Date: 20210106  
Dockets: T-2182-18  
T-2183-18  
Citation: 2020 FC 1158  
Ottawa, Ontario, January 6, 2021  
PRESENT: The Honourable Madam Justice Kane  
BETWEEN:  
TEVA CANADA INNOVATION AND  
TEVA CANADA LIMITED  
Plaintiffs  
and  
PHARMASCIENCE INC  
and  
Defendant  
YEDA RESEARCH AND  
DEVELOPMENT CO., LTD.  
Patentee added pursuant to ss 6(2)  
of the PM (NOC) Regulations and  
ss 55(3) of the Patent Act  
PUBLIC JUDGMENT AND REASONS  
Page: 2  
(The Confidential Judgment and Reasons were issued on December 16, 2020 and no redactions  
are necessary)  
Table of Contents  
I. Overview ................................................................................................................................. 4  
II. The Patents at Issue ............................................................................................................... 12  
A.  
B.  
III.  
A.  
(1)  
(2)  
(3)  
(4)  
B.  
(1)  
(2)  
(3)  
(4)  
The ‘437 Patent.................................................................................................................. 12  
The ‘802 Patent.................................................................................................................. 14  
The Witnesses and the Nature of their Evidence............................................................... 16  
The ‘437 Patent.................................................................................................................. 16  
Fact Witnesses for Teva ............................................................................................. 16  
Expert Witnesses for Teva.......................................................................................... 17  
Fact Witnesses for Pharmascience ............................................................................. 18  
Expert Witnesses for Pharmascience.......................................................................... 18  
The ‘802 Patent.................................................................................................................. 19  
Fact Witnesses for Teva ............................................................................................. 19  
Fact Witnesses for Pharmascience ............................................................................. 19  
Expert Witnesses for Teva.......................................................................................... 20  
Expert Witness for Pharmascience............................................................................. 20  
IV. MS and its Diagnosis / Criteria............................................................................................. 21  
A.  
B.  
C.  
D.  
E.  
F.  
Types of MS....................................................................................................................... 22  
Clinically Isolated Syndrome............................................................................................. 23  
Diagnosis of MS ................................................................................................................ 24  
Use of MRI ........................................................................................................................ 27  
The McDonald Criteria...................................................................................................... 28  
The Difference between the Poser and McDonald Criteria vis-à-vis a CIS patient .......... 31  
V. Overall Position of the Plaintiff Teva on the ‘437 Patent..................................................... 32  
VI. Overall Position of the Defendant Pharmascience on the ‘437 Patent ................................. 34  
VII. Overall Position of the Plaintiff Teva on the ‘802 Patent.................................................. 37  
VIII. Overall Position of the Defendant Pharmascience on the ‘802 Patent .............................. 39  
IX. Onus and Burden of Proof .................................................................................................... 40  
X. The ‘437 Patent – Description and Disclosure ..................................................................... 40  
XI. The ‘802 Patent – Description and Disclosure ..................................................................... 45  
XII. The Structure of this Judgment.......................................................................................... 47  
XIII. Overview of the Experts’ Evidence re the ‘437 Patent...................................................... 48  
A.  
B.  
C.  
D.  
Pharmascience’s Expert, Dr. Green................................................................................... 48  
Teva’s Expert, Dr. Morrow................................................................................................ 52  
Teva’s Expert, Dr. Selchen ................................................................................................ 54  
Teva’s Expert, Dr. Kreitman.............................................................................................. 56  
XIV. The POSITA for the ‘437 Patent ....................................................................................... 57  
A.  
B.  
The Principles from the Jurisprudence .............................................................................. 57  
Who is the POSITA for the ‘437 Patent?........................................................................... 58  
XV. The Construction of the Claims......................................................................................... 60  
A.  
B.  
The Principles from the Jurisprudence .............................................................................. 60  
The Claims of the ‘437 Patent ........................................................................................... 61  
Page: 3  
C.  
The Dispute regarding the Patients Included in the Claims............................................... 64  
Pharmascience’s Submissions.................................................................................... 64  
Teva’s Submissions.................................................................................................... 66  
What do the Experts Say regarding the Patients Included in the Claims?......................... 69  
Dr. Green .................................................................................................................... 69  
Dr. Morrow................................................................................................................. 71  
Dr. Selchen ................................................................................................................. 73  
The Patients Included in Claim 1 and Subsequent Claims ................................................ 76  
(1)  
(2)  
D.  
(1)  
(2)  
(3)  
E.  
XVI. Prior Art related to the ‘437 Patent.................................................................................... 84  
A.  
B.  
C.  
D.  
Prior art on the use of glatiramer acetate in MS ................................................................ 85  
Prior art on CIS progressing to MS.................................................................................... 85  
Prior art on the use of interferons in CIS ........................................................................... 86  
Prior art cited by Pharmascience as anticipatory references.............................................. 89  
XVII. Common General Knowledge............................................................................................ 90  
A.  
B.  
(1)  
(2)  
C.  
Principles from the Jurisprudence...................................................................................... 90  
What Do the Experts Say? ................................................................................................. 91  
Dr. Green .................................................................................................................... 91  
Dr. Selchen ................................................................................................................. 95  
The Common General Knowledge regarding the ‘437 Patent........................................... 98  
XVIII. Can Pharmascience rely on the Gillette Defence to the Allegations of Infringement of  
the ‘437 Patent?........................................................................................................................... 101  
A.  
B.  
C.  
D.  
Principles from the Jurisprudence.................................................................................... 101  
Pharmascience’s Submissions ......................................................................................... 102  
Teva’s Submissions ......................................................................................................... 103  
The Gillette Defence Cannot Succeed ............................................................................. 104  
XIX. Is the ‘437 Patent Anticipated?........................................................................................ 105  
A.  
B.  
C.  
D.  
(1)  
(2)  
E.  
Principles from the Jurisprudence.................................................................................... 105  
Pharmascience’s Submissions ......................................................................................... 108  
Teva’s Submissions ......................................................................................................... 111  
What do the Experts Say?................................................................................................ 114  
Dr. Green .................................................................................................................. 114  
Dr. Selchen ............................................................................................................... 116  
Karussis 2006 does Not Anticipate the Claims of the ‘437 Patent.................................. 118  
XX. Is the ‘437 Patent Obvious? ............................................................................................. 129  
A.  
B.  
C.  
D.  
(1)  
(2)  
E.  
(1)  
(2)  
Principles from the Jurisprudence.................................................................................... 129  
Pharmascience’s Submissions ......................................................................................... 134  
Teva’s Submissions ......................................................................................................... 139  
What do the Experts Say?................................................................................................ 143  
Dr. Green .................................................................................................................. 143  
Dr. Selchen ............................................................................................................... 146  
The Claims of the ‘437 Patent are Obvious..................................................................... 150  
The State of the Art .................................................................................................. 151  
The Differences between the State of the Art and the Subject Matter of the Claims155  
XXI. The ‘802 Patent................................................................................................................ 159  
A.  
B.  
The POSITA for the ‘802 Patent ..................................................................................... 160  
The Construction of the Claims of the ‘802 Patent.......................................................... 161  
Page: 4  
XXII. Prior Art and Common General Knowledge related to the ‘802 Patent .......................... 161  
A.  
B.  
C.  
D.  
Prior art on glatiramer acetate 20 mg daily vs. every-other-day (alternate-day)............. 162  
Prior art on glatiramer acetate 20 mg vs. 40 mg administered daily ............................... 165  
Prior art on glatiramer acetate 40 mg every-other-day.................................................... 167  
Prior art on injection site reaction and immediate post injection reaction....................... 167  
XXIII. Overview of the Experts’ Evidence on the ‘802 Patent ............................................... 168  
A.  
B.  
C.  
Pharmascience’s Expert, Dr. Green................................................................................. 168  
Teva’s Expert, Dr. Prat .................................................................................................... 169  
Teva’s Expert, Dr. Day.................................................................................................... 171  
XXIV. Is the ‘802 Patent Invalid due to Obviousness? ........................................................... 172  
A.  
B.  
C.  
(1)  
(2)  
D.  
(1)  
(2)  
(3)  
Teva’s Submissions ......................................................................................................... 172  
Pharmascience’s Submissions ......................................................................................... 180  
What do the Experts Say?................................................................................................ 186  
Dr. Green .................................................................................................................. 186  
Dr. Prat...................................................................................................................... 194  
The ‘802 Patent is Not Obvious....................................................................................... 206  
The State of the Art .................................................................................................. 216  
Differences between the State of the Art and the Subject Matter of the Claims...... 218  
Not Obvious to Try................................................................................................... 219  
XXV. Is the ‘802 Patent Invalid due to Lack of Utility or Sound Prediction of Utility?........... 224  
A.  
B.  
C.  
D.  
Teva’s Submissions ......................................................................................................... 224  
Pharmascience’s Submissions ......................................................................................... 228  
Principles from the Jurisprudence.................................................................................... 230  
The ‘802 Patent is not Invalid due to Lack of Sound Prediction of Utility ..................... 235  
XXVI. The Jurisdictional Issue Can Teva rely on the Regulations to assert infringement by  
Pharmascience of 20 mg Glatect?............................................................................................... 241  
XXVII. Infringement by Pharmascience................................................................................... 245  
XXVIII. Costs............................................................................................................................. 249  
I.  
Overview  
[1]  
These proceedings involve two patent infringement actions [the Action] pursuant to  
subsection 6(1) of the Patented Medicines (Notice of Compliance) Regulations, SOR/93-133  
[the Regulations].  
[2]  
At issue are medications that treat multiple sclerosis [MS]. The Teva Canada Innovation  
and Teva Canada Limited [collectively, Teva] product is Copaxone® [Copaxone]. Copaxone 20  
 
