# Teva Pharmaceuticals International GmbH v. Eli Lilly and Company

> District Court, D. Massachusetts · October 3, 2022

URL: https://www.frixlaw.com/law-library/cases/10200579

## Case

- **Court:** District Court, D. Massachusetts
- **Decided:** October 3, 2022
- **Opinion:** 100trialcourt
- **Cited by:** 0 later opinions in the Frix Law Library

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## Opinion text

UNITED STATES DISTRICT COURT
DISTRICT OF MASSACHUSETTS

TEVA PHARMACEUTICALS *
INTERNATIONAL GMBH and *
TEVA PHARMACEUTICALS *
USA, INC., *
*
Plaintiffs, *
* Civil Action No. 18-cv-12029-ADB
v. *
*
ELI LILLY AND COMPANY, *
*
Defendant. *
*

MEMORANDUM & ORDER ON CROSS-MOTIONS FOR SUMMARY JUDGMENT

Plaintiffs Teva Pharmaceuticals International GmbH and Teva Pharmaceuticals USA,
Inc. (collectively, “Teva”) and Defendant Eli Lilly and Company (“Lilly”), competing
pharmaceutical companies, have both developed antibodies capable of treating headache
disorders associated with calcitonin gene-related peptide (“CGRP”). In the instant case, Teva
alleges that Lilly has infringed three of its patents1 (the “Patents-in-Suit”), seeks a declaration
that Lilly is judicially estopped from raising arguments that conflict with arguments it made in
prior inter partes review (“IPR”) proceedings, and argues that Teva does not have unclean hands
or engage in inequitable conduct. Lilly, in turn, seeks declarations that its product, Emgality®,
also known as Galcanezumab, does not infringe the patents, willfully or otherwise, and that the
asserted patents are invalid under 35 U.S.C. § 112.

1 U.S. Patent Nos. 8,586,045 (the “’045 patent”); 9,884,907 (the “’907 patent”); and 9,884,908
(the “’908 patent”).
I. FACTUAL BACKGROUND
After weeding through the more than 1,296 pages of asserted facts and responses, the
following facts are undisputed except where otherwise noted.
A. Migraine, Headache Disorders & CGRP
“Migraine is a common chronic, recurrent neurological disorder that affects greater than

10% of adults globally and approximately 39 million individuals in the United States.” [ECF
No. 400 ¶ 106 (citation omitted)].2 It is among the more than 200 classifications of headache
disorders listed by the International Classification of Headache Disorders, 2nd edition. [Id. ¶
110].
CGRP is a neuropeptide that, as of 2005–2006,3 was understood to be involved in head
pain in a variety of contexts, including migraine headaches. [ECF No. 400 ¶¶ 114, P47]. At that
time, CGRP had been the subject of thousands of peer-reviewed articles, [id. ¶ P46], and drugs
affecting the CGRP pathway were used to treat migraine and other forms of headaches, [id. ¶
P48]. CGRP has four functional regions: (1) the N-terminal end; (2) the mid-region; (3) a hinge-

like region; and (4) the C-terminal end. [Id. ¶ 113].
B. Antibodies
An antibody, or immunoglobin, is a specialized protein molecule that recognizes and
binds to a target molecule known as an antigen. [ECF No. 400 ¶ 26]. “The main function of

2 The Court draws the facts primarily from the parties’ Reply Statements of Material Facts, [ECF
Nos. 387 (Unclean Hands), 389 (Judicial Estoppel), 395 (Willful Infringement), 400 (Written
Description), 406 (Non Infringement), and 411 (Lack of Enablement)], which contain both
parties’ positions on the material facts, and the documents referenced therein. The Court further
notes that citations to specific paragraphs are inclusive of the response to said paragraph.
3 The Court looks to scientific knowledge as of 2005 to 2006 because the Patents-in-Suit claim
priority to Provisional Application No. 60/736,623, which was filed on November 14, 2005, and
to Application No. 12/093,638, which was filed on November 2, 2006. [ECF No. 411 ¶ 142].
antibodies is to bind to antigens and neutralize them or to mark them for destruction.” [Id. ¶ 48].
The portion of an antigen that is bound by an antibody is called an epitope. [Id. ¶ 27].
Antibodies themselves are made up of amino acids that are connected to each other in linear
chains, often referred to as amino acid sequences. [Id. ¶ 29].
Typical full-length antibodies have four chains of amino acids: two identical heavy

chains and two identical light chains. [ECF No. 400 ¶¶ 30, 32]. Each heavy chain and each light
chain has a variable domain and each variable domain has three complementarity determining
regions (“CDRs”). [Id. ¶¶ 31–33]. Thus, a typical full-length antibody has six unique CDRs
and two unique variable domains. See [id. ¶¶ 32–33, 68, P35, P104]. The CDRs, which combine
to form the variable domains, form the primary binding interface between the antibody and the
epitope of the antigen, [id. ¶ 37], with the amino acid sequence of each of the CDRs causing the
variable domains to adopt unique three-dimensional structures, [ECF No. 406 ¶¶ 17–18]. The
amino acid sequence of the variable region differs for each antibody, [ECF No. 400 ¶ 34], and
contains approximately 220 amino acid residues, [id. ¶ 35].

The number of possible permutations of antibodies is extraordinarily broad. See [ECF
No. 400 ¶ 59]. The claims in the Patents-in-Suit, however, do not claim every antibody that
could possibly be generated, rather they claim “a specific subset of anti-CGRP antibodies that
antagonize CGRP function.” [Id. ¶ 66 (quoting ECF No. 296-64 ¶ 206)]. Lilly argues that this
subset of antibodies would nonetheless be extraordinarily hard to identify because “[a]s of 2005–
2006 it was not possible to predict an antibody’s function based on its amino acid sequence.”
[Id. ¶ 72]. Teva disputes this, arguing that, by that time, “it was well known that antibodies have
common amino acid sequences that contribute in known ways to known functions, including
antibodies generally and antibodies within particular known classes.” [Id.].
C. Development of Antibodies for Therapeutics
To be safe and effective as a treatment for any type of headache disorder, an antibody
must share certain general characteristics with naturally occurring human antibodies. See [ECF
No. 400 ¶¶ 93–94]. If it does not, the antibody may be recognized by the body as foreign and
become the target of a potentially dangerous immune response, resulting in the elimination of the

antibody, a loss of therapeutic efficacy, and possibly serious allergic reactions. [Id. ¶ 93].
As of 2005–2006, one of the processes used to develop new therapeutic antibodies
involved the use of murine (i.e., mouse) antibodies. [ECF No. 400 ¶ 91]. These murine
antibodies were generated by injecting mice with an antigen of interest, which caused the mouse
to produce a type of white blood cell, referred to as B cells, that, in turn, produced a large variety
of antibodies to protect against what the mouse’s immune system perceived as a foreign antigen.
See [id. ¶¶ 91–92]. Scientists then could isolate a B cell, fuse it to a cancer cell to form a hybrid
cell known as a hybridoma, which then produced antibodies having an identical amino acid
sequence (i.e., “monoclonal” antibodies). [Id. ¶ 92]. An antibody produced in this way is not

human, however, and to avoid human immune systems rejecting the foreign antibody, it was
necessary to use genetic engineering to “humanize” the murine antibodies. [Id. ¶¶ 93–94]. This
process involved replacing portions of the genes encoding the murine antibody with portions that
encode a human antibody. [Id. ¶ 94]. As of 2005–2006, humanization of murine antibodies was
sufficiently established to be considered “conventional” and “routine,” but the parties dispute
how labor intensive and time consuming the process was. See [id. ¶¶ 95–98, P8, P54, P64–66].
D. Key Antibody Attributes
To be effective in treating headache disorders caused by CGRP, an antibody produced by
the methods previously described must possess several characteristics. Among the most
important is its “affinity” for the target antigen, which refers to how strongly the antibody
attaches to the target. [ECF No. 400 ¶ 42]. One measure of affinity is the dissociation constant
of the antibody-antigen interaction, or “KD” value. See [id. ¶ 189]. A related property is an
antibody’s “neutralizing” capability, meaning its ability to inhibit the biological activities of the
antigen to which it binds. [Id.]. A high affinity is integral to an antibody’s neutralizing
capability, otherwise the antibody will not effectively inhibit the target antigen (e.g., CGRP).

See [id. ¶ P67].4
E. The Asserted Patents and Specifications
Teva asserts twenty claims from three patents: the ’045, ’907, and ’908 patents. See
[ECF No. 400 ¶ 1; ECF No. 298 at 6]. The patents each claim the use of human or humanized
anti-CGRP antagonist antibodies5 to treat vasomotor symptoms, such as headaches. [ECF No.
400 ¶ 185–86]. The ’045 patent is titled “Methods of Using Anti-CGRP Antagonist Antibodies,”
and the ’907, and ’908 patents share the title “Methods for Treating Headache Using Antagonist
Antibodies Directed Against Calcitonin Gene-Related Peptide.” [ECF No. 387 ¶¶ 1, 3, 5].
Named inventors for all three patents include, among others, Joerg Zeller, Kristian T. Poulsen,
Yasmina Noubia Abdiche, and Jaume Pons. [Id. ¶¶ 2, 4, 6]. Each of the Patents-in-Suit claim

priority to Provisional Patent Application No. 60/736,623, which was filed on November 14,
2005, and to Application No. 12/093,638, which was filed on November 2, 2006, [ECF No. 400
¶ 183], and later published on May 18, 2007 as International Publication Number WO
2007/054809 (the “’809 application”), [ECF No. 395 ¶ P2].

4 Teva objects to Paragraph P67, [ECF No. 400 ¶ P67], but does not dispute that antibodies that
bind to the C-terminal, mid-, or N-terminal regions of CGRP can all antagonize CGRP if they
exhibit high enough binding affinity and block CGRP’s interaction with the CGRP receptor.
5 The Court has construed the term “anti-CGRP antagonist antibody” as “an antibody that is able
to bind to CGRP and inhibit CGRP biological activity and/or downstream pathway(s) mediated
by CGRP signaling.” [ECF No. 101 at 11].
i. The ’045 Patent
Teva asserts one independent claim from the ’045 patent, which recites as follows:

17. A method for reducing incidence of or treating headache in a human,
comprising administering to the human an effective amount of anti-CGRP
antagonist antibody, wherein said anti-CGRP antagonist antibody is a human
monoclonal antibody or a humanized monoclonal antibody.

[ECF No. 400 ¶ 251]. The Court has previously construed the term “effective amount” to
mean “an amount sufficient to effect beneficial or desired results, including but not
limited to clinical results.” [ECF No. 101 at 31]. Teva also asserts seven dependent
claims of the ’045 patent, [ECF No. 400 ¶ 252]: claims 18 and 21 recite specific amino
acid sequences of portions of the antibodies, [id. ¶¶ 253, 256], claim 19 limits the
condition treated to several specific headache disorders, [id. ¶ 254], claim 20 specifies the
strength of binding, [id. ¶ 255], claim 24 limits the condition treated to migraine, [id. ¶
257], claim 27 limits the routes of administration, [id. ¶ 258], and claim 30 requires that
the anti-CGRP antagonist antibody is a humanized monoclonal antibody, [id. ¶ 259].
ii. The ’907 and ’908 Patents
Teva similarly asserts one independent claim of the ’907 patent, claim 1, which recites as
follows:
1. A method for treating headache in an individual, comprising: administering to
the individual an effective amount of a humanized monoclonal anti-[CGRP]
antagonist antibody, comprising: two human IgG heavy chains, each heavy chain
comprising three complementarity determining regions (CDRs) and four
framework regions, wherein portions of the two heavy chains together form an Fc
region; and two light chains, each light chain comprising three CDRs and four
framework regions; wherein the CDRs impart to the antibody specific binding to a
CGRP consisting of amino acid residues 1 to 37 of SEQ ID No:15 or SEQ ID
NO:43.

