Dr. Gwiazda. (See Gwiazda Decl., Ex. 2150, ¶ 46.) 12
Dr. Gwiazda testifies that the comparison between data presented in the first 13
box, (labeled Sce + Trex2 wt) and the last box (labeled Sce-Donor alone) 14
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demonstrates this result, wherein the percentage of mCherry positive cells 1
produced by treatment with Sce and Trex2 wild type (10.9) was greater than the 2
percentage of mCherry positive cells produced by treatment with Sce alone (0.56). 3
(See Gwiazda Decl., Ex. 2150, ¶ 47; see SCRI Motion 4, Paper 374, 22:10–24:4.) 4
According to Dr. Gwiazda, this data confirms that coupling of a homing 5
endonuclease with an end-processing enzyme increases mutagenesis. (See Gwiazda 6
Decl., Ex. 2150, ¶ 47.) 7
Dr. Gwiazda also points to the data reported on page 33 of her notebook 8
regarding variants of Trex2. (See Gwiazda Decl., Ex. 2150, ¶ 49.) She testifies 9
that the catalytically inactive variant (D193N) did not increase mutagenesis, but 10
that a variant merely unable to dimerize (K59A) retained the ability to increase 11
mutagenesis. According to Dr. Gwiazda, this result suggests the increased 12
mutagenesis was due to Trex2 catalytic activity. (See id.) 13
Dr. Urnov supports Dr. Gwiazda’s interpretation of the data reported on 14
page 33 of Exhibit 2061, testifying that: 15
an increase in mCherry expression means there has been an increase 16
in mutagenesis at the I-SceI recognition site in the cell. The data 17
shows that those cells expressing both I-SceI and wild type Trex2 18
express significantly more mCherry than those cells that express only 19
I-SceI (compare the first box on the left with the fourth box from the 20
left). I also note that the cells expressing the catalytically inactive 21
Trex2 (second box from the left) do not show an increase in mCherry 22
expression, which provides further proof that the enzymatic activity of 23
Trex2 as an exonuclease drives an increase in mutagenesis. 24
25
(Urnov Decl., Ex. 2156, ¶ 45; see SCRI Motion 4, Paper 374, 40:21–43:4.) 26
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As corroboration, Dr. Curinga testifies that she recalls Dr. Gwiazda 1
presenting the data in Exhibit 2162. (See Curinga Decl., Ex. 2154, ¶ 20; see SCRI 2
Motion 4, Paper 374, 33:7–16.) According to Dr. Curinga, pages 3 and 5 of 3
Exhibit 2162 shows that mutagenesis in a cell increases when the activity of a 4
homing endonuclease is coupled with Trex2 as demonstrated by an increase in 5
mCherry production. (See Curinga Decl., Ex. 2154, ¶ 20.) We find that the data 6
on page 3 of Exhibit 2162 shows panels that are the same as the lower panels on 7
page 33 of Dr. Gwiazda’s notebook (Ex. 2061) because they recite the same 8
values. 9
Dr. Curinga testifies that she knows that Gwiazda presented the data in 10
Exhibit 2162 on 13 May 2010 because she reviewed the storage location on 11
SCRI’s server and located a copy of Exhibit 2162 in a file labeled “10-05-13.” 12
(See Curinga Decl., Ex. 2154, ¶ 21, citing Exhibit 2165 as a screen shot of the 13
folder; see SCRI Motion 4, Paper 374, 33:17–34:6.) 14
Additional Evidence of Corroboration 15
In addition to directing us to testimony of Dr. Curinga’s recollection of 16
group meetings, SCRI also directs us to testimony about Dr. Curinga’s motivations 17
for her own work as corroboration of Dr. Gwiazda’s testimony. (See SCRI Motion 18
4, Paper 374, 35:11–37:3.) Dr. Curinga testifies that on 3 June 2010 she began 19
“Experiment 11,” recorded on pages 14–20 of her laboratory notebook (Exhibit 20
2090). (See Curinga Decl., Ex. 2154, ¶ 28; see SCRI Motion 4, Paper 374, 36:16–21
37:3.) According to Dr. Curinga, the goal of Experiment 11 was to test I-SceI 22
either alone or in combination with Trex-2 in cells isolated from a mouse, called 23
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“primary” cells, not the “transformed” HEK cell line that Dr. Gwiazda used. (See 1
Curinga Decl., Ex. 2154, ¶ 28.) Dr. Curinga testifies: 2
Prior to beginning these experiments, I knew that the system would 3
work in a transformed cell because Kamila Gwiazda had 4
demonstrated that it would work in HEK293T cells. Accordingly, I 5
knew that Kamila Gwiazda had demonstrated that the coupling the 6
activity of a homing endonuclease and an end-processing enzyme in a 7
cell would increase mutagenesis at a nucleic acid site in a cell prior to 8
June 3, 2010. This is reflected on page 20 of Exhibit 2090 where I 9
reference Kamila Gwiazda’s data. 10
11
(Curinga Decl., Ex. 2154, ¶ 28.) We reproduce the text from page 20 of Dr. 12
Curinga’s laboratory notebook below. 13
14
15
(Curinga Notebook, Ex. 2090, 20.) The text includes the notation “5. Is there a 16
difference between Trex2 constructs? G4S appears to be slightly better --- need to 17
compare cell viability with both – Kamila’s data and slight shift in live cell 18
population.” Although there is no explanation about which specific data she refers, 19
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the reference indicates that Dr. Curinga was aware of the results of at least some of 1