Page: 5  
milligram [mg] has been on the market since the mid-90s. Copaxone 40 mg is a more recent  
product.  
[3]  
The Pharmascience Inc. [Pharmascience] generic product is Glatect® [Glatect].  
Pharmascience obtained a Notice of Compliance [NOC] from the Minister of Health [Minister]  
for Glatect 20 mg, which is administered daily, in 2017 and has been marketing Glatect 20 mg  
since that time. The Glatect Product Monograph, which, among other things, describes what  
Glatect 20 mg is intended to treat, is described in more detail later in these Reasons. Teva has  
confirmed that regardless of the outcome of this Action, the NOC issued to Pharmascience for  
Glatect 20 mg daily will not be affected.  
[4]  
Pharmascience now seeks to expand its Glatect product to include a 40 mg strength to be  
administered three times per week. Pharmascience submitted a Supplementary New Drug  
Submission [SNDS] to do so and, in that context, identified Copaxone 40 mg as the reference  
product. Pharmascience describes its SNDS as a line extension to its 20 mg product.  
[5]  
This Action arises from Pharmascience’s filing of the SNDS. Teva submits that Glatect  
40 mg would be marketed in accordance with Pharmascience’s proposed Glatect Product  
Monograph that is substantially identical to Teva’s Copaxone Product Monograph.  
[6]  
Teva argues that Pharmascience’s Glatect products will infringe the two patents at issue –  
Canadian Patent Nos. 2,702,437 [the ‘437 Patent] and 2,760,802 [the ‘802 Patent]. Teva submits  
that Pharmascience will manufacture, sell and induce the use of its products, which will be for  
Page: 6  
exactly the same patient population, in the same dosage strength, and with the same dosage  
regimen to achieve the same outcomes. Teva submits that Pharmascience has not led any  
evidence to demonstrate that it will not infringe. Pharmascience argues that the patents are  
invalid.  
[7]  
The criteria for a diagnosis of MS is a point of contention between Teva and  
Pharmascience as this has an impact on the scope of the claims of the ‘437 Patent and in turn the  
allegations of infringement and invalidity. As described below, in the 1980s and 1990s, the  
diagnosis of MS was based on criteria developed by Poser (Poser CM et al, “New Diagnostic  
Criteria for Multiple Sclerosis: Guidelines for Research Protocols”, 1983 Ann Neurol 13(3): 227-  
230 [the Poser criteria]) which required the demonstration of two clinical attacks. In 2001, new  
criteria were developed by McDonald (McDonald et al, “Recommended diagnostic criteria for  
multiple sclerosis: guidelines from the international panel on the diagnosis of multiple sclerosis”,  
2001 Ann Neurol 50: 121-127 [the McDonald criteria]) which relied more extensively on  
magnetic resonance imaging [MRI] evidence to demonstrate the disease and its progression. The  
McDonald criteria were updated in 2005, 2010 and 2017. The experts noted that while the  
McDonald criteria gained wide acceptance, the Poser criteria and terminology remain within  
their knowledge and some physicians continue to refer to the Poser criteria.  
[8]  
Teva submits that the claims of the ‘437 Patent are directed only to patients who have had  
one clinical attack and have not yet been diagnosed with MS.  
Page: 7  
[9]  
Teva does not dispute that Copaxone 20 mg was known as an effective therapy for  
patients diagnosed with relapsing-remitting multiple sclerosis [RRMS], a type of MS. Teva  
argues that the ‘437 Patent was novel and inventive in identifying 20 mg of glatiramer acetate  
daily for the early treatment of patients after their first clinical attack and before the onset of MS.  
Teva argues that the prior art relied on by Pharmascience was obscure and only speculated that  
glatiramer acetate administered daily would be effective for the early treatment of patients.  
[10] Pharmascience argues that it will not infringe the ‘437 Patent because the patent is invalid  
and because its Glatect 40 mg product is not intended for the single-attack patient but for patients  
who meet the criteria for a diagnosis of MS or RRMS.  
[11] Pharmascience asserts the Gillette defence in response to Teva’s allegations of  
infringement. Pharmascience argues that it does not infringe the ‘437 Patent because its Glatect  
product merely practices the teachings of the prior art. Pharmascience submits that the claims of  
the ‘437 Patent include RRMS patients, and the prior art includes that glatiramer acetate was  
well known to be an effective treatment for RRMS.  
[12] Pharmascience also argues that the ‘437 Patent is neither novel nor inventive and, as a  
result, is invalid due to anticipation and obviousness.  
[13] Pharmascience submits that, although the claims of the ‘437 Patent reflect the Poser  
criteria, the claims include some patients who meet the McDonald criteria for MS. If  
Pharmascience’s interpretation prevails, then those patients who have had only one clinical  
Page: 8  
attack but who meet the criteria for a diagnosis of MS (i.e., based on MRI evidence) would fall  
within the claims of the ‘437 Patent. Argueably, these MS patients are no different from the  
RRMS patients for which Copaxone 20 mg was a well-known treatment.  
[14] Pharmascience also submits that if the claims of the ‘437 Patent are interpreted narrowly,  
to single-attack patients (as Teva proposes), the claims are still anticipated by the prior art, which  
recommended that glatiramer acetate should be considered for the early treatment of such  
patients.  
[15] Pharmascience argues that the claims are obvious because there was no difference  
between the state of the art in November 2007 and the subject matter of the claims.  
[16] Jurisdictional issues have been raised by Pharmascience regarding whether the scope of  
the Regulations permits Teva to assert infringement of the ‘437 Patent with respect to Glatect  
20 mg on a go-forward basis in these circumstances, given that Pharmascience has already  
obtained a NOC. This issue is addressed later in these Reasons in Part XXVI.  
[17] With respect to the ‘802 Patent, Teva argues that Pharmascience will infringe the patent  
because Pharmascience’s Glatect product is indicated for the very same patient population,  
primarily patients with RRMS, with the same dosing schedule of 40 mg three times weekly.  
Teva disputes that the ‘802 Patent is invalid for obviousness or lack of sound prediction of  
utility.  
Page: 9  
[18] Teva argues that there were material differences between the state of the art in August  
2009 and the subject matter of the claims of the patent. Teva disputes that the prior art relied on  
by Pharmascience was authoritative or known by the person skilled in the art [POSITA or skilled  
person] or would be considered as a “mosaic” by the POSITA. Teva argues that the POSITA  
would not reach the invention using their common general knowledge and routine work. Rather  
inventiveness was required. Teva submits that there is no question that the 40 mg three times per  
week invention is inventive and useful.  
[19] Pharmascience submits that it will not infringe Teva’s ‘802 Patent because the ‘802  
Patent is invalid due to obviousness.  
[20] Pharmascience alternatively submits that if the ‘802 Patent is not obvious based on the  
prior art, then Teva has neither demonstrated utility nor soundly predicted utility. Teva notes that  
there are no results set out in the ‘802 Patent, but only a proposal for a study of the expected  
results.  
[21] Generally, the parties have mapped out different paths to lead to the findings they seek  
and have pointed to excerpts in the evidence in support of their particular directional paths.  
However, the role of the Court is to take the “high road” and to consider all the relevant evidence  
in its proper context.  
[22] Both Teva and Pharmascience raised objections to particular evidence of the other party.  
Page: 10  
[23] For example, Teva submits that Pharmascience has engaged in case splitting by  
introducing new evidence, in particular, the international patent application WO 2007/081975  
[Pinchasi 2007], noted in Dr. Ari Green’s responding report on non-infringement. Pharmascience  
disputes this allegation and argues that it clearly pleaded the Gillette defence as an infringement  
issue. Pharmascience explains that Dr. Green was given and asked to review the prior art product  
monographs for Copaxone and Pinchasi 2007 and to describe how a skilled person would  
understand them. He was also asked to review the Glatect Product Monograph and to provide his  
opinion as to whether it followed the teachings of the prior art.  
[24] Pharmascience explains that it does not rely on Dr. Green’s opinion on Pinchasi 2007 in  
his responding non-infringement report for its anticipation arguments; rather it relies on this  
evidence for the Gillette defence. Pharmascience notes that Teva did not provide any reply to Dr.  
Green’s non-infringement report.  
[25] Pharmascience also notes that it clearly cited Pinchasi 2007 as an anticipatory reference  
and it can, therefore, be relied on to show anticipation.  
[26] Teva also submits that Pharmascience sought to introduce additional evidence in its  
closing arguments. Pharmascience responds that the additional 21-page compendium contains  
only excerpts of documents already in evidence to more clearly point to the references Dr. Green  
relied on in his validity opinion.  
Page: 11  
[27] More generally, each party seeks to diminish the expertise and evidence of their  
opponents’ experts by, among other things: questioning their understanding of the legal tests and  
instructions provided; suggesting that they are in the pockets of big pharmaceutical companies  
due to past research grants and consulting fees; suggesting that they have exceeded their  
mandates; suggesting that they have not published in certain top scientific journals; suggesting  
that they have cited other experts in the field in their publications who they now seem to differ  
with on specific points; and, challenging their specific expertise, such as not being part of a drug  
development team.  
[28] In my view, all the experts have established their particular expertise and all have offered  
evidence that is helpful to the Court on the issues at play. All the experts are clearly committed  
to improving the experience of persons with MS. I have considered the submissions of both  
parties who seek to discount the evidence of the other party’s witnesses. I have considered all of  
the evidence in its proper context and have weighed it. I have not discounted the evidence of any  
expert because they have been paid by the parties in this or other litigation or in their research, or  
because they have published more or less extensively than other experts. Clearly, they are all  
experts in the diagnosis and treatment of MS and have been so qualified for the purpose of this  
Action. However, the experts have provided different opinions on key issues that are not possible  
to reconcile. Cross-examination has identified some inconsistencies and frailties in some of the  
evidence. However, some of the questions posed to the experts on cross-examination were  
detailed and specific and understandably sought to elicit support for particular arguments. In  
some instances, the questions and answers were confusing and contrived and have required me to  
Page: 12  
very carefully consider the totality of the expert’s extensive evidence. The assessment of the  
evidence is addressed in the context of the relevant issues.  
[29] For the reasons that follow, I find that the ‘437 Patent is not anticipated by Karussis D et  
al, “A recommended treatment algorithm in relapsing multiple sclerosis: report of an  
international consensus meeting”, 2006 Eur J Neurol 13: 61-71 [Karussis 2006]. However, I find  
that the ‘437 Patent is obvious.  
[30] The jurisdictional issue regarding Teva’s reliance on the Regulations to allege  
infringement with respect to the 20 mg Glatect product need not be addressed given my  
conclusion that the ‘437 Patent is not valid.  
[31] I find that the ‘802 Patent is valid; it is not obvious and it soundly predicted its utility.  
[32] With respect to infringement, if Pharmascience proceeds to market Glatect 40 mg in  
accordance with its proposed SNDS, it will infringe the ‘802 Patent.  
II.  
A.  
The Patents at Issue  
The ‘437 Patent  
[33] Yeda Research and Development Co., Ltd. [Yeda] is the owner of the ‘437 Patent.  
   