[ECF No. 400 ¶ 262]. Teva has asserted five dependent claims from claim 1 of the ’907
patent: claim 4 requires that the antibody be administered intravenously or
subcutaneously, [id. ¶ 264], claim 5 limits the condition treated to one of a specific set of
headache disorders, [id. ¶ 265], claim 6 limits the condition treated to migraine, [id. ¶
266], and claim 15 specifies that the constant regions of the IgG heavy chains are IgG4
constant regions, [id. ¶ 267].
The asserted independent claim from the ’908 patent, claim 1, is identical to claim

1 of the ’907 patent, with the following information added to the end: “and wherein the
antibody binds to the CGRP with a binding affinity (KD) of about 10 nM or less as
measured by surface plasmon resonance at 37° C.” [ECF No. 400 ¶ 269]. Teva asserts
five dependent claims from the ’908 patent, which are identical in number and language
to the dependent claims asserted in the ’907 patent. [Id. ¶¶ 270–75].
iii. The Shared Specification of the Patents-in-Suit
The specifications in each of the Patents-in-Suit are substantively identical, [ECF No. 400
¶ 184], and describe the claimed invention as “concern[ing] anti-CGRP antagonist antibodies and
methods of using anti-CGRP antagonist antibodies for treating or preventing . . . headaches, such

as migraine” as well as other types of headaches. [ECF No. 411 ¶ 144]. The specification (1)
states that” [a]nti-CGRP antagonist antibodies are known in the art . . . .” [ECF No. 400 ¶ 204
(Teva, in response, citing the ’045 patent at 25:59–61)];6 (2) describes a full-length humanized
“anti-CGRP antagonist antibody referred to as Antibody G1 and later re-named
fremanezumab[,]” [ECF No. 411 ¶ 145 (citations omitted)], as well as 84 humanized anti-CGRP
antibody variants of G1 (“M1-M84”), which vary from Antibody G1 by 10 or fewer amino acids,

6 Lilly agrees that murine anti-CGRP antibodies were known in the art but disputes that
humanized or human anti-CGRP antibodies were known in the art. See, e.g., [ECF No. 400 ¶
P28].
[ECF No. 400 ¶¶ 192, P103];7 (3) discloses the complete amino acid sequence of Antibody G1,
including the variable region and CDR portions of the antibody, [id. ¶ P104]; (4) discloses, in
addition to the humanized antibodies, 12 murine anti-CGRP antibodies, seven of which were
shown to be CGRP antagonists, [id. ¶ P102]; (5) describes “the routine methods for making
humanized and human antibodies[,]” [id. ¶ P97 (citation omitted)], but does not disclose how

Antibody G1, in particular, was made, [id. ¶ 188]; (6) states that by 2005–2006, methods for
humanization of antibodies were well-known, routine, and reliable in the prior art and that
conventional humanization techniques were routinely used that preserved the affinity and
specificity of the donor antibody, [id. ¶ P64–65]; (7) discloses that there were well-known
screening techniques, such as the cAMP activation assay, that allowed researchers to determine
whether an antibody antagonized CGRP,8 [id. ¶ P63]; (8) reports that Antibody G1 binds to the
C-terminal end of CGRP, [id. ¶ 190]; (9) includes data on antibodies that bind to CGRP’s C-
terminal but do not inhibit CGRP’s effects, [ECF No. 387 ¶ 22]; (10) provides instruction about
how to formulate antibodies, including anti-CGRP antagonist antibodies, and various modes of

administration, [ECF No. 400 ¶ P135]; (11) offers specific examples of formulations for
common modes of administration and cites prior art where further detail can be found, [id.];9

7 Light chain CDR3, heavy chain CDR1, and heavy chain CDR3 of all 84 variants (M1–M84)
are identical to those of Antibody G1. [ECF No. 400 ¶ 194]. Additionally, the specification
does not report in vitro or in vivo experiments evaluating the ability of antibodies M1–M84 to
inhibit CGRP biological activity. [Id. ¶ 196]
8 The parties dispute whether the specification disclosed human anti-CGRP antagonist
antibodies: such antibodies are not explicitly referenced, but the technology to humanize
antibodies was “routine” and discussed in the specification. Compare [ECF No. 400 ¶ 205] with
[id. ¶ P66, P96].
9 Lilly purports to object to Paragraph P135, [ECF No. 400 ¶ 135], however, Lilly does not
dispute that the specification includes specific examples of formulations for common modes of
administration. Rather, Lilly argues that the specification “offer[s] no support to show that the
inventors made anti-CGRP antibody formulations that included all possible routes of
(12) describes how anti-CGRP antagonist antibodies can be used to treat headache by
administering an anti-CGRP antagonist antibody to a patient prior to, during and/or after
headache, [id. ¶ P134]; and (13) reports activity of Antibody G1 in two assays conducted in rats:
a saphenous nerve assay and a closed cranial window assay, [id. ¶ 214].10
Teva currently has an antibody product within the scope of its patents called Ajovy®

(Fremanezumab), that is prescribed to treat migraine. [ECF No. 400 ¶ 375].
iv. Information Omitted from the Specification
Lilly alleges that by not disclosing certain information in the shared specification of the
Patents-in-Suit, Teva engaged in inequitable conduct. [ECF No. 387 ¶ 13]. In particular, Lilly
points to the fact that named inventors, Drs. Zeller and Pons, did not, in the ’045 patent, disclose
to the U.S. Patent and Trademark Office (“PTO”) prior art literature of which they were aware,
specifically, Shaw et al., The effect of monoclonal antibodies to calcitonin gene-related peptide

administration in the art” and claims that “Teva’s inventors testified to not having made any anti-
CGRP antibody formulations for certain routes of administration known in the art.” [Id.].
Neither of Lilly’s assertions, however, disputes Teva’s claim that the specification includes
specific examples of formulations for common modes of administration.
10 The saphenous nerve assay tests whether an anti-CGRP antibody can inhibit CGRP biological
function in a live animal at a site of action relevant to migraine, whereas the closed cranial
window assay measures the effect of an anti-CGRP antagonist antibody on the dilation of dural
arteries, which is known to be associated with head pain. Teva asserts that a positive result in the
closed cranial window assay was understood to be predictive of efficacy for treating migraine in
humans, and although Lilly does not directly dispute this statement, Lilly claims the assertion is
contradicted by Teva’s expert who testified that “preclinical animal experiments [] will never
satisfy concerns about efficacy and safety . . . .” [Id. ¶ P79]. Lilly further claims that Teva’s
statement is unsupported because its specification states that “the precise pathophysiology of
migraine is not yet well understood.” [Id.]. The Court notes that neither piece of testimony cited
by Lilly actually contradicts Teva’s statement and therefore finds that the Teva’s assertion—that
a positive result in the closed cranial window assay was understood to be predictive of
efficacy—is not disputed. Teva acknowledges that the specification does not disclose any
experiment involving administration of anti-CGRP antibodies to non-human primates or humans.
[ECF No. 411 ¶¶ 196–97]. The parties do dispute, however, whether the results from the assay
address the blood-brain barrier (“BBB”). Cf. [ECF No. 400 ¶ 219] with [id. ¶ 115].
(CGRP) on CGRP-induced vasodilation in pig coronary artery rings, 106 Br. J. Pharmacol. 196,
196–98 (1992) (“Shaw”), which taught, in part, that no antibody studied in the paper that bound
to the mid-region of CGRP had blocked CGRP activity. [Id.]. Lilly further asserts that Drs.
Zeller and Pons committed inequitable conduct by not disclosing to the PTO (1) the results of
experiments that showed that some N-terminal antibodies bind to but, nevertheless, do not

antagonize CGRP, [ECF No. 348-1 at 9]; see [ECF No. 387 ¶ 40]; (2) certain non-C-terminal
binding data that addressed polyclonal antibodies, [ECF No. 387 ¶ 41; ECF No. 348-1 at 9]; and
(3) data from a cortical spreading depression (“CSD”) assay, [ECF No. 387 ¶ 15; ECF No. 348 at
11]. With regard to this last point, the CSD assay was, at the time, a preferred in vivo test used to
evaluate migraine pathophysiology because it allowed researchers to, among other things,
evaluate whether a drug could effect a particular migraine symptom. [ECF No. 387 ¶ 53]. Lilly
claims that Dr. Pons was on notice of the importance of the test because he was on an email
chain in which another scientist stated that if the anti-CGRP antibody “doesn’t work” in the
assay, “then the whole concept is questionable.” [Id. ¶ 57 (quoting ECF No. 354-26)]. Lilly’s

expert Dr. Charles described the CSD assay results as “material” in his report, which, in his
view, meant that the information was “germane to the patent issue.” [Id. ¶ 28 (quoting ECF No.
304-18)]. The parties dispute whether the results of the CSD assay were either inconclusive
because the experiment lacked a control (Teva’s position) or negative (Lilly’s position), and
whether a negative result means that the antibody does not work to treat migraine. [Id. ¶¶ 54–
56].
F. Lilly’s Development of Emgality® (Galcanezumab) and Knowledge of Teva’s
Patents
In 2004, Lilly began a program to develop an anti-CGRP antagonist antibody for the
therapeutic treatment of migraine, which eventually led to the creation of Emgality. [ECF No.
395 ¶ 21]. During this process Lilly successfully generated murine antibodies that bound to the
mid-region of CGRP, screened them for CGRP antagonism, and ultimately humanized an
antibody that was later named Galcanezumab. [Id. ¶¶ 28–32]. Lilly did not create
Galcanezumab, however, until 2008–2009.11 [Id. ¶ P4]. Lilly also applied for and was granted a
patent (U.S. Patent No. 9,505,838 (the “’838 patent”)) directed to the use of Galcanezumab to

treat migraine. [ECF No. 406 ¶ 125]. Galcanezumab is the only therapeutic antibody approved
by the FDA to treat episodic cluster headache. [ECF No. 411 ¶ 311].
Lilly had knowledge of the ’045 patent at least as early as October 24, 2017, and
knowledge of the ’907 and ’908 patents as early as February 6, 2018. [ECF No. 395 ¶ P1]. As
discussed above, the Patents-in-Suit claim priority to the ’809 application, [id. ¶ P2], which
shares the same specification as the Patents-in-Suit. [Id. ¶ P3]. Lilly was aware of the ’809
application as of June 7, 2011. [Id. ¶ P5].
G. Lilly’s Marketing and Sale of Emgality®
Lilly has continuously made, marketed, and sold Emgality since October 2018. [ECF

No. 395 ¶ P13]. Leading up to the launch in 2018, Lilly undertook a sales and marketing
campaign to promote its product. See [id. ¶ P14].12
Lilly’s campaign included spending $523.5 million on marketing between 2018 and
2020, [ECF No. 395 ¶ P14], and nearly $225 million on its U.S. Emgality sales force in that
same time period, [id ¶ P15]. Internal documents also state that Lilly’s focus was on “strategic
objectives to ‘Win’ and ‘Grow’ the CGRP class,” [id. ¶ P17 (quoting ECF No. 368-82)], and

11 Lilly selected a lead murine antibody for humanization in April 2008, and later decided to
advance the resulting humanized compound to clinical development in December 2009. [ECF
No. 395 ¶ P4].
12 Lilly raises objections to this statement of fact, but does not dispute the underlying assertion
that it engaged in a marketing campaign to promote Emgality.
describe the U.S. Emgality campaign as having a “land grab” mentality at the time the product
launched, [id. ¶ P18 (quoting ECF No. 368-80) (exhibit to witness deposition)]. Lilly’s
campaign also involved providing free samples to healthcare providers and offering increased
rebates to pharmacy benefits managers to ensure that health insurance formularies would cover
Emgality. [Id. ¶ P23–24].

H. Procedural Background
Teva initiated this lawsuit on September 27, 2018, claiming that Lilly infringed nine of
Teva’s patents. [ECF No. 411 ¶ 2]. Soon after, Lilly responded by filing a petition for IPR by
the Patent Trial and Appeal Board (“PTAB”) of the three Patents-in-Suit (the “Method of
Treatment patents”) as well as an additional six patents (the “Composition of Matter patents”).
[Id. ¶¶ 3–4]. The Composition of Matter patents and the Method of Treatment patents are
directed at the same type of antibodies. [Id. ¶ P3].13
During the Composition of Matter IPR proceedings, Lilly argued that it would have been
obvious to make a humanized anti-CGRP antibody within the scope of the claims, [ECF No. 290

at 16–17], and that “by 2005, conventional humanization techniques were routinely used that
preserved the affinity and specificity of the donor antibody[,]” see [ECF No. 411 ¶ P8]. Lilly
further claimed that a person of ordinary skill in the art (“POSA”)14 “would have had a
reasonable expectation of successfully making a humanized anti-CGRP antagonist antibody.”