Dr. Gwiazda’s experiments regarding Trex2 and the linker G4S prior to 3 June 2
2010. 3
In addition to Dr. Curinga’s testimony, SCRI presents the testimony of non-4
inventor Dr. Jordan Jarjour to corroborate Dr. Gwiazda’s testimony. (See SCRI 5
Motion 4, Paper 374, 29:13–40:7.) Dr. Jarjour testifies that he received a Ph.D. in 6
2010 and did graduate research in the laboratory of inventor Scharenberg. 7
(Declaration of Jordan Jarjour, Ph.D. (“Jarjour Decl.”), Ex. 2152, ¶¶ 2–3.) Like 8
Dr. Curinga, Dr. Jarjour testifies that he interacted daily with members of both the 9
Scharenberg and Rawlings laboratories, attended joint group meetings, and was 10
generally aware of their projects, and experimental results. (See id. at ¶ 9.) Dr. 11
Jarjour testifies further that his laboratory bench was next to Dr. Certo’s and one 12
bay away from Dr. Gwiazda’s and that he had personal knowledge of the 13
experiments they conducted including the results. (See id. ¶ 10) 14
Dr. Jarjour testifies: 15
I have reviewed Ex. 2061 [Gwiazda notebook] and recall 16
observing these experiments and having contemporaneous discussions 17
of the results from those experiments. I recall that I provided Kamila 18
with the I-AniI Y2 construct she used in her experiments conducted 19
on April 4-8, 2010. I also recall how the putative Trex2 dimerization 20
mutants (e.g., Trex2 K59A) did not affect the ability of Trex2 to 21
increase mutagenesis after I-SceI endonuclease cleavage (data 22
obtained May 6, 2010). 23
24
(Jarjour Decl., Ex. 2152, ¶ 15.) 25
Dr. Jarjour also testifies that he participated in an annual Department of 26
Immunology Retreat held on 13–14 September 2010. (See id. at ¶ 17; see SCRI 27
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Motion 4, Paper 374, 39:4–15.) He cites to Exhibit 2100 as a copy of the agenda 1
for the meeting. (See Jarjour Decl., Ex. 2152, ¶ 17.) Dr. Jarjour also cites to 2
Exhibit 2101, which is entitled “Student # Check List as of Sept 29, 2010” and lists 3
“Jordan Jarjour.” (See id. at ¶ 17.) Dr. Jarjour states that he recognizes Exhibit 4
2099 as the presentation Dr. Certo made at this Immunology Retreat. (See id. at 5
¶ 18.) 6
The first page of Exhibit 2099 is a copy of an e-mail and alleged attachment 7
dated 12 September 2010 sent by Dr. Certo to himself. Dr. Jarjour testifies that he 8
is sure Exhibit 2099 is a copy of the presentation Dr. Certo made at the 9
Immunology Retreat because he worked with Dr. Certo to conceive the 10
“Nucleosaurs” slide 22, which he explains was a play on the Trex2 enzyme and the 11
T-rex dinosaur. (See id.) We reproduce a copy of this slide below. 12
13
(E-mail of 12 September 2010, Ex. 2099, 22.) The slide depicts a protein structure 14
superimposed on a dinosaur skeleton. 15
Dr. Jarjour testifies further that 16
I recall that this presentation included the results of the successful 17
experiments Mike designed and that he and Kamila performed, that 18
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show that the combination of Sce and Trex in a cell increases 1
“targeted disruption” or mutagenesis to nearly 100% in cells receiving 2
a high dose of both the endonuclease and exonuclease. (See, e.g., slide 3
19 of Ex. 2099). 4
5
(Jarjour Decl., Ex. 2152, ¶ 18.) Slide 19 of Exhibit 2099, which Dr. Jarjour 6
references, is reproduced below. 7
8
(E-mail of 12 September 2010, Ex. 2099, 19.) Slide 19 is entitled “Trex2 Drives 9
Targeted Disruption Rates to Nearly 100%,” and provides data wherein the panel 10
labeled “Sce D44A” has a value of 0.051, the panel labeled “Sce D44A + Trex2” 11
has a value of 0.29, the panel labeled “Sce” has a value of 2.46, and the panel 12
labeled “Sce + Trex2” have a value of 28.1. Dr. Jarjour attributes this data to the 13
“the successful experiments Mike [Certo] designed and that he and Kamila 14
[Gwiazda] performed.” (Jarjour Decl., Ex. 2152, ¶ 18.) 15
Summary of SCRI’s Evidence 16
In summary, SCRI presents Dr. Gwiazda’s testimony to show that she 17
successfully transfected cells with both I-SceI or I-Ani(Y2) endonuclease and 18
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Trex2 end-processing exonuclease and that the combination increased mutagenesis 1
at the selected site in the TLR construct in HEK cells compared to the 2
endonuclease alone. According to Dr. Gwiazda, she concluded these experiments 3
by at least three dates: 12 April 201, 23 April 2010, and 6 May 2010. We find that 4
Dr. Gwiazda’s testimony is consistent with the evidence she cites in support. 5
SCRI also presents Dr. Urnov’s testimony to support its argument that the 6
experiments described by Dr. Gwiazda and recorded in her notebook demonstrate 7
every limitation of Count 1. We find this testimony convincing. Cellectis does not 8
dispute the substance of Dr. Urnov’s opinions. 9
SCRI presents the testimony of Drs. Curinga and Jarjour to corroborate Dr. 10
Gwiazda’s testimony. We find that Dr. Curinga testifies she recollects Dr. 11
Gwiazda presenting results from the three experiments SCRI highlights during 12
meetings of the Scharenberg and Rawlings laboratories. Dr. Curinga also testifies 13