Page: 13  
[34] Pursuant to section 42 of the Patent Act, RSC 1985, c P-4 [Patent Act], Yeda has the  
exclusive right, privilege and liberty of making, constructing, using and selling to others to be  
used, the invention claimed in the ‘437 Patent.  
[35] Yeda is a corporation with a head office in Rehovot, Israel.  
[36] Teva Canada Innovation is a corporation with a head office in Montreal Quebec, and an  
office in Toronto, Ontario. Teva Canada Limited is a corporation with a head office in Toronto,  
Ontario.  
[37] The ‘437 Patent is listed on the Patent Register maintained by the Minister pursuant to  
the Regulations in respect of Teva's 40 mg glatiramer acetate product marketed under the brand  
name Copaxone in 40 mg/1 mL pre-filled syringes for subcutaneous injection. Teva’s 20 mg  
strength glatiramer acetate is not listed on the Patent Register.  
[38] Teva notes that it has obtained Yeda’s consent for the inclusion of the ‘437 Patent on the  
Patent Register maintained by the Minister pursuant to the Regulations. Teva is authorized by  
Yeda to sell, and sells, the drug Copaxone (glatiramer acetate) in Canada.  
[39] The ‘437 Patent is titled, “Methods of Delaying the Onset of Clinically Definite Multiple  
Sclerosis”. The ‘437 Patent issued on June 25, 2013 and has not expired.  
Page: 14  
[40] The parties agree that the relevant date for claims construction is the date of the  
publication of the patent, June 4, 2009. For anticipation and obviousness, the relevant date is the  
claim date, November 28, 2007.  
[41] The ‘437 Patent contains 50 claims. The claims relate to glatiramer acetate, or  
medicaments comprising glatiramer acetate, for use in treating human patients at risk of  
developing MS. The claims at issue (Claims 1, 2, 3, 4, 13, 14, 15, 16, 19, 24, 33, 47 and 50) are  
set out at Annex 1.  
[42] On November 13, 2018, Teva was served with a Notice of Allegation [NOA] from  
Pharmascience, a generic pharmaceutical company, in respect of Glatect 40 mg regarding the  
‘437 Patent. The NOA alleges that the ‘437 Patent would not be infringed by Pharmascience  
making, constructing, using or selling Glatect and that the ‘437 Patent is invalid.  
B.  
The ‘802 Patent  
[43] Yeda is also the registered owner of the ‘802 Patent and is a party to this Action pursuant  
to subsection 6(2) of the Regulations.  
[44] Pursuant to section 42 of the Patent Act, Yeda has the exclusive right, privilege and  
liberty of making, constructing, using and selling to others to be used, the invention claimed in  
the ‘802 Patent.  
 