13 Although Lilly objects to Teva’s statement of fact, it does not dispute that the type of antibody
at issue in the Composition of Matter patents (i.e., human and/or humanized anti-CGRP
antagonist antibodies) are also at issue in the Patents-in-Suit. See [ECF No. 411 ¶ 10].
14 The parties agree that a person of ordinary skill in the art would have either (1) a Ph.D. in a
relevant field such as immunology, biochemistry, or pharmacology, with several years of post-
doctoral experience in antibody engineering, pharmacokinetics, and pharmacodynamics, or (2)
an M.D. with a residency or specialty in neurology, and several years of experience studying
CGRP or treating patients with a CGRP-related disease, such as migraine headaches. [ECF No.
411 ¶¶ 223–24].
[Id. ¶ P9 (citing ECF No. 368-2 at 95, 98; ECF No. 368-3 at 104–06)]. During the proceedings,
Teva argued that the challenged patents represented “the first time that anyone, anywhere in the
world developed a humanized anti-CGRP antibody that could successfully be used as a human
therapeutic.” [Id. ¶ 7 (quoting ECF No. 292-15 at 6)]. The PTAB sided with Lilly and found
that the six Composition of Matter patents were unpatentable as obvious. [Id. ¶ P4]. In so

concluding, it found that “anti-CGRP antagonist antibodies were well known in the art, and that
the art encouraged the development of humanized anti-CGRP antibodies.” [Id. ¶ P5 (quoting
ECF No. 368-2 at 95)]. Teva appealed the PTAB’s decision, and the Federal Circuit affirmed.
[Id. ¶ 16].
The Method of Treatment patents, generally speaking, are directed to the treatment of
headache disorders with antibodies that bind to CGRP and inhibit its function. [ECF No. 387 ¶
8].15 In the Method of Treatment IPR proceedings, Teva argued that the patents were not
obvious as a POSA “would not have used a full-length antibody to treat migraine because it

15 Lilly claims to dispute Paragraph 8 of Teva’s statement of material facts, see [ECF No. 387 at
3–4], which states, “The patent claims at issue in this case are directed to treating migraines by
using antibodies that bind to the peptide [CGRP] and inhibit its function.” Upon review,
however, Lilly’s response does not raise any dispute and merely quibbles about whether CGRP
is a singular peptide and repeats Lilly’s argument that Teva’s antibodies bind only to the C-
terminal end of CGRP whereas other antibodies inhibit CGRP by binding to its middle-region or
N-terminal end. [Id.]. To begin, it is not clear that Teva’s statement asserts that CGRP is
singular, therefore Lilly’s claim that CGRP “consists of alpha and beta isoforms” does not
necessarily reflect a dispute. [Id. at 4]. Moreover, even if there was a dispute, “[a] ‘material
fact’ is one that ‘might affect the outcome’ of the case[,]” Intercontinental Great Brands LLC v.
Kellogg N. Am. Co., 869 F.3d 1336, 1343 (Fed. Cir. 2017) (quoting Anderson v. Liberty Lobby,
Inc., 477 U.S. 242, 248 (1986)), and whether CGRP is singular does not impact the Court’s
analysis of the issues presently before it. Teva’s statement also does not make any claim as to
which portion of CGRP the antibodies bind, therefore Lilly’s discussion of antibodies that bind
to the N-terminal and mid-region does not evidence a dispute. Lilly further argues that Teva’s
statement is disputed because the claims in the Patents-in-Suit are directed towards treating other
headache conditions in addition to migraine. [Id. at 4]. That assertion, however, does not
dispute that the facts set forth in Paragraph 8, i.e., that the Patents-in-Suit pertain to the use of
antibodies to treat migraine by binding and inhibiting CGRP.
would not have been expected to cross the [blood brain barrier (““BBB”’)].”. [ECF No. 400 § P18
(quoting ECF No. 296-17 at 9)]. The PTAB agreed, finding that uncertainty about whether
antibodies would need to cross the BBB weighed against a reasonable expectation of success in
using the claimed methods, and therefore weighed against obviousness. [Id. ] P20]. Lilly
appealed and the Federal Circuit affirmed. [Id. § P17].
The parties have now filed six cross-motions for summary judgment. Teva’s motions
argue that Lilly should be judicially estopped from raising arguments contrary to the positions it
advanced in the IPR proceedings and that Lilly cannot succeed on its inequitable conduct claims.
Lilly’s motions contend that its product, Emgality, does not infringe, willfully or otherwise, the
claims of the Patents-in-Suit and, alternatively, that Teva’s patents are invalid for lack of written
description and lack of enablement.
II. STANDARD OF REVIEW
Summary judgment is appropriate where the moving party can show that “there is no
genuine dispute as to any material fact and the movant 1s entitled to judgment as a matter of
law.” Fed. R. Civ. P. 56(a). “[A]n issue is ‘genuine’ if it ‘may reasonably be resolved in favor
of either party.”” Robinson v. Cook, 863 F. Supp. 2d 49, 60 (D. Mass. 2012) (quoting Vineberg
v. Bissonnette, 548 F.3d 50, 56 (1st Cir. 2008)). “A fact is material if its resolution might affect
the outcome of the case under the controlling law.” Cochran v. Quest Software, Inc., 328 F.3d 1,
6 (1st Cir. 2003) (citation omitted). By invoking summary judgment, “the moving party in effect
declares that the evidence is insufficient to support the nonmoving party’s case.” United States
v. One Parcel of Real Prop. (Great Harbor Neck, New Shoreham, R.I.), 960 F.2d 200, 204 (1st
Cir. 1992) (citing Celotex Corp. v. Catrett, 477 U.S. 317, 325 (1986)).

14

“To succeed in showing that there is no genuine dispute of material fact, the moving
party must . . . ‘affirmatively produce evidence that negates an essential element of the non-
moving party’s claim,’ or, using ‘evidentiary materials already on file . . . demonstrate that the
non-moving party will be unable to carry its burden of persuasion at trial.’” Ocasio-Hernández
v. Fortuño-Burset, 777 F.3d 1, 4–5 (1st Cir. 2015) (quoting Carmona v. Toledo, 215 F.3d 124,

132 (1st Cir. 2000)).
Conversely, “[t]o defeat a properly supported motion for summary judgment, the
nonmoving party must establish a trial-worthy issue by presenting enough competent evidence to
enable a finding favorable to the nonmoving party.” ATC Realty, LLC v. Town of Kingston,
N.H., 303 F.3d 91, 94 (1st Cir. 2002) (internal quotations and citation omitted). That is, the
nonmoving party must set forth specific, material facts showing that there is a genuine
disagreement as to some material fact. One Parcel of Real Prop., 960 F.2d at 204 (citing
Anderson., 477 U.S. at 247–48).
In reviewing the record, the Court “must take the evidence in the light most flattering to

the party opposing summary judgment, indulging all reasonable inferences in that party’s favor.”
Cochran, 328 F.3d at 6 (citation omitted). The First Circuit has noted that this review “is
favorable to the nonmoving party, but it does not give him a free pass to trial.” Hannon v. Beard,
645 F.3d 45, 48 (1st Cir. 2011). “The factual conflicts upon which he relies must be both
genuine and material[,]” Gomez v. Stop & Shop Supermarket Co., 670 F.3d 395, 397 (1st Cir.
2012), and the Court may discount “conclusory allegations, improbable inferences, and
unsupported speculation.” Cochran, 328 F.3d at 6 (quoting Medina-Muñoz v. R.J. Reynolds
Tobacco Co., 896 F.2d 5, 8 (1st Cir. 1990)).
III. Discussion
A. Judicial Estoppel
Teva contends that Lilly should be precluded from advancing certain factual arguments in
the instant proceedings because Lilly took the opposite position in the IPR proceedings and won.
[ECF No. 315 at 6]. Those alleged contradictory arguments pertain to the following three fact

issues: (1) what a POSA would understand about anti-CGRP antagonist antibodies and the
process for preparing them; (2) the techniques available to that POSA to screen anti-CGRP
antibodies for antagonistic activity; and (3) the techniques available to that POSA to humanize
anti-CGRP antagonist antibodies. [ECF No. 356-1 at 14, 23–25]. Teva asks that the Court hold
Lilly to the positions that it took in the IPR proceedings and find that the following facts are
established:
1. Anti-CGRP antagonist antibodies were well-known in the art as of 2005;

2. By 2005, a POSA would have considered the techniques for generating anti-CGRP
antagonist antibodies “routine” and “conventional”;

3. By 2005, the techniques for preparing humanized antibodies from non-human
antibodies were well-established and conventional to a POSA;

4. By 2005, conventional humanization techniques that were routinely used preserved
the affinity and specificity of the donor antibody.

5. By 2005, assays that measured antagonism, such as cAMP activation assays and
radioligand binding assays were conventional and routine means of evaluating
whether an anti-CGRP antibody was able to antagonize CGRP.
[ECF No. 315 at 25].
“As a general matter, the doctrine of judicial estoppel prevents a litigant from pressing a
claim that is inconsistent with a position taken by that litigant either in a prior legal proceeding
or in an earlier phase of the same legal proceeding.” InterGen N.V. v. Grina, 344 F.3d 134, 144
(1st Cir. 2003). The purpose of the doctrine is to safeguard the integrity of the courts and avoid
the “perception that either the first or the second court was misled[,]” New Hampshire v. Maine,
532 U.S. 742, 750 (2001), and it applies to a variety of positions a party may take, including an
“expression of intention, a statement of fact, or a legal assertion[,]” Alt. Sys. Concepts, Inc. v.
Synopsys, Inc., 374 F.3d 23, 34 (1st Cir. 2004) (quoting Wagner v. Prof’l Eng’rs in Cal. Gov’t,
354 F.3d 1036, 1044 (9th Cir. 2004)). Judicial estoppel is applied at the court’s discretion, but

“with caution to avoid impinging on the truth-seeking function of the court.” Sexual Minorities
Uganda v. Lively, 899 F.3d 24, 32 (1st Cir. 2018) (quoting Perry v. Blum, 629 F.3d 1, 11 (1st
Cir. 2010)).
In general, the party seeking to invoke judicial estoppel must satisfy three conditions.
Díaz-Báez v. Alicea-Vasallo, 22 F.4th 11, 21 (1st Cir. 2021). First, the prior position of the party
to be estopped must be directly inconsistent with its current position such that they are mutually
exclusive. Id. It is not enough for the moving party to simply point to an “appearance of
inconsistency.” Lampi Corp. v. Am. Power Prods., Inc., 228 F.3d 1365, 1377 (Fed. Cir. 2000).
Second, the accused party must have persuaded the prior court to accept or otherwise rely on its

previous position. Díaz-Báez, 22 F.4th at 21. Third, “the party seeking to assert the inconsistent
position must stand to derive an unfair advantage if the new position is accepted by the court.”
Id. (quoting Knowlton v. Shaw, 704 F.3d 1, 10 (1st Cir. 2013)); see also RFF Family P’ship, LP
v. Ross, 814 F.3d 520, 528 (1st Cir. 2016); Alt. Sys., 374 F.3d at 33 (1st Cir. 2004). Courts also
“often inquire as to whether judicial acceptance of a party’s initial position conferred a benefit on
that party.” Alt. Sys., 374 F.3d at 33 (citation omitted).
Judicial estoppel is not limited to Article III proceedings, and also applies where a party
takes a position in a judicial proceeding that is inconsistent with a position that party took before
an administrative tribunal, including in an IPR proceeding before the PTAB. See e.g., Portela-
Gonzalez v. Sec’y of the Navy, 109 F.3d 74, 78 (1st Cir. 1997) (“Equitable doctrines of estoppel
apply in administrative and judicial fora.”); see also Egenera, Inc. v. Cisco Sys., Inc., 972 F.3d
1367, 1380 (Fed. Cir. 2020) (“[W]e agree that judicial estoppel can occur in an administrative
tribunal.”)
The Court analyzes in turn each category of Lilly’s allegedly inconsistent arguments. To

be “clearly inconsistent,” positions must be “mutually exclusive” and “directly inconsistent.”
RFF, 814 F.3d at 528 (quoting Alt. Sys., 374 F.3d at 33).
i. Anti-CGRP Antibodies and the Processes to Make Them
Lilly argued in the Composition of Matter IPRs that murine anti-CGRP antibodies were
well-known in the art, [ECF No. 389 ¶ 6], and that “murine monoclonal anti-CGRP antagonist
antibod[ies] . . . . were extensively described in the prior art[,]” [id. ¶ 7 (quoting ECF No. 317-2
at 5–6)].16 Lilly also asserted that “[b]y 2005, several publications had described anti-CGRP
antagonist antibodies[,]” [id. ¶ 8 (quoting ECF No. 317-5 at 5)], and that “anti-CGRP antagonist
antibodies could be created by known, established, and standard techniques[,]” [id. ¶ 9 (quoting

ECF No. 317-5 at 10–11)]. Lilly further claimed that techniques for making murine monoclonal
anti-CGRP antagonist antibodies that bind to human CGRP “were extensively described in the
prior art[,]” [id. ¶ 11 (quoting ECF No. 317-2 at 5–6)], such that a POSA “would have expected
that a similar antibody [i.e., other anti-CGRP antagonist antibodies] could be prepared using