that she knows that she was aware of Dr. Gwiazda’s experiments and result by 14
3 June 2010 because she based her own experiments in primary cells on these 15
results. 16
Dr. Jarjour testifies that he recollects a presentation Dr. Certo made on 17
12 September 2010 at a department retreat because he remembers a slide that he 18
helped to make for that presentation. He testifies that he also remembers the 19
presentation including slides with results from Dr. Gwiazda’s experiments in the 20
presentation. We find that the testimony of Drs. Curinga and Jarjour is consistent 21
with the exhibits they cite and with Dr. Gwiazda’s testimony. 22
Cellectis does not direct us to evidence that specifically contradicts any of 23
these findings. 24
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Cellectis disputes whether this testimony and other evidence cited by SCRI 1
is appropriate and sufficient for corroboration. (See Cellectis Opp. 4, Paper 389, 2
1:10.) We review Cellectis’s arguments and the evidence cited to determine if the 3
relevant evidence SCRI offers is admissible and if it supports SCRI’s arguments. 4
Cellectis Motion to Exclude 5
We first review Cellectis’s Motion to Exclude (Cellectis Motion 5, Paper 6
411) because Cellectis argues that almost all of the evidence relied upon by SCRI 7
in its priority case is inadmissible. (See Cellectis Motion 5, Paper 411, 14:14–23 8
(“SCRI built its entire priority case on more than 100 Exhibits, disregarding the 9
inadmissibility of these Exhibits as hearsay.”).) According to Cellectis, SCRI 10
relies on the truth of the content of the non-declaration exhibits it presents, for 11
example, the dates provided on e-mails, notebook pages, and presentations, but that 12
because these documents are out of court statements, they are inadmissible 13
hearsay. (See id. at 1:19–20.) Cellectis argues further that “SCRI’s Declarations 14
are saturated with references to these hearsay Exhibits . . .” and that therefore, “the 15
sections of the Declarations relying on this hearsay should be stricken as 16
inadmissible hearsay under FRE 802.” (Id. at 14:16–22.) (See Cellectis Reply 5, 17
Paper 421, 5:17–21 (“It is incontestable that SCRI’s non-Declaration Exhibits are 18
out of court statements that are being used by SCRI for the truth of the dates on 19
which certain events allegedly occurred. Thus, these Exhibits are hearsay and are 20
inadmissible. See FRE 802. Similarly, the discussions of these Exhibits in SCRI’s 21
Declarations are also hearsay and are inadmissible.”).) 22
Hearsay is a statement that “the declarant does not make while testifying at 23
the current trial or hearing” and that “a party offers in evidence to prove the truth 24
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of the matter asserted in the statement.” (Fed. R. Evid. (“FRE”) 801(c).) To 1
prevail Cellectis must show that SCRI’s exhibits are statements made outside of 2
the proceeding and that they are being offered to prove the matter asserted in the 3
document. 4
Cellectis fails to persuade us that both conditions are met by the declarations 5
of Drs. Gwiazda (Ex. 2150), Certo (Ex. 2149), Curinga (Ex. 2154), Jarjour (Ex. 6
2152), and Urnov (Ex. 2156), which we cite in our review of SCRI’s evidence. 7
These declarations were made by each witness during the interference proceeding 8
and each witness was subject to cross-examination. They are not out of court 9
statements. Accordingly, they are not hearsay. 10
We are not persuaded that citations to exhibits in these declarations make 11
them hearsay, even if those other exhibits are themselves hearsay. (See Cellectis 12
Motion 5, Paper 411, 11:14–12:11.) Cellectis cites to the Federal Rules of 13
evidence 801-803 to support its argument that “[t]o the extent that these 14
Declarations are based on hearsay Exhibits, the Declarations should likewise be 15
excluded as hearsay.” (Cellectis Motion 5, Paper 411, 11:3–4.) Rules 801-803 do 16
not support the argument. Rule 801 defines hearsay, Rule 802 provides the general 17
rule against hearsay, and Rule 803 provides for exceptions from the rule against 18
hearsay. None of these rules discusses the citation of hearsay within a non-hearsay 19
declaration. Cellectis cites no other authority for its assertion that citation of 20
hearsay makes an in-court statement hearsay and we do not know of any. 21
Cellectis argues further that the declarations are hearsay because SCRI’s 22
witnesses rely on the content and dates in Dr. Gwiazda’s laboratory notebook to 23
prove the truth of the matter asserted. (See Cellectis Motion 5, Paper 411, 11:8–24
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13.) According to Cellectis, “[t]he Declarants have simply assumed these Exhibits 1
to be the truth and then testified as if they are the truth.” (Cellectis Motion 5, 2
Paper 411, 12:4–5; see also Cellectis Reply 5, Paper 421, 1:13–15 (“Instead of 3
limiting their testimony to events within their personal knowledge, SCRI’s 4
witnesses base their testimony on inadmissible hearsay documents, relying on them 5
as if they all contain the truth.”) 6