Page: 15  
[45] The ‘802 Patent is listed on the Patent Register maintained by the Minister pursuant to  
the Regulations in respect of Teva’s glatiramer acetate product marketed under the brand name  
Copaxone in 40 mg /1 mL pre-filled syringes for subcutaneous injection.  
[46] Teva notes that it has obtained Yeda's consent for the inclusion of the ‘802 Patent on the  
Patent Register maintained by the Minister pursuant to the Regulations. Teva asserts that it is  
authorized by Yeda to sell, and sells, the drug Copaxone (glatiramer acetate) in Canada.  
[47] The ‘802 Patent is titled, “Low Frequency Glatiramer Acetate Therapy”.  
[48] The parties agree that the relevant date for construing the claims is the publication date of  
the patent application, February 24, 2011. The relevant date for the allegations of obviousness is  
the claim date, August 20, 2009. The relevant date to assess utility is the filing date, August 19,  
2010.  
[49] The ‘802 Patent contains 66 claims. All claims relate to glatiramer acetate, or  
medicaments comprising glatiramer acetate, for use in treating human patients with, or at risk of  
developing, MS. The claims at issue are Claims 1, 2, 3, 4, 22, 24, 25, 36-39, 47-57, 59, 60, 63-66  
and are set out at Annex 2.  
[50] On November 13, 2018, Teva was served with a NOA from Pharmascience in respect of  
Glatect regarding the ‘802 Patent. The NOA alleges that the ‘802 Patent would not be infringed  
by Pharmascience making, constructing, using or selling Glatect and the ‘802 Patent is invalid.  
Page: 16  
III.  
The Witnesses and the Nature of their Evidence  
[51] The parties presented their evidence in both written reports from fact and expert  
witnesses and oral testimony from many of the witnesses. The witnesses and a brief synopsis of  
the nature of their evidence is set out below.  
A.  
The ‘437 Patent  
(1)  
Fact Witnesses for Teva  
[52] Ms. Sigalit Zecharia Daniel is the Senior Director, Head of Global Clinical Quality at  
Teva Pharmaceutical Industries Ltd. Ms. Daniel attached to her affidavit documents related to  
clinical studies that Teva had conducted, including the clinical study protocols and reports.  
[53] Dr. Rivka Kreitman holds a Ph.D. in biochemistry and completed a post-doctoral  
fellowship in molecular biology and genetics. She joined Teva in 1993 and left in 2018. During  
her time at Teva, among other things, she and her team were responsible for the research,  
development, regulatory filings and clinical studies of Copaxone. Dr. Kreitman provided  
documents related to the development of Copaxone. Dr. Kreitman has also provided evidence in  
proceedings in other jurisdictions regarding the patents at issue.  
     
Page: 17  
(2)  
Expert Witnesses for Teva  
[54] Dr. Sarah Morrow is a neurologist with expertise in neurological disorders, including the  
diagnosis and treatment of MS. Dr. Morrow described the POSITA, the disclosure of the ‘437  
Patent and the construction of the claims. Dr. Morrow’s evidence focussed on whether the using  
or selling of Pharmascience’s Glatect products, as described in the Glatect Product Monograph,  
would infringe the claims of the ‘437 Patent.  
[55] Dr. Selchen is a neurologist with expertise in neurological disorders, including the  
diagnosis and treatment of MS. Dr. Selchen responded to Dr. Green’s invalidity opinion.  
Dr. Selchen addressed the POSITA, common general knowledge, construction of the claims and  
the state of the art in relation to the ‘437 Patent.  
[56] Mr. Neil Palmer is an expert on the Canadian pharmaceutical marketplace. He is the  
Founder, Senior Adviser, and President Emeritus of PDCI Market Access Inc., an Ottawa-based  
pricing and reimbursement consultancy. Mr. Palmer’s evidence addressed, among other things,  
the public and private reimbursement regimes relevant to glatiramer acetate including Copaxone  
and Glatect. The parties agreed that Mr. Palmer’s report be accepted without oral testimony.  
[57] Dr. Gregory Grant is a biochemist and professor of developmental biology and  
biochemistry in medicine. Dr. Grant’s evidence addressed a biochemist’s understanding of  
“glatiramer acetate” relative to the ‘437 and ‘802 Patents and assessed whether Glatect contains  
 
Page: 18  
glatiramer acetate. The parties agreed that Dr. Grant’s evidence be accepted without oral  
testimony.  
(3)  
Fact Witnesses for Pharmascience  
[58] Mr. Graham McKinnon is a registered patent agent in Canada and the United States.  
Mr. McKinnon attached to his affidavit documents related to the filing history of the U.S. Patent  
Application No. 11/651,212 and Canadian Patent No. 2,191,088 [the ‘088 Patent].  
[59] Mr. Deirdre Cozier is the Director of Global Regulatory Affairs at Pharmascience,  
responsible for compiling information and data and making submissions related to  
Pharmascience’s pharmaceutical products to regulatory authorities worldwide, including Health  
Canada. Mr. Cozier attached to his affidavit documents related to the regulatory filings of  
Glatect, including the product monograph and SNDS.  
(4)  
Expert Witnesses for Pharmascience  
[60] Dr. Ari Green is a neurologist with expertise in neurological disorders, including the  
diagnosis and treatment of MS. He provided two reports with respect to the ‘437 Patent.  
Dr. Green first set out his opinion on the validity of the ‘437 Patent and addressed anticipation,  
citing Karussis 2006, and obviousness with reference to the prior art and common general  
knowledge. Dr. Green also provided a second report in response to Dr. Morrow’s infringement  
report. In the second report, Dr. Green addressed product monographs, elaborated on the target  
   
Page: 19  
patient population and cited additional prior art. Dr. Green has also provided expert evidence in  
proceedings in other jurisdictions regarding the patents at issue or their equivalents.  
[61] Ms. Susanne Picard is a pharmacist and regulatory affairs consultant with expertise in the  
regulatory approval of pharmaceutical products. Ms. Picard’s evidence addressed, among other  
things, the requirements for New Drug Submissions [NDS] and SNDS, the use of product  
monographs and, more particularly, the Glatect SNDS and Product Monograph.  
B.  
The ‘802 Patent  
(1)  
Fact Witnesses for Teva  
[62] Ms. Sigalit Zecharia Daniel and Dr. Rivka Kreitman, described above, also provided  
evidence for the ‘802 Patent.  
(2)  
Fact Witnesses for Pharmascience  
[63] Mr. Graham McKinnon and Mr. Deirdre Cozier, described above, also provided evidence  
for the ‘802 Patent.  
     
Page: 20  
(3)  
Expert Witnesses for Teva  
[64] Dr. Reza Vosoughi is a neurologist with expertise in neurological disorders, including the  
diagnosis and treatment of multiple sclerosis. Dr.Vosoughi’s evidence addressed the POSITA,  
construction of the claims and infringement of the claims of the 802 Patent.  
[65] Dr. Alexandre Prat is a neurologist with expertise in neurological disorders, including the  
diagnosis and treatment of multiple sclerosis. Dr. Prat responded to Dr. Green’s opinion on the  
invalidity of the ‘802 Patent.  
[66] Dr. Simon Day is a biostatistician with expertise in clinical trial design and interpretation.  
Among other things, Dr. Day addressed how the POSITA would have regardedthe results of  
clinincal studies and other abstracts relating to glatiramer acetate.  
[67] Mr. Neil Palmer and Dr. Gregory Grant, described above, also provided evidence for the  
‘802 Patent.  
(4)  
Expert Witness for Pharmascience  
[68] Dr. Ari Green, described above, also provided his opinion on the validity of the ‘802  
Patent.  
   