16 Although Lilly claims to dispute Paragraph 7 of Teva’s statement of material facts, after
careful consideration of Lilly’s response, the Court concludes that there is no factual dispute.
Lilly’s petition seeking inter partes review of one of the Composition of Matter patents states
that “The first step in making a humanized anti-CGRP antagonist antibody . . . would have been
to make a murine monoclonal anti-CGRP antagonist antibody that binds to human CGRP. Such
antibodies, and techniques for making them, were extensively described in the prior art.” There
can be no good faith dispute that in the latter sentence, Lilly was referring to murine anti-CGRP
antagonist antibodies.
routine and conventional antibody preparation methods[,]” [id. ¶ 12 (quoting ECF No. 317-3 at
5)].
In the instant case, Lilly posits that the “state of the art” was “nascent” and “contained
minimal information about CGRP antibodies.” [ECF No. 389 ¶ 22 (quoting ECF No. 317-1 at
20)].17 Lilly additionally claims that there were “few reported murine anti-CGRP antibodies” in

the prior art and that those that were known “had unpredictable properties and functions, with
some enhancing CGRP’s activity rather than antagonizing it.” [Id. ¶ 20 (quoting ECF No. 317-6
at 3)]. Further, with respect to the process for making anti-CGRP antagonist antibodies, Lilly
asserts that “[a]s of 2005 and 2006, the art of antibody engineering . . . was highly unpredictable”
because “[t]he diversity of antibody repertoire generated by immunizing a live animal, like a
mouse, is vast, highly variable, and uncontrollable.” [Id. ¶¶ 24–25 (quoting ECF No. 317-1 at
11)].
With the exception of Lilly’s contention that the prior art “contained minimal information
about CGRP antibodies[,]” [ECF No. 389 ¶ 22 (quoting ECF No. 317-1 at 20)], Lilly’s current

and prior positions are not so clearly inconsistent as to warrant summary judgment. Lilly’s
claims in the IPR proceedings that murine anti-CGRP antagonist antibodies were extensively
described by multiple publications in the prior art and its argument here, that only a few murine
anti-CGRP antibodies had been reported, are not mutually exclusive. The same reasoning
applies to Lilly’s comments about the processes used to make anti-CGRP antagonist antibodies:
that the techniques to make the antibodies were extensively described, such that a POSA could

17 Lilly also disputes Paragraph 22 of Teva’s statement of material facts and argues that Teva’s
“excerpted and strung together quotations mischaracterize Lilly’s disclosures and [its expert’s]
opinions.” [ECF No. 389 ¶ 22]. The Court has closely reviewed the full excerpt offered by
Lilly, and does not agree that Teva has misrepresented Lilly’s position in the present case.
expect to make other anti-CGRP antagonist antibodies using said techniques, does not foreclose
the possibility that the process was also unpredictable and that the outcomes of the process were
highly variable.
Conversely, it is exceedingly difficult to square Lilly’s argument to the PTAB that
murine anti-CGRP antagonist antibodies were well known and extensively described in the prior

art with its current argument that the prior art “contained minimal information about CGRP
antibodies.” [ECF No. 389 ¶ 22 (quoting ECF No. 317-1 at 20)]. As this is a motion for
summary judgment, however, the Court must draw all ambiguities and factual inferences in the
light most favorable to the non-moving party, Lilly. Lilly’s current position is that the prior art
contained minimal information about CGRP antibodies, generally, whereas it argued to the
PTAB that anti-CGRP antibodies, specifically, were well known and extensively described in the
prior art. Drawing all inferences in Lilly’s favor, as it must, the Court concludes that it’s
conceivable that while a subset of CGRP antibodies (i.e., anti-CGRP antibodies) was well
known, little was known about the larger class of antibodies (i.e., CGRP antibodies, generally).

Therefore, the Court concludes that Lilly’s positions on this fact issue are not contradictory
enough to support summary judgment.
ii. Screening for Antibodies that Antagonize CGRP
In the Composition of Matter IPRs, Lilly argued that by 2005–2006 a POSA had access
to routine and conventional assays (i.e., tests) to screen humanized anti-CGRP antibodies to
determine whether they possessed desired attributes such as binding to and inhibiting CGRP.
[ECF No. 389 ¶ 28]; see e.g., [id. ¶ 29 (“Lilly asserted that ‘Teva’s own disclosures established
that the use of the radioligand binding in SK-N-MC cells is a routine and conventional assay.’”)
(alteration omitted); id. ¶ 30 (“Lilly asserted that “[a] POSA would . . . have expected to generate
a humanized anti-CGRP antagonist antibody with similar properties that could be evaluated by
the well-known and routine radioligand assay in SK-N-MC cells.’”); id. ¶ 33 (Lilly asserted that
“as of Teva’s earliest filing date, radioligand binding assays in SK-N-MC cells were routinely
used for measuring the ability of a CGRP antagonist from [sic] binding of human CGRP with its
receptor.”)]. Lilly also took the position that “measuring inhibition of cAMP activation [was] a

conventional means of evaluating whether an anti-CGRP antagonist antibody is, in fact, an anti-
CGRP antagonist.”18 [Id. ¶ 27 (quoting ECF No. 317-4 at 3)]. In addition to asserting that the
tests were routine and conventional, Lilly further claimed that “SK-N-MC cells were a
commercially available assay medium that a POSA would have had readily available for
measuring inhibition of cAMP activation,” as “evidenced by [a prior scientific publication].”
[Id. ¶ 31 (quoting ECF No. 317-4 at 5)].
Lilly presently argues that the Patents-in-Suit “fail to provide adequate guidance on how
to screen for humanized anti-CGRP antagonist antibodies that would be efficacious in treating a
human disease.” [ECF No. 389 ¶ 41 (quoting ECF No. 317-1 ¶ 285)]. Lilly also avers that the

screening process required to practice the claimed methods “would require that same lengthy
trial-and-error process for as many as 20220 different antibody sequences . . . .” [Id. ¶ 42 (quoting
ECF No. 317-1 ¶ 278)]. Further, Lilly claims that “conducting cAMP and in vivo animal assays
to adequately characterize a single compound requires significant work and time for setting up
the experimentation, selecting and evaluating appropriate controls, testing the compound of
interest itself, and appropriately evaluating the results . . . . Overall, conducting such assays for

18 Lilly claims to dispute that it took this position in the IPRs, asserting that its petition merely
cited to Teva’s patent’s admissions, not the prior art. [ECF No. 389 ¶ 27]. Having reviewed
Lilly’s petition for inter partes review, it is clear that, whether or not Lilly was citing Teva’s
patent’s admissions, it was adopting the position that measuring the inhibition of cAMP
activation was a conventional means of evaluating CGRP antagonism.
even a single compound would take at least four months.” [Id. ¶ 43 (quoting ECF No. 317-6 ¶
329)].
Here, again, Lilly’s positions are not so contradictory as to warrant summary judgment.
In the IPR proceedings, Lilly argued that tests used to screen antibodies for desired traits were
conventional, routine, and commercially available. Lilly did not argue, importantly, that tests

that identified whether, for example, an antibody binds to CGRP, also indicate whether the test
will be efficacious in treating human disease such as migraine. Further, Lilly’s position before
the PTAB that a test was routine is not inconsistent with its present argument that the screening
process to identify antibodies covered by the claimed methods would be lengthy and require
significant time and effort. Because Lilly’s positions are not more specifically contradictory, the
Court will not impose the harsh sanction of judicially estopping Lilly from making arguments in
the instant action that merely differ from positions asserted in prior proceedings, although the
Court will, where appropriate, allow cross examination on this topic.
iii. Humanizing murine anti-CGRP antagonist antibodies

In the IPRs, Lilly argued that the process of humanizing non-human (e.g., murine)
antibodies “was a well-established and routine procedure by 2005.” [ECF No. 389 ¶ 44 (quoting
ECF No. 317-5 at 3)]. Lilly also discussed a prior art reference, Queen, U.S. Pat. No. 6,180,370,
issued Jan. 30, 2001, and observed that it “describes routine and conventional humanization
technologies that have been recognized as the ‘gold standard’ years before 2005.” [Id. ¶ 45
(quoting ECF No. 317-5 at 10)]; see also [id. ¶ 47 (quoting ECF No. 315-5 at 18) (Lilly asserting
that Queen “discloses well-established prior art techniques to generate humanized antibodies for
therapeutic use that maintained the original binding attributes of the donor non-human
antibodies.”)]. Lilly further argued that, relying on Queen’s “routine humanization process,” a
POSA “would have readily been able to” humanize an antibody “while maintaining or even
improving the binding specificity and affinity for human CGRP.” [Id. ¶ 46 (quoting ECF No.
317-2 at 7)].
Lilly now argues that in 2005–2006, the methods for humanization “were both laborious
and fraught with unpredictability” and it “was an empirical, unpredictable, time-consuming, and

expensive process, taking anywhere from four months to a full year, requiring multiple full-time
employees, and costing about $500,000 for each humanized antibody.” [ECF No. 389 ¶¶ 55
(quoting ECF No. 317-6 ¶ 331), 60 (quoting ECF No. 317-10 ¶ 50)]. Lilly additionally alleges
that humanization was a “trial and error exercise,” required “experimentation,” with “no
guarantee of success at the end,” and that the process “typically reduced or eliminated the ability
of the antibody to bind to its target[.]” [Id. ¶¶ 56–57 (quoting ECF No. 317-1 ¶¶ 62, 270, 288–
89)].
Here, again, Lilly’s arguments regarding humanization techniques, while different from
the points advanced during the IPR proceedings, are not so different as to be considered mutually

exclusive. A process may be routine and conventional while also being unpredictable, costly,
and burdensome. The former does not preclude the latter and therefore the sanction of judicial
estoppel is not warranted.
Having concluded that Lilly’s arguments to this Court are not so obviously inconsistent
as to warrant summary judgment, it is not necessary to further consider whether Lilly persuaded
the PTAB to adopt its prior arguments or whether Lilly would derive an unfair advantage if this
Court accepted its new position. The Court similarly need not consider Lilly’s argument that
Teva’s motion failed to comply with Fed. R. Civ. P. 56(a) because it did not seek judgment on
any claim or defense.
B. Inequitable Conduct and Unclean Hands
Lilly asserts that the Patents-in-Suit are unenforceable because (1) during prosecution
before the PTO, Teva intentionally withheld material prior art references and data from certain
preliminary experiments, and (2) with respect to the ’907 and ’908 patents, because doctors
involved in patent prosecution on Teva’s behalf intentionally delayed filing paperwork that was

necessary to correct otherwise defective patent applications and falsely averred that the delay
was unintentional. [ECF No. 302 at 6–7]. Teva moves for summary judgment on these
defenses, contending that Lilly cannot shoulder the heavy evidentiary burden of proving
inequitable conduct. [Id. at 11, 23–24].
The burden of proof is significant. “Inequitable conduct is an equitable defense to patent
infringement that, if proved, bars enforcement of a patent.” Therasense, Inc. v. Becton,
Dickinson & Co., 649 F.3d 1276, 1285 (Fed. Cir. 2011) (en banc). “The remedy for inequitable
conduct is [known as] the ‘atomic bomb’ of patent law,” because “inequitable conduct as to any
individual claim renders the entire patent unenforceable.” Id. at 1288.

Inequitable conduct has two requirements: materiality and intent. Therasense, 649 F.3d
at 1290. “[T]he materiality required to establish inequitable conduct is but-for materiality[,]” id.
at 1291, for present purposes “meaning that ‘the PTO would not have allowed a claim had it
been aware of the undisclosed prior art[,]’” TransWeb, LLC v. 3M Innovative Properties Co.,
812 F.3d 1295, 1304 (Fed. Cir. 2016) (quoting Therasense, 649 F.3d at 1291–92).
To show intent, “the accused infringer must prove that the patentee acted with the
specific intent to deceive the PTO.” Therasense, 649 F.3d at 1290. In cases involving
nondisclosure of information, as alleged here, “the accused infringer must prove by clear and
convincing evidence that the applicant knew of the undisclosed information, knew it was
material, and made a deliberate decision to withhold it.” Id. In other words, “[p]roving that the
applicant knew of a reference, should have known of its materiality, and decided not to submit it
to the PTO does not prove specific intent to deceive.” Id. Courts may infer intent from indirect
and circumstantial evidence, however, “to meet the clear and convincing evidence standard, the
specific intent to deceive must be ‘the single most reasonable inference able to be drawn from

the evidence.’” Id. (quoting Star Sci., Inc. v. R.J. Reynolds Tobacco Co., 537 F.3d 1357, 1366
(Fed. Cir. 2008)).
Here, Lilly contends that Teva, and specifically Drs. Zeller and Pons, engaged in
inequitable conduct by intentionally omitting (1) a prior art reference, Shaw, (2) the results of
internal data from failed attempts to identify anti-CGRP antagonist antibodies that bound to the
N-terminal end or mid-region of CGRP, and (3) data from a cortical spreading depression
(“CSD”) assay. [ECF No. 302 at 7].
i. Shaw
Shaw is a prior art reference that includes data on an antibody that bound to the mid-