This argument is not persuasive because Cellectis fails to direct us to any 7
evidence in support. Each of SCRI’s witnesses state in their declaration that they 8
rely on their own knowledge and belief. (See Gwiazda Decl., Ex. 2150, ¶ 1; Certo 9
Decl., Ex. 2149, ¶ 1; Curinga Decl., Ex. 2154, ¶ 1; Jarjour Decl., Ex. 2152, ¶ 1; and 10
Urnov Decl., Ex. 2156, ¶ 1.) Without evidence to the contrary, we have no reason 11
to doubt these statements. Because the witnesses were available for cross-12
examination, Cellectis had an opportunity to elicit contradictory evidence from 13
them, highlighting any differences between their in-court declarations and the 14
evidence they cite. (See In re Epstein, 32 F.3d 1559, 1565 (Fed. Cir. 1994) (“As 15
has been articulated by Professor Wigmore, ‘[t]he theory of the hearsay rule ... is 16
that the many possible sources of inaccuracy and untrustworthiness which may lie 17
underneath the bare untested assertion of a witness can best be brought to light and 18
exposed, if they exist, by the test of cross-examination.’ 5 John H. Wigmore, 19
Evidence in Trials at Common Law § 1420, at 251 (James H. Chadbourn rev. 20
1974).”).) 21
Cellectis argues that “[i]n view of the pervasive reliance of SCRI’s 22
Declarants on these inadmissible Exhibits for their testimony, neither Cellectis nor 23
the Board are in a position to determine what portions of the Declarations, if any, 24
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are dependent on the witnesses’ personal knowledge – it is simply an impossible 1
task.” (Cellectis Reply 5, Paper 421, 2:15–18.) Because Cellectis had an 2
opportunity to question SCRI’s witnesses about whether they actually participated 3
in the activities or authored the documents about which they testify, it is not clear 4
why such a task would be impossible. 5
Cellectis provides an example of the use of cross-examination in its 6
arguments regarding Dr. Ankit Gupta’s testimony. (See Cellectis Motion 5, Paper 7
411, 12:17–14:12.) Cellectis argues that Dr. Gupta provided inconsistent 8
testimony on cross-examination regarding knowledge of the TLR system in the art 9
because his testimony was contradicted by documentary exhibits. Although 10
Cellectis argues that Dr. Gupta’s testimony “highlights the dangers of testimony 11
based on hearsay” (Cellectis Motion 5, Paper 411, 12:17–18), Cellectis’s argument 12
actually highlights why declarations made during the proceeding, when the witness 13
is available for cross-examination, are not hearsay and are not inadmissible under 14
FRE 802. That is, the truth of the matters asserted in statements made during the 15
proceeding may be questioned on cross-examination. We need not reach Dr. 16
Gupta’s declaration for a determination of priority. Thus, even if Dr. Gupta’s 17
testimony is flawed, our opinion does not differ and the issue of whether to exclude 18
it is moot. Furthermore, even if Cellectis is correct that Dr. Gupta’s testimony is 19
flawed, Cellectis has not directed us to similar evidence regarding any of the SCRI 20
testimonies we do cite. Cellectis’s arguments regarding exclusion of or the merits 21
of Dr. Gupta’s declaration is not persuasive regarding any of SCRI’s other 22
evidence that we cite in support of our decision. 23
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Cellectis argues further that many of the non-declaration exhibits presented 1
by SCRI and relied upon by its witnesses are inadmissible hearsay.7 (See Cellectis 2
Motion 5, Paper 411, 1:16–8:23.) According to Cellectis, SCRI uses these exhibits 3
to support “nearly all aspects” of its priority case. (Id. at 8:5.) For example, 4
Cellectis argues that SCRI relies on Exhibit 2061, Dr. Gwiazda’s notebook, to 5
prove that she performed experiments by specific dates in 2010. 6
Contrary to Cellectis’s characterization, SCRI presents its priority case 7
based on the testimony of its inventors, as corroborated by the non-inventor 8
witnesses and the other exhibits it cites. We do not agree that Cellectis argues its 9
case primarily on these other exhibits. Although SCRI’s witnesses cite other 10
exhibits, they testify to their personal recollections and activity related to these 11
exhibits. 12
The evidence SCRI’s witnesses cite supports their testimony about their 13
personal knowledge and activities, but does not prove the truth of the matters 14
asserted in the documents. For example, SCRI does not offer Dr. Gwiazda’s 15
laboratory notebook pages (Ex. 2061) to prove that she performed the experiments 16
recorded or that the experiments showed increased mutagenesis at a selected site. 17
Instead, SCRI presents Dr. Gwiazda’s testimony and Dr. Urnov’s testimony to 18
prove these facts. We agree with SCRI that exhibits such as Exhibit 2061 do not 19
meet the second prong of the definition of hearsay, wherein the reason the party 20

7 Cellectis lists Exhibits 2054–2069, 2071–2077, 2079, 2080, 2082–2093, 2095,
2096, , 2098–2104, 2106–2125, 2127–2133, 2136, 2138–2140, 2143–2148, 2162–
2167, 2169–2182, 2184–2202, and 2210. (See Cellectis Motion 5, Paper 411, 2–
7.)