Page: 21  
IV.  
MS and its Diagnosis/Criteria  
[69] MS is a disease of the central nervous system [CNS], which includes the brain, optic  
nerve and spinal cord. MS is considered to be an inflammatory or autoimmune disease in which  
the patient’s own immune system attacks the myelin of the CNS.  
[70] As explained by Teva’s witness Dr. Morrow, and reiterated by the other experts, the CNS  
is composed of grey matter and white matter. Grey matter contains neuron cell bodies, while  
white matter contains axons, which are the projecting portions of neurons. The axons of the CNS  
white matter are wrapped in a fatty substance known as myelin. The myelin forms a sheath  
(analogous to insulation) that enables rapid transmission of electrical signals generated in neuron  
cell bodies that are propagated along the length of axons.  
[71] With MS, the body’s immune system attacks elements of the CNS and leads to the  
destruction of the myelin sheath in the brain, optic nerve and spinal cord (referred to as  
“demyelination”) and axonal loss, which causes CNS damage, or lesions over time.  
[72] Demyelination may occur at various sites within the CNS. The symptoms experienced by  
an MS patient depend upon the site or sites within the CNS that are affected by demyelination  
and by the size of the lesions.  
[73] Pharmascience’s expert, Dr. Green, explained that MS is characterized early on by  
intermittent but potentially debilitating inflammatory and demyelinating events (also called  
 
Page: 22  
“attacks”, “relapses”, “exacerbations”, and “episodes”). One of the common presenting clinical  
attacks is optic neuritis (which manifests itself as a loss of vision and pain behind the eye). Other  
common clinical attacks include episodes of numbness, tingling, muscle weakness and spasticity,  
incoordination, loss of control of bowel and bladder, general fatigue, dizziness and depression.  
A.  
Types of MS  
[74] The expert witnesses all described the categories of MS in a similar manner noting that  
the categories are related to the course or progression of the disease.  
[75] The experts explained that as of November 2007, with respect to the ‘437 Patent, and as  
of August 2009, with respect to the ‘802 Patent, four distinct clinical courses or categories of MS  
had been described:  
a. RRMS is characterized by intermittent and clearly defined relapses with at least partial  
recovery or remission of some symptoms over weeks to months;  
b. Secondary progressive MS [SPMS], which follows a diagnosis of RRMS is characterized  
by progressive worsening of symptoms over time with fewer or no intermittent relapses  
interspersed with periods of partial recovery;  
c. Primary progressive MS [PPMS] is characterized by a steady decline in neurological  
function without distinct relapses or remissions; and,  
 
Page: 23  
d. Progressive-relapsing MS [PRMS] is characterized by a steady decline in neurological  
function from onset overlaid with occasional relapses and periods of recovery during  
which progressive worsening of symptoms continues.  
[76] Several experts explained that RRMS remains the most common type of MS.  
B.  
Clinically Isolated Syndrome  
[77] Teva’s witness, Dr. Selchen explained that, as of November 2007, patients presenting  
with a single clinical attack having features typical of MS were diagnosed as having a clinically  
isolated syndrome [CIS]. Dr. Selchen noted that when examining a patient presenting with a  
possible CIS, it would be important for the clinician to consider whether the CIS is caused by  
something other than MS. Dr. Selchen also noted that it was recognized that many, but not all,  
cases of MS begin as a CIS.  
[78] MRI could be used for patients who had a single clinical attack to determine if the attack  
was suggestive or supportive of an MS diagnosis.  
[79] Dr. Green also explained that the term CIS was generally applied to patients who had a  
single episode of clinical neurological worsening that was suspicious for demyelination with  
MRI evidence of other lesions (at least one or two). CIS with evidence of MRI lesion(s) was  
often distinguished from an episode that was suspicious for inflammatory demyelination but did  
 
Page: 24  
not have MRI lesions by calling it “high risk” CIS. Dr. Green stated that most of these “high  
risk” CIS patients go on to develop RRMS.  
[80] Dr. Green added that the primary means of distinguishing who is at risk of developing  
future attacks is evidence of prior episodes that preceded the clinical event (the CIS event). As of  
November 2007, this risk was largely assessed via the identification of suspect lesions on MRI.  
C.  
Diagnosis of MS  
[81] All the experts agreed that the diagnosis of MS has evolved over time.  
[82] The experts also agreed that there is no single diagnostic test for any type of MS. The  
diagnosis is based on a combination of findings from a patient’s history, physical exam, ancillary  
diagnostic tests (such as MRIs of the brain and spinal cord) and examination of cerebrospinal  
fluid through lumbar puncture.  
[83] As Dr. Green elaborated, by November 2007, MS diagnosis depended upon (and still  
depends upon) numerous objective and subjective analyses. Objective analyses include clinical  
examination, formalized clinical evaluations scored to measure disability, MRI scans, extended  
clinical assessments (e.g., neuropsychological assessments and neurovisual assessments) and  
relapse frequency assessments. Subjective assessments include patient questionnaires targeting  
measurement of clinical progression.  
 
Page: 25  
[84] Although MS was diagnosed long before the 1980s, the criteria of relevance to this  
Action are the Poser and McDonald criteria.  
[85] The “Poser criteria” were developed in the 1980s. The Poser criteria depended to a great  
extent on clinical observation.  
[86] The concepts or pillars of the criteria are “dissemination in space” [DIS], described as  
evidence of lesions at multiple locations in the CNS, and “dissemination in time” [DIT],  
described as the occurrence of distinct episodes separated in time.  
[87] Dr. Green explained that DIT and DIS continue to be crucial characteristic features of  
MS.  
[88] Dr. Selchen also explained that a diagnosis of MS can be made only after demonstration  
of both DIT and DIS.  
[89] Under the Poser criteria, a diagnosis of MS (also referred to as “clinically definite MS” or  
CDMS) required evidence of multiple CNS lesions. This could be demonstrated by neurological  
examination (referred to as clinical signs of neurological dysfunction) or by tests and procedures  
that demonstrate the existence of a lesion without the patient having reported or observed a  
clinical sign (referred to as paraclinical signs of neurological dysfunction, e.g., relying on MRI).  
Patients had to have evidence that there was more than one lesion separated in space (i.e., DIS)  
and evidence of more than one prior episode or relapse (i.e., DIT).  
Page: 26  
[90] Under the Poser criteria, a diagnosis of CDMS required:  
Two attacks and clinical evidence of two separate lesions; or  
Two attacks and clinical evidence of one lesion and paraclinical evidence (i.e., MRI) of  
another, separate lesion.  
[91] In simpler terms, the diagnosis in accordance with the Poser criteria (and in accordance  
with the McDonald criteria) requires that the disease is demonstrated to affect different parts of  
the CNS and at different times.  
[92] Dr. Green explained that the Poser criteria initially established that, to make out a  
diagnosis of CDMS, it was necessary to demonstrate that the disease involved more than one  
pathway (DIS) and was not “monophasic” (i.e., a single phase) (DIT). This depended on clinical  
evaluation and typically required that a patient have two identified attacks (i.e., relapses) of more  
than 24 hours duration separated by more than a one-month interval together with clinical  
evidence of lesions in at least two different places within the CNS.  
[93] Dr. Morrow explained that according to the Poser criteria, a patient that has only  
experienced one attack and had clinical or paraclinical signs of at least one CNS lesion was  
referred to as having CIS.  
[94] Dr. Morrow stated that the majority of CIS patients progress to being diagnosed with  
CDMS. Dr. Green agreed. Dr. Selchen also agreed but noted that some patients would need to be  
followed for a longer period of time.  
Page: 27  
[95] Dr. Selchen explained that CIS has been called a “clinical event suggestive of MS”  
because in many patients it precedes a diagnosis of MS.  
D.  
Use of MRI  
[96] By the early 2000s, MRI was increasingly relied on in the MS clinical setting.  
Dr. Morrow explained that MRI is a highly sensitive technique for detection of tissue changes in  
patients with MS. MRI is used as a paraclinical measure for the diagnosis of MS and to monitor  
both disease activity and progression in patients.  
[97] The experts explained how MRI of the brain to identify lesions that are characteristic of  
MS depicts the disease and its progression and can guide the management of the disease. The  
two main types of images are “T1-weighted” and “T2-weighted” images.  
[98] Dr. Vosoughi and the other experts noted that inflammation in the brain can be observed  
with the injection of Gadolinium (referred to as Gd or GAD). This was described as an imaging  
technique in which the patient is given an “enhancing agent”, like a dye, to increase the contrast  
between healthy and damaged tissues. Dr. Morrow and Dr. Green similarly explained the  
visualization using MRI T1-weighted images and T2-weighted images and the use of Gd on  
post-contrast images.  
[99] Dr. Vosoughi explained that in patients with MS, T1 lesions tend to increase in number  
and volume over time. In addition, when the immune system attacks the brain (or spinal cord) in  
 