region of CGRP but failed to antagonize it, [ECF No. 387 ¶¶ 32, 68], and, among other things,
discussed antibodies that bound to the N-terminal end of CGRP, one of which antagonized
CGRP, and others that did not, [id. ¶ 33]. Prior to submitting applications for any of the Patents-
in-Suit, Dr. Zeller summarized Shaw’s findings, with respect to antibodies that bind to the mid-
region of CGRP, to other named inventors. See [ECF No. 387 ¶ 13]. Lilly alleges that Teva
acted inequitably by failing to disclose Shaw in the ’045 application and by burying it in the ’907
and ’908 applications among 400 other references without discussing its significance. [ECF No.
348 at 10].
According to Lilly, Shaw is material, and not cumulative, because it teaches that some
antibodies that bind to the N-terminal end and mid-region do not antagonize CGRP. [ECF No.
348 at 22]. This teaching, in Lilly’s view, undermines Teva’s argument to the PTO during
prosecution that because the antibodies in the Patents-in-Suit bind to the C-terminal end of
CGRP—the epitope furthest from the region responsible for activating CGRP—“any antibody

that effectively binds CGRP may reasonably be expected to have the claimed effect,” i.e.,
antagonize CGRP. [ECF No. 387 ¶ 64 (quoting ECF No. 354-14 at 11)]. Lilly contends that if
Shaw had been disclosed, the patent examiner would have rejected Teva’s argument and the ’045
patent would not have issued because Shaw identifies antibodies that bind to epitopes other than
the C-terminal and do not in fact antagonize CGRP. See [id. ¶¶ 25–27 (Lilly citing to Dr.
McDonnell’s opening and reply reports)]. Lilly also argues that even though Shaw was
disclosed in the ’907 and ’908 patents, it was buried and Teva did nothing to highlight it despite
its significance and tendency to contradict Teva’s prior assertion. [Id. ¶¶ 25, 29, 51]. Given
Shaw’s alleged significance, Teva’s failure to disclose it in the ’045 application and its decision

to bury it in the ’907 and ’908 applications, Lilly contends that a reasonable juror could conclude
that the most reasonable inference is that Teva withheld it with the intent to deceive the PTO.
[ECF No. 348 at 20–22].
Teva responds that Shaw was cumulative and not material because the patent, and a prior
publication—Tan et al., Demonstration of the neurotransmitter role of calcitonin gene-related
peptides (CGRP) by immunoblockade with anti-CGRP monoclonal antibodies, 111 Br. J.
Pharmacol. 703–10 (1994) (“Tan 1994”)—already disclosed certain antibodies that bind to
CGRP but do not antagonize it. [ECF No. 302 at 15]. Therefore, according to Teva, Shaw’s
teaching—that antibodies that bind to the mid-region and N-terminal of CGRP may not
antagonize it—was unlikely to change the patent examiner’s view of patentability. [Id.].
The Court finds that there is a genuine dispute about Shaw’s materiality. While Teva
argues that Shaw was cumulative because the patent specification and Tan 1994 also teach that
antibodies that bind to CGRP may not antagonize it, that argument overlooks the fact that Shaw

specifically and additionally teaches that antibodies that bind to the N-terminal and mid-region
may fail to antagonize CGRP. See [ECF No. 387 ¶¶ 37–38]. That additional disclosure
undermines Teva’s argument that Shaw is merely cumulative of information disclosed in the
patent specification. Drawing all inferences in favor of the non-moving party, the Court further
finds that a reasonable juror could conclude that if Shaw had been disclosed the patent examiner
would have rejected Teva’s claim that antibodies that bind to regions other than the C-terminal
(e.g., the mid-region or N-terminal) can be reasonably expected to antagonize CGRP, and, in
turn, not allow the patent to issue.
As to intent, Teva argues there is no direct evidence that Drs. Zeller or Pons considered

disclosing Shaw to the PTO and deliberately chose to withhold it and that there are other
reasonable inferences the jury could reach. [ECF No. 302 at 21]. To begin, the question is not
whether there are simply other reasonable inferences, as Teva appears to suggest in its motion,
see [id. at 19–21], rather, at summary judgment, the question is if there is a genuine dispute
regarding whether a reasonable factfinder could conclude that the most reasonable inference is
that Shaw was withheld with the intent to deceive the PTO. Therasense, 649 F.3d at 1290.
Having closely considered the record, the Court cannot conclude that a reasonable juror could
not find that the most reasonable inference is that Drs. Zeller and Pons sought to deceive the
PTO by withholding Shaw in the ’045 application and not highlighting it in the ’907 and ’908
applications. The Court thus finds that these are factual matters best left to the factfinder and
summary judgment is denied.
ii. Internal Binding Data & CSD Assay Data
Lilly next claims that Teva, and Drs. Zeller and Pons, engaged in inequitable conduct by
withholding the results of internal data from failed attempts to identify anti-CGRP antagonist

antibodies that bound to the N-terminal end or mid-region of CGRP (“Binding Data”). See [ECF
No. 387 ¶ 14]. In Lilly’s view, the Binding Data is material because it shows that Teva did not
possess the full scope of the claimed methods. [ECF No. 348 at 20]. For that reason, Lilly
suggests that Drs. Zeller and Pons were incentivized to withhold the data as disclosing it would
have potentially prevented Teva from securing a broad patent. [Id. at 15–16].
Lilly also alleges that during prosecution of the Patents-in-Suit, Teva, and specifically
Drs. Zeller and Pons, withheld the results of a CSD assay that showed that an anti-CGRP
antagonist antibody did not inhibit a signal related to migraine.19 [ECF No. 387 ¶ 55]. Lilly
claims that Dr. Pons was on notice of the importance of the test because he was on an email

chain in which another scientist stated that if the anti-CGRP antibody “doesn’t work” in the
assay, “then the whole concept in questionable.” [Id. ¶ 57 (quoting ECF No. 354-26 at 2) (email
from Robert Klein to, among others, Dr. Pons)]. Dr. Zeller was similarly on notice of the CSD
assay’s relevance, says Lilly, because he stated that the data from the study would “be crucial in
identifying whether or not the peptide is an effective therapeutic for migraine.” [Id. ¶ 54
(quoting ECF No. 364-21 at 3)]. In light of the alleged importance of the test, Lilly argues (1)
that if the results had been disclosed, the PTO would not have allowed the patent to issue based

19 In addition to disputing whether the results of the CSD assay were material, the parties also
dispute whether the test results were negative or merely inconclusive. See [ECF No. 348 at 17].
on lack of utility and possession, [id. ¶ 56], and (2) that a factfinder could conclude that the most
reasonable inference is that the results were withheld with the intent to deceive the PTO, [ECF
No. 348 at 23–24].
In response, Teva argues that Lilly has not pointed to any evidence to suggest that the
Binding Data or the CSD assay results are material or, in other words, would have led the PTO to

reject any claims of the Patents-in-Suit. [ECF No. 302 at 13, 16]. Teva notes that Lilly’s own
expert, Dr. McDonnell, testified that when he described the Binding Data as material, he meant
only that it “could have been relevant for [the PTO’s patentability] assessment,” [ECF No. 387 ¶
25 (quoting ECF No. 354-7 at 151:5–10); ECF No. 302 at 13], and, with respect to the CSD
assay, another of Lilly’s experts described the results as merely “germane to the patent issue[.]”
[ECF No. 387 ¶ 28 (quoting ECF No. 304-18 at 214:3–8)]. Teva further argues that the CSD
assay is not material because the results were not dispositive in determining whether an anti-
CGRP antibody can treat migraine or other head pain. [ECF No. 302 at 16].
As for intent, Teva asserts that no reasonable factfinder could exclude the possibility that

Drs. Zeller and Pons did not consider disclosing the results of the internal testing or the results of
the CSD assay to the PTO because they did not make final decisions about what information to
disclose or that they did not view it as particularly relevant because, for example, they thought it
was inconclusive. [ECF No. 302 at 20–23; ECF No. 387 ¶ 57].
The Court again finds that there are genuine disputes with respect to materiality and
intent that preclude summary judgment. Drawing all inferences in favor of Lilly, a reasonable
factfinder could conclude that disclosure of the Binding Data, which revealed that Teva’s
scientists had been unable to identify an anti-CGRP antagonist antibody that bound to a region
other than the C-terminal, may have caused the PTO to refrain from issuing the broad Patents-in-
Suit. A similar inference is reasonable with respect to the results of the CSD assay, which could
be interpreted to suggest that the claimed invention was inoperative, and thus cause the examiner
to reject the application. Based on the potential negative impacts of disclosing the data, the
Court further finds that a reasonable factfinder could conclude that the most reasonable inference
is that the data and results were withheld with the intent to deceive the PTO.

iii. Petitions for Unintentional Delay
Lilly next argues that Teva is liable for inequitable conduct committed by patent agent
Adam Cole and patent attorney Jeffery Giering during prosecution of the patent applications that
led to the ’907 and ’908 patents. [ECF No. 348 at 12]. In particular, Lilly claims that Cole and
Giering intentionally delayed filing petitions to correct three patent applications that had initially
claimed priority to an abandoned application (the ’394 application). [Id.]. The intentional delay
can be inferred, according to Lilly, from the fact that, after receiving notice that the ’394
application had been abandoned, Cole and Giering waited more than a year to file the first
petition to correct the ’871 application. [Id. at 13]. They then waited an additional five months

to file identical corrections in two other pending applications (the ’816 and ’925 applications).
[Id. at 24; ECF No. 387 ¶ 85]. Lilly asserts that because Cole and Giering were on notice of the
errors in all three applications at least as early as the date they filed the motion for the first
petition, it is not conceivable that the entire period of delay was unintentional. [ECF No. 348 at
24; ECF No. 387 ¶¶ 85, 87]. Lilly thus argues that Cole and Giering’s attestation that the delay
was unintentional, at least as to the second and third petitions, was false and evidences an intent
to deceive the PTO to hide their error and save the patents. [ECF No. 348 at 24]. The
submission, and later approval, of the petitions was material to the issuance of the ’907 and ’908
patents, in Lilly’s view, because the patents would have been considered invalid and would not
have issued. [Id.].
Teva does not contest that the petitions were material but argues that intent to deceive is
not the most reasonable inference because there is no evidence that the delay was intentional or
that Cole and Giering knew the statements were wrong and made them with the intent to deceive.

[ECF No. 302 at 24].
Here, again, the Court finds that there is a genuine dispute of fact as to intent such that
summary judgment is not warranted. Teva appears to argue, in part, that the Court should grant
summary judgment because there is no direct evidence that the delay was intentional. However,
“a district court may infer intent from indirect and circumstantial evidence.” Therasense, 649
F.3d at 1290 (citation omitted). Lilly has presented circumstantial evidence that the
representations in the second and third petitions were false and also proffered an explanation as
to why Drs. Cole and Giering would have been motivated to deceive the PTO. A factfinder
could thus conclude that the most reasonable inference is that Drs. Cole and Giering made a false

representation to the PTO with the intent to deceive. Therefore, the Court declines to grant
summary judgment on this issue.
C. Willful Infringement
Lilly requests the Court enter summary judgment against Teva on its claim for willful
infringement, arguing that even if Lilly infringed—which it denies—there is no evidence it did
so willfully. [ECF No. 306 at 5–6]. Under 35 U.S.C. § 284, a district court may enhance
damages for patent infringement up to three times the amount found or assessed. The awarding
of enhanced damages, however, is “generally reserved for egregious cases of culpable behavior.”
Halo Elecs., Inc. v. Pulse Elecs., Inc., 579 U.S. 93, 104 (2016); see also Crane Sec. Techs., Inc.
v. Rolling Optics AB, 337 F. Supp. 3d 48, 57 (D. Mass. 2018). Indeed, “[t]he sort of conduct
warranting enhanced damages has been variously described . . . as willful, wanton, malicious,
bad-faith, deliberate, consciously wrongful, flagrant, or—indeed—characteristic of a pirate.” Id.
at 103–04.
Willfulness requires “specific intent to infringe at the time of the challenged conduct.”