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offers the evidence is to prove the truth of the matter asserted in the evidence. (See 1
SCRI Opp. 5, Paper 417, 7:6–10:2.) We are not persuaded by Cellectis’s 2
arguments regarding the evidence cited by Drs. Certo, Gwiazda, Curinga, Jarjour, 3
and Urnov to support their testimony. 4
Cellectis cites to Chen v. Bouchard, 347 F.3d 1299, 1308 (Fed. Cir. 2003), 5
in support of its argument that laboratory notebooks are inadmissible hearsay not 6
falling within any exception. (See Cellectis Motion 5, Paper 411, 8:2–5, and 8:16–7
21.) In Chen the author of notebooks was not called to testify and, thus, the 8
notebooks themselves were the evidence offered to prove the truth of the matters 9
asserted. The court noted that “notebook records are obviously of prime 10
importance in proving the elements of invention” (id.), but also noted that without 11
testimony by their author or other evidence to show their veracity, the notebooks 12
were properly excluded. See also Medichem, S.A. v. Rolabo, S.L., 437 F.3d 1157, 13
1172-73 (Fed. Cir. 2006) (“It is clear to this court, therefore, that Medichem's 14
claim of corroboration stands or falls with the modicum of additional corroborative 15
value that can properly be assigned to non-inventor Casas' notebook. However, 16
Casas did not testify regarding the notebook or the genuineness of its contents. . . . 17
without testimony from Casas, the court lacked any non-inventor testimony 18
regarding the genuineness of the notebook's contents.”). 19
In contrast, the witnesses who testify that they authored the exhibits on 20
which we rely also provided direct testimony. Cellectis had an opportunity to 21
reveal fabrications or other inconsistencies in this testimony through cross-22
examination. Thus, we are not persuaded that they should be excluded as 23
inadmissible hearsay and we deny Cellectis Motion 5 in regard to the documentary 24
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exhibits we cite, specifically, Exhibits 2053, 2058, 2061, 2099, 2064, 2065, 2090. 1
We note that we also rely on Exhibits 2063, 2162, and 2163 to reach our 2
decision. Dr. Gwiazda reportedly presented these slides to show the results of her 3
experiments. (See Gwiazda Decl., Ex. 2150, ¶¶ 26, 38, and 50.) SCRI presented 4
Dr. Curinga’s testimony about when she saw these presentations and her 5
understandings of them. (See SCRI Motion 4, Paper 374, 29:13–35:5.) Because 6
SCRI presents Dr. Curinga’s testimony for her recollections of the documents in 7
Exhibits 2162 and 2163, not whether the results presented in them actually show 8
increased mutagenesis, they are not inadmissible hearsay. 9
Cellectis states that “[a] similar analysis applies to all of the above-10
referenced Exhibits relied on by SCRI.” (Cellectis Motion 5, Paper 411, 8:22–23.) 11
No other explanation is provided for the 120 exhibits Cellectis argues should be 12
excluded, other than Exhibit 20558 and 2061. Because, as explained above, we 13
rely only on exhibits authored or prepared by witnesses who also testify for SCRI 14
in the interference and because Cellectis fails to provide any different reason why 15
the other exhibits should be excluded, we dismiss Cellectis Motion 5 as moot in 16
regard to these other exhibits. 17
Cellectis Opposition to SCRI Priority Motion 18
Having determined that none of the evidence we cite in our review of 19
SCRI’s priority motion should be excluded, we turn to Cellectis’s arguments 20
against that motion. In general, Cellectis asserts that SCRI failed to present 21

8 We do not rely on Exhibit 2055 to reach our decision. Thus, even if it is
inadmissible hearsay, excluding it would not change our decision.
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sufficient corroborating evidence to prove priority. (See Cellectis Opp. 4, Paper 1
389, 1:10.) Cellectis’s arguments are not persuasive either because the evidence 2
Cellectis cites was not presented for corroboration or because Cellectis’s 3
arguments are based on an incorrect standard. 4
“Sufficiency of corroboration is determined by using a ‘rule of reason’ 5
analysis, under which all pertinent evidence is examined when determining the 6
credibility of an inventor's testimony.” Medichem, 437 F.3d at 1170. “The law 7
does not impose an impossible standard of ‘independence’ on corroborative 8
evidence by requiring that every point of a reduction to practice be corroborated by 9
evidence having a source totally independent of the inventor; indeed, such a 10
standard is the antithesis of the rule of reason.” Knorr v. Pearson, 671 F.2d 1368, 11
1374 (Fed. Cir. 1982). In practice, the “rule of reason” may apply when there is 12
not an actual eye-witness account, but there is sufficient circumstantial evidence of 13
an independent nature to corroborate facts of priority. See Cooper, 154 F.3d at 14
1330. 15
First, Cellectis argues: 16
SCRI’s arguments for reduction to practice rely predominantly 17
on Ex. 2149 and 2150, which are the Declarations of Drs. Certo & 18
Gwiazda, two of the inventors. However, these are statements by the 19
inventors and, by definition, are not evidence independent of the 20
inventor’s own statements and documents. Thus, these documents 21
cannot corroborate SCRI’s alleged reductions to practice. 22
23
(Cellectis Opp. 4, Paper 389, 7:13–17.) Although Cellectis is correct that the 24
testimony of inventors Certo and Gwiazda alone would be insufficient for a 25
corroborated priority argument, SCRI presents the testimony of non-inventors 26
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Curinga and Jarjour for corroboration. (See SCRI Reply 4, Paper 407, 1:10–16.) 1
Cellectis’s argument is not persuasive because SCRI’s case for priority does not 2