Page: 28  
MS patients, new T2 lesions appear. Over time, the number of T2 lesions and their volume  
increases. In addition to diagnosis and progression of the disease, the measurement of the  
number and volume of T1 and T2 lesions is used in clinical trials to monitor the effects of what  
is being tried.  
E.  
The McDonald Criteria  
[100] In 2001, the International Panel on MS Diagnosis published a report proposing revised  
diagnostic criteria for MS, known as the “McDonald criteria”. The McDonald criteria permitted  
the diagnosis of “monosymptomatic” disease (i.e., one attack) suggestive of MS, which was not  
previously treated as MS, but would have been diagnosed under the Poser criteria as CIS (i.e.,  
patients who had only one confirmed attack). The McDonald criteria also relied on the concepts  
of DIS and DIT and highlighted the use of MRI along with other diagnostic methods.  
[101] Dr. Green noted that the McDonald criteria were developed in response to the need for  
earlier diagnosis of MS and the increasing use of MRI. Dr. Selchen explained that the McDonald  
criteria responded to the need to diagnose with specificity and sensitivity; in other words, to  
identify for treatment those patients that had MS and to exclude from treatment those that did not  
have MS. MRI provided a means to document DIS and to standardize how to document DIT.  
[102] The experts agreed that, by November 2007, it was routine to use MRI findings to  
confirm a diagnosis of MS.  
 
Page: 29  
[103] In accordance with the McDonald criteria, a patient could be diagnosed with MS after a  
single attack where MRI results could be relied upon to show objective evidence of DIT and DIS  
(i.e., even if there is no clinical evidence of a second attack or no reporting of a second attack by  
the patient).  
[104] An excerpt from the abstract from McDonald 2001 states:  
The revised criteria facilitate the diagnosis of MS in patients with a  
variety of presentations, including “monosymptomatic” disease  
suggestive of MS, disease with a typical relapsing-remitting  
course, and disease with insidious progression, without clear  
attacks and remissions. Previously used terms such as “clinically  
definite” and “probable MS” are no longer recommended. The  
outcome of a diagnostic evaluation is either MS, “possible MS”  
(for those at risk for MS, but for whom diagnostic evaluation is  
equivocal), or “not MS.”  
[105] The McDonald criteria permitted a diagnosis of MS based on one clinical attack as long  
as additional evidence was available. Two scenarios were described:  
1. One attack with objective evidence of two or more lesions, which required:  
dissemination in time demonstrated by MRI or  
a second clinical attack  
2. One attack with objective clinical evidence of one lesion (monosymptomatic or  
CIS), which required:  
dissemination in space demonstrated by MRI, or  
two or more MRI detected lesions consistent with MS plus positive  
cerebral spinal fluid, and  
Page: 30  
dissemination in time demonstrated by MRI.  
[106] The experts agreed that the McDonald criteria result in a diagnosis of either “MS”,  
“possible MS” (where the diagnostic evaluation is equivocal) or “not MS”.  
[107] All the experts noted how the criteria for diagnosis have evolved and agreed that the  
McDonald criteria gained general acceptance. The experts agreed that the term CDMS has given  
way to simply MS. Dr. Morrow explained, however, that the McDonald criteria did not  
immediately replace the Poser criteria and that practicing neurologists remain familiar with the  
terms CDMS and CIS. All the experts noted that the POSITA would still be familiar with the  
terms under the Poser criteria and the McDonald criteria.  
[108] The McDonald criteria were refined in 2005, 2010 and 2017.  
[109] Dr. Green explained that under the McDonald criteria (Polman et al, “Diagnostic criteria  
for multiple sclerosis: 2005 Revisions to the “McDonald Criteria”, 2005 Ann Neurol 58: 840-  
846), in addition to characteristic symptoms and signs on neurological examination, patients  
could be diagnosed based on characteristic findings on MRI of the brain and spinal cord. For  
example, where a patient presented with a history of two episodes or attacks characteristic of MS  
but only one lesion was confirmed by objective clinical evidence, the McDonald criteria  
permitted MRI findings to be relied upon to establish that the disease had affected more than one  
area of the CNS and to support a diagnosis of MS. Alternatively, where neurological  
examination revealed objective clinical evidence of two or more lesions in the CNS, but the  
Page: 31  
patient history suggested only one attack, the McDonald criteria permitted MRI findings to be  
relied upon to establish that the disease was sufficiently disseminated in time to make a diagnosis  
of MS.  
[110] The experts noted that with the introduction of the 2005 McDonald criteria, relatively  
more CIS patients were diagnosed as having MS (typically RRMS) on the sole basis of  
appearance of new MRI lesions, regardless of whether new clinical symptoms developed or  
whether the lesions were “clinically silent”.  
F.  
The Difference between the Poser and McDonald Criteria vis-à-vis a CIS patient  
[111] A point of contention in this Action is whether the claims of the ‘437 Patent are directed  
to a single attack (or CIS) patient, i.e., a patient who has had a single attack without more, or are  
also directed to a single attack patient who meets the McDonald criteria for a diagnosis of MS,  
but has not yet had a second clinical attack. Teva submits that the claims are clearly directed to  
administering glatiramer acetate to a CIS patient who has not yet had a second clinical attack  
and, as a result, has not been diagnosed with CDMS. Teva submits that the claims are not  
directed at patients who have been or could be diagnosed with MS pursuant to the McDonald  
criteria.  
[112] Pharmascience argues that the McDonald criteria were the applicable diagnostic criteria  
in 2007 and that some single attack (or CIS) patients that are diagnosed pursuant to the  
 
Page: 32  
McDonald criteria with MS and who have not yet had a second attack would also fall within the  
claims of the ‘437 Patent.  
[113] This issue is addressed below in the context of the construction of the claims.  
V.  
Overall Position of the Plaintiff Teva on the ‘437 Patent  
[114] Teva notes that its glatiramer acetate product, Copaxone, is a therapy effective for the  
treatment of patients in the relapsing-remitting phase of MS (i.e., RRMS) to reduce the  
frequency of clinical relapses.  
[115] Teva explains that after the initial approval of Copaxone in the 1990s, it spent over 10  
years engaged in research and development to improve its product. Teva notes that it had failures  
but also successes, notably the invention of the ‘437 and ‘802 Patents.  
[116] Teva submits that Pharmascience seeks to benefit from Teva’s hard work, investment and  
inventiveness.  
[117] Teva disputes Pharmascience’s allegation or suggestion that it is seeking to extend the  
life of its patents, referred to as “evergreening”. Teva acknowledges that its 20 mg Copaxone  
product has been available for many years. The 40 mg Copaxone product was approved for sale  
in Canada in 2016. Teva also acknowledges that Pharmascience already obtained a NOC to  
market its 20 mg glatiramer acetate, Glatect.  
 