Bayer Healthcare LLC v. Baxalta Inc., 989 F.3d 964, 987 (Fed. Cir. 2021) (citing Halo, 579 U.S.
at 105–06). Therefore, “[k]nowledge of the asserted patent and evidence of infringement is
necessary, but not sufficient, for a finding of willfulness.” Bayer, 989 F.3d at 988. Instead, a
determination of willfulness also requires a finding of “deliberate or intentional” infringement.
See SRI Int’l, Inc. v. Cisco Sys., Inc., 14 F.4th 1323, 1330 (Fed. Cir. 2021) (quoting Eko Brands,
LLC v. Adrian Rivera Maynez Enterps., Inc., 946 F.3d 1367, 1378 (Fed. Cir. 2020)). Whether
the infringement was deliberate or intentional must be determined, based on all the
circumstances, by the factfinder. See WCM Indus., Inc. v. IPS Corp., 721 F. App’x 959, 970
(Fed. Cir. 2018) (quoting Gustafson, Inc. v. Intersystems Indus. Prods., Inc., 897 F.2d 508, 510–

11 (Fed. Cir. 1990)). “[A] patentee need only establish willfulness by a preponderance of the
evidence . . . .” SiOnyx, LLC v. Hamamatsu Photonics K.K., 330 F. Supp. 3d 574, 609 (D.
Mass. 2018) (citation omitted).
There is no dispute that Lilly had knowledge of the Patents-in-Suit prior to the date of the
first alleged infringement. See [ECF No. 395 ¶ 105 (“In a September 27, 2021 email, Lilly
agreed to stipulate that ‘Lilly possessed knowledge of [the ’045 patent] as of October 24, 2017’
and that ‘Lilly possessed knowledge of [the ’907 and ’908 patents] as of February 6, 2018.”)
(quoting ECF No. 308-72 at 2, 7)]. Therefore, the Court need only determine whether there is a
genuine dispute as to whether Lilly, if it infringed at all, did so willfully.
When determining whether alleged infringement was willful, courts look to evidence of
the accused infringer’s intent “at the time of the challenged conduct” based on the totality of the
circumstances. See Bayer, 989 F.3d at 987; BASF Plant Science, LP v. Commonwealth Sci. and
Indus. Rsch. Org., 28 F.4th 1247, 1274 (Fed. Cir. 2022) (citation omitted). Here, the alleged
infringing conduct—Lilly’s sale of Emgailty—began in October 2018. [ECF No. 395 ¶ 94].

Lilly argues that summary judgment is warranted because there is no evidence, as of October
2018, that Lilly intentionally or deliberately infringed Teva’s patents, [ECF No. 306 at 6], and
because Lilly’s reasonable belief of noninfringement is evidenced by its immediate filing of
petitions for IPR. [ECF No. 395 ¶ 3–4]. Even excluding all evidence related to actions that Lilly
took after the first alleged infringement, the Court finds that there are genuine disputes of fact
that preclude summary judgment. To begin, the parties dispute whether Lilly, in its development
of Emgality, copied the Patents-in-Suit, which would be “strong evidence of willful infringement
. . . .” L.A. Gear, Inc. v. Thom McAn Shoe Co., 988 F.2d 1117, 1127 (Fed. Cir. 1993); KAIST
IP US LLC v. Samsung Elecs. Co., 439 F. Supp. 3d 860, 884–85 (E.D. Tex. 2020), appeal

dismissed sub nom. KIPB LLC v. Samsung Elecs. Co., Ltd., 2020-1619, 2020 WL 9175080
(Fed. Cir. Sept. 3, 2020) (upholding a jury’s willfulness finding based, in part, on the accused
infringer copying the patented technology). Moreover, Lilly admits that it had knowledge of the
Patents-in-Suit at the time of infringement yet, leading up to October 2018, began an expensive
marketing campaign to promote and sell its allegedly infringing product. Lilly urges the Court to
disregard that evidence and accept its claim that it always believed the Patents-in-Suit were
invalid or otherwise unenforceable and thus, at a minimum, did not infringe willfully, if at all. A
determination of Lilly’s subjective belief, however, turns on a review of the totality of the
evidence, including the credibility of witnesses and the weight to be given to certain evidence,
which is properly left to the jury. The Court therefore will not grant summary judgment on the
issue of willful infringement.
D. Non-Infringement
Lilly moves the Court to find that Lilly’s Galcanezumab (i.e., Emgality) does not infringe
claims 18 and 21 of Teva’s ’045 patent. [ECF No. 298 at 6]. Of the 20 claims that Teva claims

Lilly has infringed, claims 18 and 21 are the only claims that set forth specific amino acid
sequences for, respectively, the CDRs and variable regions, as shown below:
18. The method according to claim 17,20 wherein the anti-CGRP antagonist
antibody is:

(a) an antibody having a CDR H121 as set forth in SEQ ID NO: 3; a CDR H2 as set
forth in SEQ ID NO: 4; a CDR H3 as set forth in SEQ ID NO:5; a CDR L1 as
set forth in SEQ ID NO: 6; a CDR L2 as set forth in SEQ ID NO: 7; and a CDR
L3 as set forth in SEQ ID NO: 8; or

(b) a variant of an antibody according to (a) as shown in Table 6.22

* * *
21. The method according to claim 17, wherein the anti-CGRP antagonist antibody
comprises a VH23 domain comprising SEQ ID NO: 1 and VL domain comprising
SEQ ID NO: 2.

[ECF No. 406 ¶¶ 43, 47]. Therefore, claim 18 recites the use of an anti-CGRP antagonist
antibody that either has the same sequence in its CDRs as either Antibody G1 or one of

20 Claim 17 recites: “A method for reducing incidence of or treating headache in a human,
comprising administering to the human an effective amount of an anti-CGRP antagonist
antibody, wherein said anti-CGRP antagonist antibody is a human monoclonal antibody or a
humanized monoclonal antibody. [ECF No. 406 ¶ 41].
21 The designations “H1,” “H2,” and “H3” refer to the first, second and third CDRs located on
the heavy chain. [ECF No. 406 ¶ 44]. The designations “L1,” “L2,” and “L3” refer to the first,
second and third CDRs located on the light chain. [Id. ¶ 45].
22 Table 6 refers to the amino acid sequences of the 84 variants of Antibody G1 that are listed in
Table 6 of the ’045 patent. [ECF No. 406 ¶ 66].
23 VH refers to the variable domain of the heavy chain and VL refers to the variable domain of the
light chain.
the variants of Antibody G1 that are listed in Table 6 of the ’045 patent. [Id. ¶¶ 43, 46].
Claim 21, in turn, recites the use of antibodies that have variable domains with amino
acid sequences identical to those of Antibody G1. See [id. ¶ 48].
Lilly’s antibody, Galcanezumab, has amino acid sequences in its CDRs and
variable regions that differ from Antibody G1 or any of the variants listed in Table 6 of

the ’045 patent. [ECF No. 406 ¶ 130]. For example, the amino acid sequences of
Galcanezumab’s CDRs have 29.9% sequence identity (i.e., similarity) with Antibody G1.
[Id. ¶ 132]. Additionally, the heavy and light chain variable domains of Galcanezumab
and Antibody G1 have 50.8% and 64.5% sequence identities, respectively. [Id. ¶ 135].
As for the variants, Antibody M2 is the variant with the most similar heavy chain variable
domain as compared to Galcanezumab, but its amino acid sequence has only 52.5%
similarity. [Id. ¶ 136].
In addition to having distinct amino acid sequences in its CDRs and variable
regions, Galcanezumab has functional differences from Antibody G1. [ECF No. 406 ¶¶

147–50]. Galcanezumab, for instance, binds to the mid-region of CGRP, whereas
Antibody G1 binds to the C-terminal end. [Id. ¶¶ 147–48].24 Further, and among other
functional differences, Galcanezumab binds to CGRP five-times more rapidly than
Antibody G1. [Id. ¶ 165].
“The patentee has the burden of proving infringement by a preponderance of the
evidence.” Amgen Inc. v. Sandoz Inc., 923 F.3d 1023, 1027 (Fed. Cir. 2019). “To
establish literal infringement, every limitation set forth in a claim must be found in an

24 Lilly claims that all of the antibodies disclosed in the Patents-in-Suit bind to the C-terminal
end of CGRP, but Teva disputes this. [ECF No. 406 ¶ 149].
accused product, exactly.” Duncan Parking Techs., Inc. v. IPS Grp., Inc., 914 F.3d 1347,
1360 (Fed. Cir. 2019) (internal quotation marks and citation omitted). “[A] product or
process that does not literally infringe upon the express terms of a patent claim may
nonetheless be found to infringe if there is ‘equivalence’ between the elements of the
accused product or process and the claimed elements of the patented invention.” Warner-

Jenkinson Co. v. Hilton Davis Chem. Co., 520 U.S. 17, 21 (1997) (citing Graver Tank &
Mfg. Co. v. Linde Air Prods. Co., 339 U.S. 605, 609 (1950)).
The Supreme Court has created two frameworks for evaluating equivalence: the
function-way-result test (“FWR”) (whether the accused product performs substantially
the same function in the same way to obtain the same result) and the insubstantial
differences test (whether the accused product is substantially different from what is
patented). Mylan Institutional LLC v. Aurobindo Pharma Ltd., 857 F.3d 858, 866–67
(Fed. Cir. 2017) (citing Graver Tank, 339 U.S. at 608, 609). The Supreme Court has
acknowledged that the suitability of the two tests may vary, depending on the

circumstances of the case, and the Federal Circuit has further advised that the FWR test
“may be less appropriate for evaluating equivalence in chemical compounds” because it
can fail to “capture substantial differences between a claimed and accused compound.”
Id. at 869.
Under either framework, the doctrine of equivalence is limited by the “all
elements rule,” which holds that “an accused product or process is not infringing unless it
contains each limitation of the claim, either literally or by an equivalent.” Freedman
Seating Co. v. Am. Seating Co., 420 F.3d 1350, 1358 (Fed. Cir. 2005). In other words,
the doctrine of equivalence may not be applied in such a way as to “effectively eliminate”
or “vitiate” any claim element. Warner-Jenkinson, 520 U.S. at 29–30. Vitiation,
however, “is not an exception to the doctrine of equivalents, but instead a legal
determination that ‘the evidence is such that no reasonable jury could determine two
elements to be equivalent.’” Deere & Co. v. Bush Hog, LLC, 703 F.3d 1349, 1356 (Fed.
Cir. 2012) (quoting Warner-Jenkinson, 520 U.S. at 39 n.8).

Lilly argues that Teva’s equivalence theory, with respect to claims 18 and 21 of
the ’045 patent, is overbroad and impermissibly vitiates multiple claim limitations. [ECF
No. 298 at 7]. In Lilly’s view, claims 18 and 21 are limited by specific amino acid
sequences and Teva’s product, Galcanezumab, has substantially different sequences. [Id.
at 13]. In addition to differences in the specific amino acid sequence, those differences
cause Galcanezumab to have different functional properties than Lilly’s product,
Fremanezumab. Lily asserts that these functional differences as well as the differences in
amino acid sequence, place Galcanezumab far beyond any permissible scope of
equivalents. [Id. at 15–16]. Lilly also argues that the Court should apply the

insubstantial differences framework when analyzing equivalence instead of the FWR test.
[Id. at 17]
Teva’s main argument in response to Lilly’s motion is that there is a genuine
dispute as to whether Lilly’s Galcanezumab infringes claims 18 and 21 of the ’045
patent. [ECF No. 360 at 6]. While Teva concedes that Galcanezumab’s amino acid
sequences are not identical to the limitations in claims 18 and 21, and therefore does not
literally infringe, it argues that Galcanezumab is equivalent because the differences in
amino acid sequence do not translate into meaningful real-world biological differences
when the antibodies are deployed to treat headache patients. [Id.]. Teva avers that the
corresponding sequences: “(i) perform substantially the same biochemical function by
binding to CGRP such that CGRP is blocked from engaging with its receptor; (ii) do this
in substantially the same way by binding to the particular regions of CGRP required for
receptor engagement with high affinity, selectivity, and duration; and (iii) achieve
substantially the same result—the treatment of headache symptoms in patients due to a

reduction in CGRP signaling.” [Id.]
Teva further claims that there are additional genuine disputes that preclude
summary judgment, including that the parties disagree about: (1) the proper scientific
framework used to perform the FWR test, [ECF No. 360 at 8 (citing Crown Packaging
Tech., Inc. v. Rexam Beverage Can Co., 559 F.3d 1308, 1315 (Fed Cir. 2009))]; (2) the
meaning and significance of clinical and pre-clinical data, [id. at 11–12]; (3) the
substance and impact of the research of the named inventors of the ’045 patent, [id. at
12–13]; and (4) whether Lilly independently developed Galcanezumab or relied on
Teva’s patents to do so, [id.].

In addition to there being disputed material facts, Teva argues that summary
judgment should be denied because Lilly’s statement of facts violates the Federal Rules
of Civil Procedure and Local Rules of the District of Massachusetts, and because Lilly’s
argument that Teva’s theory of equivalences conflicts with the equitable rationale
underlying the doctrine of equivalents fails. [ECF No. 360 at 15–16].
As the parties agree that Galcanezumab’s amino acid sequences are, at minimum,
nominally different from the limitations of claims 18 and 21 of the ’045 patent, there is
no dispute that the accused product does not literally infringe the patents claims. Thus
the Court need only determine whether there is a genuine dispute as to whether
Galcanezumab infringes claims 18 and 21 of the ’045 patent under the doctrine of
equivalents. As discussed above, the Supreme Court has “blessed two equivalent
tests”—the FWR and insubstantial differences tests—and “le[ft] to the lower courts in
future cases the choice of which to apply.” Mylan, 857 F.3d at 867. In deciding which
test to use, the Court considers the observations by the Supreme Court and Federal

Circuit that “non-mechanical cases may not be well suited to consideration under the
FWR test” and that is “particularly true in the chemical arts.”25 Id. With respect to the
claims at issue, which recite specific amino acid sequences (i.e., specific structures), the
Court finds that the FWR test is poorly suited for the equivalence analysis and elects to
apply the insubstantial differences test.
Teva’s primary argument is that even though Galcanezumab’s amino acid
sequences differ, it is nonetheless equivalent because it achieves the same result—
binding to CGRP with sufficient strength to reduce CGRP signaling—and also because it
has six CDRs and two variable domains as required by claims 18 and 21. See [ECF No.