rely entirely on inventor testimony. 3
Cellectis also argues that “SCRI relies entirely on experiments allegedly 4
performed by Dr. Gwiazda as evidence of reduction to practice, specifically Ex. 5
2061.” (Cellectis Opp. 4, Paper 389, 9:12–13.) According to Cellectis, SCRI 6
cannot use unwitnessed notebooks for corroboration, citing Reese v. Hurst, 661 7
F.2d 1222, 1231 (C.C.P.A. 1981). (See Cellectis Opp. 4, Paper 389, 6:7–8 and 8
8:19–20.) Again, these arguments do not persuade us because SCRI’s case for 9
priority is not entirely based on Exhibit 2061. Despite Cellectis’s characterization, 10
SCRI presents inventor testimony, documentary evidence, corroborating witness 11
testimony, and expert witness testimony to support its argument for priority. (See. 12
e.g., SCRI Motion 4, Paper 374, 6:13–23.) We disagree that SCRI’s case relies 13
entirely on any one type of evidence. In contrast to the facts of Reese, wherein the 14
inventor performed experiments in secrecy and his notebooks were unwitnessed or 15
signed, Dr. Curinga and Dr. Jarjour testify to their personal recollections of 16
presentations given by Dr. Gwiazda and to their own activities in the broader 17
research of the Scharenberg and Rawlings laboratories. See Reese, 661 F.2d at 18
1231. 19
Similarly, Cellectis argues that Dr. Gwiazda’s slide presentations (e.g. 20
Exhibits 2063, 2162, and 2163) are not evidence that is independent of an 21
inventor’s own statements and documents and, therefore, cannot corroborate 22
SCRI’s assertions of reduction to practice. (See id. at 9:18–10:6.) This argument 23
does not persuaded us because, as Cellectis recognizes, Dr. Curinga testifies about 24
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her recollections of these presentations and the screen shots of their files that she 1
took. It is Dr. Curinga’s testimony that is corroborative, not the presentations or 2
screen shots themselves. 3
Cellectis bases other arguments on the misapprehension that to corroborate 4
an actual reduction to practice properly, a non-inventor witness must independently 5
recreate the reduction to practice. For example, Cellectis argues that Dr. Certo 6
failed to provide any records documenting his own experiments with I-SceI and 7
Trex. (See id. at 9:3–11.) Similarly, Cellectis argues, at length, that because Dr. 8
Curinga’s experiments with I-SceI and Trex2 in primary cells did not demonstrate 9
higher levels of mutagenesis, SCRI has not presented corroborating evidence in 10
those cells. (See id. at 10:15–13:3 and 28:8–35:19.) According to Cellectis, the 11
lack of recollection by Dr. Curinga and Dr. Certo of any results showing increased 12
mutagenesis in primary cells is an admission that such results never existed. (See 13
id. at 13:2–3; see also 35:11–12.) 14
These arguments do not persuade us because SCRI need not show 15
corroboration of Dr. Gwiazda’s experiments in HEK with separate experiments in 16
primary cells. SCRI must provide independent evidence of Dr. Gwiazda’s 17
activities but it can do so in several different ways, including by presenting the 18
recollections of Dr. Gwiazda’s results. “[T]here is no final single formula that 19
must be followed in proving corroboration.” Kridl, 105 F.3d at 1450. 20
SCRI relies on Dr. Curinga’s testimony that 21
[p]rior to beginning these experiments, I knew that the system would 22
work in a transformed cell because Kamila Gwiazda had 23
demonstrated that it would work in HEK293T cells. Accordingly, I 24
knew that Kamila Gwiazda had demonstrated that the coupling the 25
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activity of a homing endonuclease and an end-processing enzyme in a 1
cell would increase mutagenesis at a nucleic acid site in a cell prior 2
to June 3, 2010. This is reflected on page 20 of Exhibit 2090 where I 3
reference Kamila Gwiazda’s data. 4
5
(Curinga Decl., Ex. 2154, ¶ 28 (emphasis added).) Instead of presenting the results 6
of Dr. Curinga’s experiments, this testimony shows Dr. Curinga’s knowledge of 7
Dr. Gwiazda’s experiments and the results. (See SCRI Reply 4, Paper 407, 2:17–8
20 and 6:22–7:3.) Dr. Curinga’s rationale for doing the experiments in primary 9
cells is the relevant aspect, not her results. Cellectis argues that the testimony of 10
SCRI’s witnesses regarding Dr. Curinga’s experiments is inconsistent, and 11
therefore not credible, (see Cellectis Opp. 4, Paper 389, 28:7–35:19), but the 12
testimony Cellectis cites relates to the performance of Dr. Curinga’s experiments, 13
not her reasons for doing them. 14
Furthermore, Count 1 does not specify a cell type, thus, the lack of success 15
in primary cells has no bearing on the achievement of success in HEK cells. Were 16
we to require reduction to practice in primary cells as well as HEK cells, we would 17
be requiring SCRI to prove reduction to practice of two embodiments of Count 1, 18
where only one is necessary. 19
Cellectis also argues that a corroborating witness must have observed the 20
actual work of reducing to practice for sufficient corroboration. For example, 21
Cellectis argues that Dr. Gwiazda’s testimony is uncorroborated because she was 22
unable, during cross-examination, to identify anyone who witnessed her 23
experiments. (Cellectis Opp. 4, Paper 389, 7:18–8:3, citing Gwiazda Dep., Ex. 24
1108, 44:11–21.) Cellectis argues that Dr. Curinga and Dr. Jarjour’s testimonies 25
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are insufficient because they did not witness the actual activities recorded in 1
Gwiazda’s laboratory notebook. (See Cellectis Opp. 4, Paper 389, 10:7–14 and 2
13:4–15:8.) 3
Under the “rule of reason” standard of evaluating corroborating evidence, 4
Dr. Curinga need not have watched every action of Dr. Gwiazda and remembered 5