Page: 33  
[118] Teva explains that it designed and conducted a Phase III clinical trial in the early 2000s  
(the PreCISe trial) to study the effect of glatiramer acetate in patients who had experienced a  
single attack suggestive of MS and prior to development of CDMS.  
[119] Teva characterizes patients who have experienced a single attack suggestive of MS, but  
who have not yet been diagnosed with MS, as CIS patients.  
[120] Teva filed and obtained the ‘437 Patent based on the results of the PreCISe trial. Teva  
received regulatory approval for the new indication of CIS in its Product Monograph in 2009.  
[121] Teva submits that the claims of the ‘437 Patent are directed to the use of glatiramer  
acetate to treat CIS patients, including a claim specifying a reduction of at least 50% in new T2  
lesions.  
[122] Teva submits that Copaxone and Glatect will be used in the same manner if approved in  
accordance with Pharmascience’s SNDS and draft combined Product Monograph. Teva also  
submits that Glatect 40 mg would be marketed in accordance with a Product Monograph that is  
substantially identical to Teva’s Copaxone Product Monograph.  
[123] Teva notes that Pharmascience has not provided any evidence to establish  
non-infringement.  
Page: 34  
[124] Teva submits that Pharmascience cannot rely on the Gillette defence to infringement.  
Teva submits that Pharmascience is splitting its case and has taken Teva by surprise by seeking  
to introduce new evidence in Dr. Green’s responding report to the report of Dr. Morrow, Teva’s  
infringement expert. Teva further submits that the law and the facts do not support the Gillette  
defence.  
[125] Teva disputes that the ‘437 Patent is anticipated by the art cited by Pharmascience,  
Karussis 2006, discussed more fully below.  
[126] Teva also disputes that the ‘437 Patent is obvious. Teva submits that there are material  
differences between the state of the art in 2007 which, among other things, did not establish  
with any evidence that glatiramer acetate would be effective for CIS patients and the subject  
matter of the claims. Teva argues that arriving at the invention required inventiveness.  
[127] More generally, Teva alleges that the evidence of Pharmascience’s expert on validity,  
Dr. Green, was inconsistent and should be approached with caution. Teva goes further in  
challenging Dr. Green’s evidence suggesting that Dr. Green went beyond the role of an expert  
witness and strayed into an advocate for Pharmascience’s position.  
VI.  
Overall Position of the Defendant Pharmascience on the ‘437 Patent  
[128] Pharmascience notes that Teva’s Copaxone products have benefited from a 20-year  
monopoly in the Canadian market.  
 
Page: 35  
[129] Pharmascience submits that Teva has attempted to extend its monopoly and “evergreen”  
its invention of glatiramer acetate (Copaxone) through successive patents, which purport to add  
old uninventive features.  
[130] Pharmascience argues that its manufacture, marketing, sale and the overall use of its  
Glatect products will not infringe the ‘437 Patent.  
[131] Pharmascience raises the Gillette defence against Teva’s allegations of infringement of  
the ‘437 Patent. Pharmascience submits that it is merely practising the teachings of the prior art  
which recognized that glatiramer acetate was effective for RRMS and, as a result, Teva’s patent  
is invalid. Alternatively, if Teva’s patent is valid it cannot be infringed by Pharmascience.  
[132] Pharmascience also argues that the ‘437 Patent is invalid due to anticipation and  
obviousness.  
[133] Pharmascience submits that, as drafted, the claims of the ‘437 Patent would encompass  
patients diagnosed pursuant to the modern and prevailing McDonald criteria. More specifically,  
patients who have had a single attack but have not yet had a second clinical attack would be  
included where they meet the criteria for MS pursuant to the McDonald criteria.  
[134] Pharmascience notes that, by November 2007, glatiramer acetate was a first-line  
treatment for patients with RRMS, which would include patients who had experienced a single  
attack and met the McDonald criteria for MS.  
Page: 36  
[135] Pharmascience also argues that if the claims are interpreted narrowly, as advanced by  
Teva, the claims are still anticipated and are obvious.  
[136] Pharmascience disputes what it characterizes as Teva’s “extreme” position i.e., that  
until a Phase III clinical trial had been completed to demonstrate that early treatment of single  
attack or CIS patients with glatiramer acetate was successful, the use of glatiramer acetate to  
treat such patients remained novel and inventive.  
[137] In support of its position that the ‘437 Patent is anticipated, Pharmascience points to  
Karussis 2006. Pharmascience describes Karussis 2006 as the consensus of an international  
group of 13 MS specialists [the Karussis Working Group] that indicates that glatiramer acetate  
should be used to treat single-attack patients who meet the McDonald criteria and also those who  
fall short of meeting the McDonald criteria.  
[138] Pharmascience submits that Karussis 2006 indicated that glatiramer acetate “should  
work” in the treatment of single-attack patients (including those who fell short of the McDonald  
criteria for MS) and that it would be reasonable to use it to treat such patients.  
[139] With respect to anticipation, Pharmascience submits that Karussis 2006 meets the  
requirements of disclosure and enablement.  
[140] Pharmascience further submits that claim 16 of the ‘437 Patent is anticipated by Pinchasi  
2007 as it disclosed the use of 40 mg glatiramer acetate for the treatment of RRMS.  
Page: 37  
[141] Pharmascience also argues that there are no differences between the state of the art in  
November 2007, which includes Karussis 2006, and the claims of the ‘437 Patent. As a result,  
the ‘437 Patent was obvious. Pharmascience submits that, to the extent that there were any  
differences, these would easily be bridged by the POSITA using the common general knowledge  
and information found by conducting a reasonably diligent search.  
[142] Pharmascience challenges Teva’s reliance on the Regulations to obtain declarations of  
patent infringement in respect of both of Pharmascience’s products – Glatect 20 mg administered  
daily and Glatect 40 mg administered three times per week given that Pharmascience obtained  
a NOC for Glatect 20 mg in 2017 and has been marketing it since that time.  
VII. Overall Position of the Plaintiff Teva on the ‘802 Patent  
[143] Teva reiterates that it worked over the years to improve its products, including to develop  
an oral formulation, which proved unsuccessful in a Phase III clinical trial (CORAL), and to  
develop a 40 mg daily dose of glatiramer acetate, which did not prove to be more effective than  
the 20 mg dose in the Phase III clinical trial (FORTE).  
[144] Teva notes that the ‘802 Patent was the result of a successful Phase III clinical trial  
(GALA) that showed that 40 mg glatiramer acetate administered three times weekly was  
effective for the treatment of RRMS.  
 
Page: 38  
[145] Teva argues that Pharmascience’s Glatect product will infringe the ‘802 Patent as  
Pharmascience’s product will be used in exactly the same manner as Copaxone 40 mg if it is  
approved in accordance with Pharmascience’s SNDS and proposed draft Product Monograph.  
Teva notes that Pharmascience has not provided any evidence that it will not infringe, rather it  
alleges only that the ‘802 Patent is invalid.  
[146] Teva disputes that the ‘802 Patent is invalid due to obviousness or lack of sound  
prediction of utility.  
[147] Teva submits that Pharmascience has adopted a hindsight approach to obviousness and  
has “cherry-picked” the prior art, some of which is obscure, to carve a path to show that the state  
of the art was such that an every other day dose of 40 mg glatiramer acetate was known and that  
it would be self-evident to simply change the administration to three times a week.  
[148] Teva submits that the evidence of its experts should be preferred as it was more balanced.  
Teva submits that without knowledge of the invention as claimed it would not have been obvious  
to a POSITA to administer 40 mg glatiramer acetate three times per week to RRMS patients.  
[149] Teva notes that Pharmascience has led no evidence to support its argument that the ‘802  
Patent lacks utility. Teva notes that all that is required is a scintilla of utility and there is no doubt  
that Copaxone 40 mg is useful.  
Page: 39  
[150] With respect to the allegations regarding lack of sound prediction of utility, Teva notes,  
among other things, that the ‘802 Patent includes a detailed description of the GALA study, a  
Phase III clinical trial, including efficacy and safety results of 40 mg glatiramer acetate three  
times per week, and includes at least 18 references to support the invention.  
VIII.  
Overall Position of the Defendant Pharmascience on the ‘802 Patent  
[151] Pharmascience submits that the ‘802 Patent is invalid due to obviousness. Alternatively,  
it is invalid due to inutility or lack of sound prediction of utility.  
[152] Pharmascience submits that Teva had already publicly disclosed an every-other-day  
dosing regimen for 40 mg glatiramer acetate. Pharmascience relies on a mosaic of the prior art to  
argue that the state of the art was that 40 mg glatiramer acetate was known to be effective (as  
was 20 mg) on an alternate day basis. Pharmascience submits that the difference between the  
state of the art and the claims of the ‘802 Patent is only the difference of one less 40 mg dose in a  
two-week period. Pharmascience argues that it is easier for a patient to remember to take their  
medication three times a week on fixed days rather than every other day. Pharmascience argues  
that the difference between the state of the art and the claims would be easily bridged by the  
POSITA who would move to the fixed day regime.  
[153] Pharmascience also suggests that the Court’s determination of the validity of the ‘802  
Patent should be informed by related proceedings. Pharmascience notes that the ‘802 Patent is  
 