360 at 18–19]. In Teva’s view, the key inquiry is not whether the amino acid sequences
are different, but whether the differences matter in the claimed method—i.e., treating
headache. [Id. at 19]. Teva’s argument is a bridge too far. Claims 18 and 21 of the ’045
patent recite specific amino acid sequences for the CDRs and variable domains,
respectively, which reflects that Teva chose to limit these claims to require these specific

25 The shortcomings of the FWR test in the context of pharmaceutical treatments is exemplified
by the comparison of aspirin and ibuprofen. Persons of skill in the art would not consider these
two medications to have structural equivalents under the insubstantial differences test. If you
analyze them under the FWR test, however, they would appear to be equivalents because they
“each provide analgesia and anti-inflammatory activity (‘function’) by inhibiting prostaglandin
synthesis (‘way’) in order to alleviate pain, reduce fevers, and lessen inflammation (‘result’).”
Mylan, 857 F.3d at 869.
sequences despite the fact that “claim[s] that contain[] [] detailed recitation of structure
[are] properly accorded correspondingly limited recourse to the doctrine of equivalents.”
Bicon, Inc. v. Straumann Co., 441 F.3d 945, 955 (Fed. Cir. 2006) (citation omitted).
Here, “by defining the claim in a way that clearly excluded certain subject matter, the
patent implicitly disclaimed the subject matter that was excluded and thereby barred the

patentee from asserting infringement under the doctrine of equivalents.” Id. (quoting
SciMed Life Sys., Inc. v. Advanced Cardiovascular Sys., Inc., 242 F.3d 1337, 1346 (Fed.
Cir. 2001)).
Because Lilly’s antibody, Galcanezumab has CDRs and variable regions with
amino acid sequences that are substantially different from Antibody G1 or any of its
variants, the amino acid sequences in Galcanezumab are clearly excluded from the amino
acid sequences recited by claims 18 and 21. Moreover, Teva’s equivalence argument
would read the amino acid sequence limitation out of claims 18 and 21 and effectively
expand the scope of that limitation to encompass any amino acid sequence in a full-length

antibody that has the effect of sufficiently antagonizing CGRP. As discussed, however,
claims 18 and 21 list the amino acid sequences of the CDRs and variable domains of
Antibody G1 and its variants, not the antibody sequences of Galcanezumab.
Accordingly, the Court finds that Galcanezumab does not infringe claims 18 or 21 under
the doctrine of equivalents.
The Court also disagrees with Teva that summary judgment is inappropriate based
on the parties’ disputes over clinical and pre-clinical data, the substance and impact of the
research of the named inventors of the ’045 patent, and whether Lilly relied on the
Patents-in-Suit to develop Galcanezumab. These issues, even if disputed, do not bear on
whether Galcanezumab infringes claims 18 and 21 under the doctrine of equivalents and
therefore are not material. The Court further declines Teva’s invitation to deny summary
judgment based on Lilly’s statement of fact. Together the parties have filed far in excess
of 1,000 pages of claimed statements of facts that improperly contain legal arguments and
disputed facts with the result being a time-consuming process to identify the much

smaller subset of facts that are actually undisputed. Where both parties have engaged in
the same malfeasance, the Court will not reward one and punish the other. Therefore the
Court grants Lilly’s motion for partial summary judgment of non-infringement with
respect to claims 18 and 21 of the ’045 patent.
E. Written Description
Lilly claims that all of Teva’s asserted claims from the ’045, ’907, and ’908 patents are
invalid because they do not satisfy 35 U.S.C. § 112’s written description requirement and seeks
summary judgment on this dispositive issue. [ECF No. 294-1 at 7]. Section 112 states that a
patent specification “shall contain a written description of the invention.” 35 U.S.C. § 112.

“[T]he hallmark of written description is disclosure,” and the test is “an objective inquiry into the
four corners of the specification from the perspective of a [POSA].” Ariad Pharms., Inc. v. Eli
Lilly & Co., 598 F.3d 1336, 1351 (Fed. Cir. 2010) (en banc). “A specification adequately
describes an invention when it ‘reasonably conveys to those skilled in the art that the inventor
had possession of the claimed subject matter as of the filing date.’” Juno Therapeutics, Inc. v.
Kite Pharma, Inc., 10 F.4th 1330, 1335 (Fed. Cir. 2021) (quoting Ariad, 598 F.3d at 1351).
Context matters, however, and “[w]hat is required to meet the written description requirement
‘varies with the nature and scope of the invention at issue, and with the scientific and technologic
knowledge already in existence.’” Juno, 10 F.4th at 1335 (quoting Capon v. Eshhar, 418 F.3d
1349, 1357 (Fed. Cir. 2005)). “Whether a patent claim is supported by an adequate written
description is a question of fact . . . .” AbbVie Deutschland GmbH & Co., KG v. Janssen
Biotech, Inc., 759 F.3d 1285, 1297 (Fed. Cir. 2014).
The Federal Circuit has set forth a number of factors to consider when evaluating the
adequacy of disclosure for generic claims, including “the existing knowledge in the particular

field, the extent and content of the prior art, the maturity of the science or technology, and the
predictability of the aspect at issue.” Id. at 1299 (internal quotation marks and citation omitted).
“For genus claims using functional language, . . . the written description ‘must demonstrate that
the applicant has made a generic invention that achieves the claimed result and do so by showing
that the applicant has invented species sufficient to support a claim to the functionally-defined
genus.” Juno, 10 F.4th at 1335 (quoting Ariad, 598 F.3d at 1349). “Where representative
[species] are necessary to satisfy the written description requirement, the number of such
[species] that must be disclosed depends on the context, including the knowledge already
available in the art.” Erfindergemeinschaft UroPep GbR v. Eli Lilly and Co., 276 F. Supp. 3d

629, 650 (E.D. Tex. 2017); see also Ariad, 598 F.3d at 1351 (“[No] bright-line rules govern[] . . .
the number of species that must be disclosed to describe a genus claim, as this number
necessarily changes with each invention, and it changes with progress in a field.”). In deciding
this issue, the Court looks to the specification as it would be viewed by a POSA, which, in effect,
incorporates the knowledge in the prior art and, as it must, draws all inferences in favor of Teva,
the non-moving party.
i. Disclosure of Claimed Antibodies
Lilly first argues that Teva’s specifications do not provide a sufficient number and variety
of humanized or human anti-CGRP antagonist antibodies to show possession of its functionally
defined genus, which, Lilly says, is necessary for an adequate written description. Lilly asserts
that “the need [for Teva] to adequately describe the claimed antibodies is particularly acute
because the patents claim the use of an entirely new genus of compounds.” [ECF No. 399 at 11].
Teva responds that Lilly has framed the inquiry incorrectly because Teva is only claiming a new
method for using certain antibodies to treat headaches, rather than claiming the invention of a

new genus of antibodies. [ECF No. 347 at 18]. Although Teva acknowledges that no humanized
or human anti-CGRP antibody had been created or tested in the prior art prior to 2005–2006,
[ECF No. 400 ¶ 155], it nevertheless contends that it is not claiming a “new” genus of antibodies
because, as Lilly argued and the PTAB found, as of 2005–2006 anti-CGRP antagonist antibodies
were “well known in the art,” and the methods of preparing them were “routine.” [ECF No. 347
at 26].
Lilly relies heavily on AbbVie, in which the Federal Circuit affirmed a verdict of
invalidity for lack of written description because the patent disclosed one very limited subgenus
within a diverse claimed genus. AbbVie, 759 F.3d 1285, 1300–01 (Fed. Cir. 2014). There, the

patent claimed a genus of antibodies having a neutralizing function with respect to a particular
antigen. Id. at 1299. The patent disclosed several antibodies that served the claimed function
and shared a particular structure, that included a 90% or more amino acid sequence similarity in
the variable regions. Id. at 1291, 1300. The defendant, however, created an antibody (the
accused antibody) that shared the function but differed greatly in structure (e.g., it had about 50%
sequence similarity with the asserted antibodies). Id. at 1300. The patentee’s experts also
“conceded that the [asserted patents] d[id] not disclose structural features common to the
members of the claimed genus[,]” id. at 1299, and “d[id] not describe any example, or even the
possibility, of [the antibodies] having heavy and light chains other than the [disclosed] types.”
Id. at 1300. The court thus concluded that “the claimed genus covers structurally diverse
antibodies,” id., and that the written description requirement was not met because the patent
disclosed no species representative of the structural breadth demonstrated by the accused
antibody, id. at 1300–01.
Teva disputes that it has claimed a new genus, but argues in the alternative that even if

the specification is required to describe the full genus of anti-CGRP antagonist antibodies used in
the claimed methods, a reasonable factfinder could conclude that, taking into account the prior
art, the specification’s disclosure of Antibody G1, 84 variants of Antibody G1, and seven murine
anti-CGRP antagonist antibodies is sufficient to show possession of the entire genus. [ECF No.
347 at 24–25]. Teva relies on Abbott GmbH & Co., KG v. Centocor Ortho Biotech, Inc., 870 F.
Supp. 2d 206 (D. Mass. 2012), which involved claims to a “functionally-defined genus . . . of
antibodies [defined by] their ability to bind to and neutralize” certain proteins. Id. at 233. The
accused infringer argued that “the patents’ disclosure of a limited number of representative
examples of antibodies within each family [was] an insufficient written description to support

the[] genus claims.” Id. The Abbott court reiterated that there is no bright line number of
species that must be disclosed to satisfy the written description requirement. Id. It further
observed that some courts have found that a written description is invalid as a matter of law
where the patent fails to disclose a single species of the claimed genus but, in other
circumstances, disclosure of “a single representative embodiment may . . . be sufficient to
describe a functionally-defined genus.” Id. at 234 (citation omitted). The court ultimately found
that where the patents at issue disclosed 50 antibodies within the scope of the genus claims that
was sufficient to preclude summary judgment. Id. The court noted that the disclosed antibodies
“represent[ed] a narrower class than the claimed genuses because the genuses encompass[ed] a
varied range of amino-acid sequences,” and the disclosed antibodies “all derived from a single
‘lineage’” and had highly similar amino-acid sequences. Id. Nonetheless, “because the parties’
experts dispute[d] the significance of the differences in amino-acid sequences” relied upon by
the accused infringer, the court found that summary judgment was inappropriate. Id. at 235.
The facts of the present case hew closer to Abbott than AbbVie. Even assuming that

Teva is required to disclose sufficient species representative of the genus of claimed antibodies,
the record is replete with conflicting evidence, including contradictory expert testimony,
regarding (1) the significance of amino acid sequences as compared to antibody structure, (2) the
functional similarity between the antibodies disclosed in the patents and Galcanezumab, and (3)
the diversity of antibodies disclosed in the prior art. The Court discusses each in turn.
First, Teva and its experts dispute whether the use of amino acid sequences is an
appropriate comparison to determine whether the disclosed antibodies were representative of the
genus. See [ECF No. 347 at 30–31]. Teva’s expert testified that the anti-CGRP antibodies have
well-known common structural features, including, among others, a Y-shaped structure and the

formation of binding sites (i.e., paratopes) that are structurally complementary to the target
antigen. [ECF No. 411 ¶¶ 153, P77]. Additionally, Teva argues that the disclosed antibodies do
in fact encompass Galcanezumab’s structure because Galcanezumab also contains six CDRs and
two variable domains, despite having different amino acid sequences. [ECF No. 360 at 6].
Second, the parties dispute the functional similarity, or dissimilarity, between Antibody
G1 and Galcanezumab, which bears on the written description analysis. [ECF No. 294 at 7–8].
In particular, if the patents disclose antibodies that encompass the function of Galcanezumab,
that determination would weigh in favor of finding an adequate written description. On the other
hand, if Galcanezumab is determined to be functionally different, that would weigh in favor of
invalidating the patents. Lilly claims that the antibodies have clearly distinct functions because
Galcanezumab binds to the mid-region of CGRP whereas Antibody G1 binds to the C-terminal
end. [Id. at 7]. Teva and its experts contend, however, that the antibodies “are not functionally
different because binding to one of those regions rather than the other does not affect whether the
antibody will block CGRP’s biological function.” [ECF No. 347 at 29; ECF No. 400 ¶ P153].