every detail years later for her testimony to be sufficiently corroborating. “[I]t is 6
not necessary to produce an actual over-the-shoulder observer. Rather, sufficient 7
circumstantial evidence of an independent nature can satisfy the corroboration 8
requirement.” Medichem, 437 F.3d at 1171 (citing Cooper, 154 F.3d at 1330). 9
Cellectis cites Hahn v. Wong, 892 F.2d 1028, 1033-34 (Fed. Cir. 1989), to support 10
its argument that a witness must provide facts independent of the inventor’s 11
testimony to be corroborating. (See Cellectis Opp. 4, Paper 389, 10:11–14.) In 12
Hahn, though, the witness testified that he had “read and understood” laboratory 13
notebook pages, but this testimony only showed only that the pages existed on the 14
date that the witness saw them. See Hahn, 892 F.2d at 1033. The testimony did 15
not provide a contemporaneous recollection of the inventor’s activities. 16
In contrast, Dr. Curinga testifies that 17
during [the March 2010 – February 2011 timeframe she] regularly 18
attended joint group meetings between the Rawlings and Scharenberg 19
laboratories. During these group meetings, various laboratory 20
members would present their most recent data to the group. 21
22
(Curinga Decl., Ex. 2154, ¶ 8.) Dr. Curinga testifies that she was present for Dr. 23
Gwiazda’s presentations and provides her own recollections, as well as citing to 24
copies of the presentations. (See id. ¶ 9, citing Exhibit 2063.) 25
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Similarly, Dr. Jarjour testifies to his own recollections about the presentation 1
of Dr. Gwiazda’s results. Like Dr. Curinga, Dr. Jarjour testifies to the laboratory 2
organization and structure, wherein each investigator was focused on his or her 3
own project, gathering for group meetings to discuss each members work in turn. 4
(See Jarjour Decl., Ex. 2152, ¶ 9 (“During these group meetings, various laboratory 5
members would present their most recent data to the group.”); see also Curinga 6
Decl., Ex. 2154, ¶ 8.) Dr. Jarjour testifies further that he “would have observed 7
certain results from these experiments. . . . [u]sually in the form of assembled data 8
slides and presentations . . . .” (Jarjour Dep., Ex. 1107, 30:4–9.) Given the 9
laboratory atmosphere and structure, which Cellectis does not dispute, it is 10
reasonable that Dr. Jarjour would have been aware of Dr. Gwiazda’s experiments 11
and results. 12
Dr. Jarjour also testifies that he specifically remembers a presentation of 13
results increased mutagenesis from expression of Sce-I and Trex2 because of his 14
contribution to one of the slides. (See Jarjour Decl., Ex. 2152, ¶¶ 17–18.) (See 15
SCRI Reply, Paper 407, 8:4–8.) Each of these recollections is independent of the 16
inventors’ testimony. 17
Both Dr. Curinga and Dr. Jarjour corroborate Dr. Gwiazda’s testimony 18
regarding Dr. Gwiazda’s experiments even if neither witness watched her doing 19
the actual experiments because they provide independent bases for their 20
recollections. These recollections are consistent with the other evidence SCRI 21
cites, such as laboratory notebooks and slide presentations. Cellectis fails to direct 22
us to evidence of a motivation for either Dr. Curinga or Dr. Jarjour to falsify their 23
testimony and fails to direct us to positive evidence that Dr. Gwiazda failed to 24
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conduct the experiments that she testifies she did. Accordingly, under the rule of 1
reason standard, we are persuaded that Dr. Curinga and Dr. Jarjour sufficiently 2
corroborate the inventors’ testimony. 3
Cellectis also attacks Dr. Urnov’s testimony, arguing, in part, that Dr. 4
Urnov’s testimony does not corroborate that the experiments in Dr. Gwiazda’s 5
notebook are a reduction to practice. (See Cellectis Opp. 4, Paper 389, 19:18–21.) 6
SCRI does not present Dr. Urnov’s testimony for corroboration. Thus, we are not 7
persuaded by this argument. SCRI presents Dr. Urnov’s testimony to explain Dr. 8
Gwiazda’s work and how it relates to the elements of Count 1, not whether she did 9
it. (See SCRI Motion 4, Paper 374, 40:25–41:1 (“[Dr. Urnov] has reviewed Ex. 10
2061, namely experiments performed by Kamila Gwiazda in the spring of 2010, 11
and based on his extensive experience in the field, confirms that those experiments 12
constituted SCRI reductions to practice of the invention of the Count.”) 13
Cellectis argues that Dr. Urnov’s testimony is also insufficient because he 14
bases his conclusions on exhibits that were unavailable to skilled artisans at the 15
time of the invention. (See Cellectis Opp. 4, Paper 389, 17:5–24:21.) Specifically, 16
Cellectis argues that Dr. Urnov improperly relied on Dr. Gwiazda’s declaration 17
(Ex. 2150) to know that the HEK cells she used stably expressed a TLR construct 18
containing an I-SceI recognition site. (See id., 17:12–18.) Cellectis argues that Dr. 19
Urnov improperly relied on the Nature Methods publication (Ex. 2053), which was 20
published in 2011, for his testimony that increased mCherry production 21
corresponds to an increase in mutagenesis. (See id., 17:18–18:1.) According to 22
Cellectis, Dr. Urnov should not have been allowed to use these exhibits to form his 23
opinions regarding Dr. Gwiazda’s experiments and that doing so taints his 24
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testimony. (See id., 19:9–12.) Cellectis argues further that without these 1
documents, it would have been impossible to understand Dr. Gwiazda’s 2
experiments. (See id., 19:12–18.) 3
These arguments are not persuasive. Dr. Urnov testified that he did not need 4
the Nature Methods publication to understand Dr. Gwiazda’s experiments. (See 5
Urnov Dep., Ex. 1110, 25:6–8 (“Q Did you rely on Exhibit 2053 to understand the 6