Third, there is conflicting evidence regarding the type of antibodies disclosed in the
Patents-in-Suit and in the prior art. Lilly argues that Teva has only disclosed anti-CGRP
antagonist antibodies that bind to the C-terminal end of CGRP, but Teva contends that in
addition to Antibody G1, the variants, and the murine anti-CGRP antagonist antibodies, its
specification also disclosed, through its reference to Tan 1995, anti-CGRP antibodies that bind to
the N-terminal region of CGRP. [ECF No. 400 ¶¶ 197, P67–70]. Teva additionally claims that
the techniques used to make, screen, and humanize anti-CGRP antibodies were well-known in
the prior art, which decreases the number of species of antibodies they needed to disclose to
satisfy the written description requirement. [ECF No. 347 at 21–24]. Given this dispute, the

Court cannot conclude, that Teva’s “patents d[id] not describe any example, or even the
possibility, of [the antibodies] having heavy and light chains other than the [disclosed] types,”
AbbVie, 759 F.3d at 1300, and will not grant summary judgment based on insufficient disclosure
of representative species.
ii. Remaining Arguments
This conclusion does not end the analysis, however, because Lilly asserts that Teva’s
patents further fail the written description requirement because (1) the patents claim types of
antibodies that the named inventors tried but failed to make, (2) the specification fails to
demonstrate possession of the claimed methods of treatment, and (3) the specification does not
contain information that would permit a POSA to conclude that the antibodies disclosed could
cross the BBB and thus treat headache. [ECF No. 294 at 7–9]. Teva, however, disputes each of
Lilly’s carguments. [ECF No. 347 at 7].
Regarding whether the named inventors tried but failed to make anti-CGRP antagonist
antibodies that bound to CGRP’s N-terminal end or mid-region and therefore did not possess

what they claimed, Teva argues that Lilly is wrong on the law and the facts. [ECF No. 347 at
31]. The Court finds that it need not reach Lilly’s legal argument because there is a genuine
dispute of fact, namely, whether the inventors tried and failed to make antibodies that bound to
regions other than the C-terminal meaning that they did not possess what they claimed or, as
Teva alleges, merely discontinued their research due to the acquisition of the research
organization (Rinat) by Pfizer. Cf. [ECF No. 400 ¶ 287–89] with [id. ¶ P161–66 (“By late 2006,
the named inventors of the ’045 patent were ‘well underway’ to making antibodies that bound to
the N-terminus and ‘linker region’ (i.e., mid-region) of CGRP. Early characterization showed
that at least one was an anti-CGRP antagonist antibody (i.e., antagonized CGRP biological

activity). The inventors ‘did not fully complete the analysis’ because their research organization
(Rinat) had just been acquired by Pfizer and ‘the focus towards generating more anti-CGRP
antibodies had shifted.’”) (quoting ECF Nos. 368-19 at 179; and 368-27 at 223:1–8, 223:18-
224:7) (internal citations omitted)].
The parties also dispute whether the specification describes the claimed methods. Lilly
argues that the specification is insufficient because it does not disclose any specific method
tailored to treat headache disorder and instead merely suggests various routes of administration,
leaving it up to a future POSA to determine an “effective amount” of antibody to be used for
treatment based on several factors. [ECF No. 290-1 at 25–26]. Thus, according to Lilly, a
POSA would not have believed that the named inventors possessed a treatment for each listed
headache disorder. See [id. at 29–30]. In response, Teva claims that the specification
demonstrates that the inventors did possess the claimed methods because, in part, it discloses
data from two animal assays that would be understood by a POSA to demonstrate that Antibody
G1 would be effective at treating migraine in humans. [ECF No. 347 at 33–34].

Although Lilly claims that several cases support its position, including Ariad, Univ. of
Rochester v. G.D. Searle & Co., 358 F.3d 916 (Fed. Cir. 2004), and FWP IP ApS v. Biogen MA
Inc., 749 F. App’x 969 (Fed. Cir. 2018), none of these cases are availing. In Ariad, the full
extent of the specification’s disclosure was an assertion that the claimed molecules would
function as intended and accomplish the desired result. Ariad, 598 F.3d at 1357. The Federal
Circuit held that even though “[p]rophetic examples are routinely used in the chemical arts, and
[] certainly can be sufficient to satisfy the written description requirement[,]” the disclosure at
issue was merely a mention of a desired outcome with “no descriptive link” between the
molecules and the desired result. Id. Here, in contrast, the specification disclosed the results

from two animal assays that, according to Teva, would be understood by a POSA to demonstrate
that the antibodies would be useful for treating headache. [ECF No. 347 at 33–34]. The alleged
positive results from in vivo tests are, in the Court’s view, much more than a bare assertion that a
claimed invention will work absent supporting data.
In Rochester, the court affirmed summary judgment for no written description because
the patent “does not provide any guidance that would steer the skilled practitioner toward
compounds that can be used to carry out the claimed methods . . . and has not provided evidence
that any such compounds were otherwise within the knowledge of a person or ordinary skill in
the art . . . .” 358 F.3d at 929. The specification at issue here, however, is a far cry from what
the Rochester court confronted. The specification discloses Antibody G1 as well as the results of
the in vivo animal tests that would purportedly indicate to a POSA that Antibody G1 works in the
claimed method. It further discloses prior art references that discuss anti-CGRP antibodies and,
as the PTAB concluded, anti-CGRP antagonist antibodies were “well-known” in the prior art.
The Court therefore concludes that, unlike in Rochester, the specification’s disclosure does direct

a POSA toward compounds that can be used in the claimed methods.
Finally, in FWP IP, the court held that the written description was inadequate where the
specification did not demonstrate that the claimed compounds “were in fact effective for treating
the entire list of enumerated conditions” which was presented as a “laundry list of diseases and
conditions include[ing] psoriasis; psoriatic arthritis; neurodermatitis; inflammatory bowel
disease; neurodermatitus; autoimmune diseases (including [multiple sclerosis] as one of the
eleven listed); pain associated with radibulopahty, neuropathy, or sciatica; organ transplantation”
and several more. 749 F. App’x 969, 972, 975 (Fed. Cir. 2018). This case is easily
distinguishable because the list in FWP IP included a far greater variety of diseases that the

claimed invention purported to treat, as opposed to the present case where the condition to be
treated was “headache.” Moreover, Teva contends that the two in vivo assays do demonstrate the
effectiveness of its claimed inventions, which further distinguishes the present case from FWP IP
where the specification did not demonstrate that the claimed compounds were effective. At
minimum, there remains a genuine dispute over the extent of the specification’s disclosure.
Accordingly, based on the numerous factual disputes discussed above, the court denies
Lilly’s motion for summary judgment for lack of written description.
F. Lack of Enablement
Lilly argues that Teva’s asserted patents are not enabled because it would require undue
experimentation to (1) make the full scope of functionally-defined antibodies referenced in the
claims and (2) use the antibodies in the claimed method. [ECF No. 290 at 7–8]. Teva responds
that practicing the full scope of the claims does not require undue experimentation and, at the

very least, there are genuine disputes of fact as to whether the claims are enabled. [ECF No. 353
8–10].
“The requirement of enablement, stated in 35 U.S.C. § 112, enforces the essential ‘quid
pro quo of the patent bargain” by requiring a patentee to teach the public how ‘to practice the full
scope of the claimed invention.” McRO, Inc. v. Bandai Namco Games Am., Inc., 959 F.3d
1091, 1099–100 (Fed. Cir. 2020) (quoting AK Steel Corp. v. Sollac, 344 F.3d 1234, 1244 (Fed.
Cir. 2003)). “To prove that a claim is invalid for lack of enablement, a challenger must show by
clear and convincing evidence that a person of ordinary skill in the art would not be able to
practice the claimed invention without ‘undue experimentation.’” Amgen Inc. v. Sanofi,

Aventisub LLC, 987 F.3d 1080, 1084 (Fed. Cir. 2021) (quoting Alcon Rsch. Ltd. v. Barr Lab’ys,
Inc., 745 F.3d 1180, 1188 (Fed. Cir. 2014)). “Whether undue experimentation is needed is not a
single, simple factual determination, but rather is a conclusion reached by weighing many factual
considerations.” In re Wands, 858 F.2d 731, 737 (Fed. Cir. 1988). The factual consideration,
known as the “Wands factors,” are:
(1) the quantity of experimentation necessary, (2) the amount of direction or
guidance presented, (3) the presence or absence of working examples, (4) the nature
of the invention, (5) the state of the prior art, (6) the relative skill of those in the art,
(7) the predictability or unpredictability of the art, and (8) the breadth of the claims.
Id.
Lilly first argues that Teva’s claims are not enabled because they do not provide the
amino acid sequences for all the antibodies that have the function of binding to CGRP, inhibiting
CGRP biological activity, and, in turn, treating migraine or other headache disorders. [ECF No.
290 at 19]. As a result, undue experimentation becomes necessary as the number of possible
antibodies is so enormous that modifying the amino acids only within the CDRs of a single

antibody “results in 5 x 1080 antibodies—more than the number of stars in our galaxy (1x1011),
atoms in the Earth (1x1051), or hydrogen atoms in the universe (4x1079).” [Id. at 20]. Lilly
also claims that “A POSA Had No Prior Experience with the Claimed Antibodies in This New
Field” and “would have had no experience with the claimed methods” and would therefore have
to undertake undue experimentation. [Id. at 22].
The Court finds that Lilly has failed to carry its burden to show that there is no genuine
dispute of material fact as to whether a POSA would need to engage in undue experimentation,
as opposed to routine experimentation, to make the antibodies used in the claimed methods. This
is true even assuming, as Lilly argues, that Teva has claimed all humanized or human anti-CGRP

antagonist antibodies. “Undue experimentation is a matter of degree. Even a considerable
amount of experimentation is permissible, as long as it is merely routine or the specification
provides a reasonable amount of guidance regarding the direction of experimentation.” Wyeth &
Cordis Corp. v. Abbott Lab’ys, 720 F.3d 1380, 1385–86 (Fed. Cir. 2013) (internal citations and
quotation marks omitted). Here, the parties agree that the relevant POSA has either a Ph.D. in a
field such as immunology, biochemistry, or pharmacology with several years of post-doctoral
experience in antibody engineering, pharmacokinetics, and pharmacodynamics, or is a M.D. with
a residency or specialty in neurology, and several years of experience studying CGRP or treating
patients with a headache disorder such as migraine. [ECF No. 411 ¶¶ 223–24]. Given this high
degree of expertise, Lilly’s argument focusing on the immense possible diversity of antibodies
resulting from the randomization of every amino acid in every CDR in a single antibody is of no
moment. The suggestion that someone with that degree of knowledge would engage in such a
dramatic and disorganized substitution in search of an antibody that binds to and antagonizes
CGRP is not credible or persuasive.

Moreover, Teva has presented substantial evidence that the state of the prior art of
antibody engineering was advanced and predictable, the relative skill of those in the art was high,
and any experimentation needed to practice the claimed invention was “routine” and
“conventional.” As just one example, the evidence proffered by Teva suggests that screening to
identify CGRP antagonist antibodies was accomplished via automated, high-throughput,
commercially available assays. [ECF No. 411 ¶¶ P68–P73]. Moreover, as Lilly itself argued
and the PTAB agreed, by 2005–2006, anti-CGRP antagonist antibodies were well known in the
prior art. [ECF No. 411 ¶ 14].
Lilly’s next argues that because the asserted claims encompass administering an effective

amount of any anti-CGRP antagonist antibody to treat one of numerous headache disorders, the
specification amounts to an invitation for further research and experimentation. [ECF No. 290 at
24–25]. Further, because as of 2005–2006 a POSA would have had no experience using the
claimed antibodies to treat headache, extensive trial-and-error experimentation and clinical trials
would be necessary to practice the claimed methods. [Id. at 25]. Here, again, the Court finds
that Lilly fails to carry its burden. Among others, the parties dispute (1) whether a POSA would
be starting from a blank slate when identifying an effective amount to treat headache, (2)
whether the specification provided sufficient guidance on dosing, (3) whether Teva needed to
provide dosing regimens for each of the sub-types of headache disorders listed in the
specification, (4) whether the only headaches linked to CGRP were migraines and some forms of
cluster headaches, and (5) whether testing in humans was essential to practice the claimed
methods. These numerous factual disputes reflect that summary judgment is wholly
inappropriate on the issue, and Lilly’s motion for summary judgment for lack of enablement is
therefore denied.

IV. CONCLUSION
Accordingly, Lilly’s motions for summary judgment for lack of enablement, insufficient
written description, and no willful infringement are DENIED, its partial motion for summary
judgment for non-infringement is GRANTED and Teva’s motions for summary judgment
regarding judicial estoppel and inequitable conduct are DENIED.
SO ORDERED.

October 3, 2022 /s/ Allison D. Burroughs
ALLISON D. BURROUGHS
U.S. DISTRICT JUDGE

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/10200579. Public record. Not legal advice.