experiments in Exhibit 2061? A I did not.”).) Dr. Urnov testified further that he 7
was able to understand the relationship between mCherry production and 8
mutagenesis based on an analysis of the results reported in Dr. Gwiazda’s 9
notebook. (See id.; see SCRI Reply 4, Paper 407, 11:6–17.) 10
Although Cellectis is correct that Dr. Urnov required the Nature Methods 11
publication or Dr. Gwiazda’s declaration to understand some aspects of her 12
notebook, we are not persuaded that these details are necessary to Dr. Urnov’s 13
opinion about performance of the elements of Count 1. For example, Dr. Urnov 14
testifies that he did not know the meaning of the abbreviations “TLR” and “BFP,” 15
the nucleotide sequence of the SceI portion of the TLR construct, the sequence of 16
“donors,” the form of the Trex2 protein, or the order of elements in the BFP 17
construct, from Dr. Gwiazda’s notebook alone. (See Cellectis Opp. 4, Paper 389, 18
19:22–24:21, citing Urnov Decl., Ex. 1110, 31:19–32:4, 34:3–10; 36: 2–8; 37:22–19
38:13, 47:1–6; 49:7–14, 51:18–52:3, 59:6–18, and 60:8–62:10.) Cellectis fails to 20
explain, though, why an understanding of these details is necessary to understand 21
activities that are a reduction to practice of Count 1. (See SCRI Reply 4, Paper 22
407, 12:1–7.) 23
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For example, we are not persuaded that one would need to know that “TLR” 1
stands for “traffic light reporter” to know that Dr. Gwiazda selected a sequence for 2
targeted mutagenesis, selected an endonuclease that cleaved at that site, coupled its 3
activity to an end-processing enzyme, and achieved increased mutagenesis at the 4
selected site. Similarly, we are not persuaded that one would need to know the 5
specific sequence of I-SceI in the construct Dr. Gwiazda used to know that Dr. 6
Gwiazda had achieved increased mutagenesis at a selected site by coupling the 7
activity of an endonuclease and an end-processing enzyme to reduce an 8
embodiment of Count 1 to practice. 9
In general, Dr. Urnov testifies that he did not need to rely on any outside 10
information to understand Dr. Gwiazda’s experiments. (See Urnov Dep., Ex.1110, 11
24:6–19 (“Q Did you rely on any information outside this document to understand 12
the experiments that are in this document? **** Q Do you need to rely on anything 13
external to this document, other documents, to support your opinion? A I 14
understand, I see. I did not.”).) Cellectis fails to direct us to evidence that this 15
testimony is untrustworthy. 16
Cellectis also asserts that SCRI fails to present sufficient evidence of actual 17
reduction to practice and falls short of proving prove priority. (See Cellectis Opp. 18
5, Paper 389, 1:11–13.) Because Cellectis does not direct us to any specific aspect 19
of SCRI’s priority case that is missing or inadequate, other than corroboration, 20
Cellectis’s assertion is not persuasive. 21
Instead, we are persuaded that the after considering and evaluating the 22
record as a whole, SCRI inventor’s testimony is corroborated by the testimony of 23
Drs. Curinga and Jarjour. Even if Drs. Curinga and Jarjour did not actually 24
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observe Dr. Gwiazda’s each and every action by looking over her shoulder, their 1
testimony and the circumstantial evidence of Dr. Gwiazda’s presentations are 2
consistent with Dr. Gwiazda’s testimony and her notebook pages. This evidence 3
persuades us that Dr. Gwiazda performed the experiments and obtained the results 4
to which she testifies. Cellectis does not direct us to evidence showing that any of 5
this evidence or testimony is untrustworthy. Accordingly, the preponderance of all 6
the evidence before us persuades us that Dr. Gwiazda actually reduced to practice 7
embodiments of Count 1 by 12 April, 30 April, and 6 May in 2018. See Lacotte v. 8
Thomas, 758 F.2d 611, 613 (Fed. Cir. 1985) (holding that the combination of 9
corroborating testimony and independent circumstantial evidence within an 10
organized research program, including testimony of the inventor, written evidence 11
in his notebook, and testimony of the inventor’s associate, was more than adequate 12
for the board to conclude the facts establishing an actual reduction to practice by a 13
preponderance of the evidence). 14
Conclusion 15
In light of the arguments presented by both SCRI and Cellectis, we consider 16
the preponderance of the evidence to support SCRI’s assertion that its inventors 17
reduced to practice an embodiment of Count 1 at least by 12 April 2010, and then 18
subsequently by 30 April 2010 and 6 May 2010. Because these dates are earlier 19
than Cellectis’s asserted date of conception, 27 October 2010, we exercise our 20
discretion and decline to review Cellectis’s arguments for an earlier conception or 21
diligence to a reduction to practice. (See Cellectis Motion 4, Paper 231.) The 22
issues presented by Cellectis’s priority motion, earlier conception and diligent 23
reduction to practice, are moot. We also decline to review SCRI’s arguments for 24
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conception by 29 March 2010 and diligence, because they are also moot in light of 1
SCRI’s earlier reduction to practice. (See SCRI Motion 4, Paper 374, 8:20–13:6.) 2
We enter judgment against Cellectis under 35 U.S.C. § 102(g) in a separate paper. 3

cc (via e-mail):

Attorney for Junior Party Cellectis:

Salvatore J. Arrigo
Scott M. K. Lee
LAW OFFICE OF SALVATORE ARRIGO AND SCOTT LEE, LLP
sal@arrigo.us
scott.lee@arrigo.us

Attorney for Senior Party SCRI:
E. Anthony Figg
R. Danny Huntington
Sharon E. Crane
Seth E. Cockrum
ROTHWELL, FIGG, ERNST & MANBECK, P.C.
efigg@rfem.com
dhuntington@rfem.com
scrane@rfem.com