Page: 40  
being examined by the Canadian Intellectual Property Office [CIPO], and that equivalent patents  
have been found to be obvious in the U.K. and U.S.  
[154] Pharmascience argues that if the ‘802 Patent is not obvious due to the state of the prior  
art, then Teva cannot resort to the prior art that it discounts or rejects to support the utility or  
sound prediction of utility of the ‘802 Patent.  
[155] Pharmascience argues that the evidence of its experts should be preferred. Pharmascience  
submits that Teva’s experts were misinstructed regarding the test for obviousness and, more  
generally, are not of the same caliber as its expert Dr. Green who, among other expertise, is  
experienced in clinical trial design.  
IX.  
Onus and Burden of Proof  
[156] The burden is on the Defendant, Pharmascience, to prove each ground of invalidity on a  
balance of probabilities. The burden is on the Plaintiff, Teva, to prove infringement on a balance  
of probabilities. Where the validity of a patent is at issue, the starting point is that the patent is  
presumed to be valid.  
X.  
The ‘437 Patent – Description and Disclosure  
[157] The ‘437 Patent is titled, “Method of Delaying the Onset of Clinically Definite Multiple  
Sclerosis”.  
   
Page: 41  
[158] The ‘437 Patent acknowledges that it cites various publications and that these  
publications are incorporated by reference into the patent application “to more fully describe the  
state of the art to which this invention pertains”. These references include: the Poser criteria;  
Brex PA et al, “A longitudinal study of abnormalities on MRI and disability from multiple  
sclerosis”, 2002 N Engl J Med 346(3): 158-164 [Brex 2002]; Frohman EM et al, “The utility of  
MRI in suspected MS: report of the Therapeutics and Technology Assessment Subcommittee of  
the American Academy of Neurology”, 2003 Neurology 61(5): 602-611 [Frohman 2003];  
Johnson KP et al, “Copolymer 1 reduces relapse rate and improves disability in relapsing-  
remitting multiple sclerosis: results of a phase III multicenter, double-blind, placebo-controlled  
trial. The Copolymer 1 Multiple Sclerosis Study Group”, 1995 Neurology 45: 1268-1276  
[Johnson 1995]; Cohen JA et al., Rovaris, “9006 Study Group. Randomized, double-blind, dose-  
comparison study of glatiramer acetate in relapsing–remitting MS”, Neurology, 2007, 68(12):  
939-944 [Cohen 2007 or FORTE Phase II]; and, Comi G et al, “European/Canadian Multicenter,  
Double-Blind, Randomized, Placebo-Controlled Study of the Effects of Glatiramer Acetate on  
Magnetic Resonance Imaging-Measured Disease Activity and Burden in Patients with Relapsing  
Multiple Sclerosis”, 2001 Ann Neurol 49: 290-297 [Comi 2001].  
[159] In the Background of the Invention, the authors state that MS is “one of the more  
common chronic neurological diseases in human adults” and that it is a “chronic, inflammatory  
[CNS] disease characterized pathologically by demyelination” and “classified as an autoimmune  
disease”.  
Page: 42  
[160] The ‘437 Patent states that “MS disease activity can be monitored by cranial scans,  
including [MRI] of the brain, accumulation of disability, as well as rate and severity of relapses”.  
[161] The ‘437 Patent further states that that the diagnosis of CDMS as determined by the  
Poser criteria “requires at least two neurological events suggesting demyelination in the CNS  
separated in time and in location”.  
[162] The ‘437 Patent notes that a CIS is a single monosymptomatic attack suggestive of MS  
such as optic neuritis, brain stem symptoms, and partial myelitis. It states that “[p]atients with  
CIS that experience a second clinical attack are generally considered to have [CDMS]” and that  
“[o]ver 80 percent of patients with a CIS and MRI lesions go on to develop MS, while  
approximately 20 percent have a self-limited process”.  
[163] The ‘437 Patent describes five types of MS: benign, RRMS, secondary progressive MS,  
progressive relapsing MS and primary progressive MS.  
[164] The ‘437 Patent describes glatiramer acetate and notes that it is marketed as Copaxone  
which had been approved as a 20 mg glatiramer acetate injection for patients with RRMS.  
[165] The ‘437 Patent also notes that the synthesis of Copaxone had been disclosed in several  
U.S. patents and that the formulation of 40 mg Copaxone has been disclosed in a U.S. patent.  
Page: 43  
[166] The ‘437 Patent further states that the “efficacy of Copaxone® in reducing the frequency  
of relapses in patients with RRMS is well established” and that both the 20 and 40 mg daily  
subcutaneous dose have been shown to reduce the total number of enhancing lesions in MS  
patients as measured by MRI (citing Cohen 2007).  
[167] The ‘437 Patent notes that it was an open question whether Copaxone would be effective  
in patients suffering from earlier stages of MS and that there was a debate in the medical and  
scientific community as to the benefits of commencing MS therapy at the early stage. It states:  
“[s]pecifically, questions exist regarding whether the benefits of early treatment outweigh the  
inconvenience, cost, potential adverse effects of treatment, and the risk of submitting patients  
that independently of treatment would not experience further events to unnecessary long-term  
therapy”.  
[168] The Summary of the Invention states that the invention “provides a method for delaying  
the onset of [CDMS] in a patient at risk of developing [CDMS], the method comprising  
periodically administering a pharmaceutical composition comprising a therapeutically effective  
amount of glatiramer acetate to the patient, thereby delaying onset of [CDMS] in the patient”.  
[169] The Summary adds, among other things, that the invention also provides a method to  
reduce progression of MRI-monitored disease activity in a patient at risk of developing CDMS, a  
method for reducing the progression of symptoms, and a method of delaying the progression to  
CDMS. The Summary adds that the invention of the medicament of glatiramer acetate is for the  
treatment of a patient who: “experienced a single demyelinating event and an active  
Page: 44  
inflammatory process, which are indicative of the patient being at high risk of developing  
CDMS”; and, who “experienced a first clinical event suggestive of [MS] and is at risk of  
developing [CDMS]”.  
[170] The ‘437 Patent sets out definitions of the terms used therein. These definitions are noted  
in the discussion in Part XV, Construction of the Claims.  
[171] The ‘437 Patent includes five examples to illustrate the invention and to “aid in an  
understanding of the invention” but not to “limit in any way the invention as set forth in the  
claims”. The examples describe a clinical trial to assess the effect of treatment with daily  
subcutaneous injections of 20 mg of glatiramer acetate compared to placebo on the time to  
conversion to CDMS as determined by the Poser criteria. Examples 1, 2 and 5 specifically refer  
to evaluating the effect of glatiramer acetate on patients presenting with CIS.  
[172] The ‘437 Patent states that the results of the examples “show that early, pre-diagnosis i.e.,  
pre-CDMS, [glatiramer acetate] treatment confers long-term benefits on MS symptoms and on  
the progression of disability”.  
[173] The ‘437 Patent further states that the results show that glatiramer acetate “delays the  
development of [CDMS] when administered to patients presenting a single, clinically isolated  
syndrome (CIS) suggestive of MS”.  
Page: 45  
XI.  
The ‘802 Patent – Description and Disclosure  
[174] The 802 Patent is entitled, “Low Frequency Glatiramer Acetate Therapy”.  
[175] The ‘802 Patent acknowledges that “[t]hroughout this application various publications are  
referenced by their full citations. The disclosures of these publications are referenced in this  
application in order to more fully describe the state of the art”.  
[176] In the Background of the Invention, MS is described, as are the various types of MS and  
methods to monitor the disease. Glatiramer acetate is also described.  
[177] The ‘802 Patent explains that patients suffering from RRMS “experience sporadic  
exacerbations or relapses, as well as periods of remission” and that “[l]esions and evidence of  
axonal loss may or may not be visible on MRI for patients with RRMS”.  
[178] The ‘802 Patent notes that glatiramer acetate “is marketed under the tradename  
Copaxone®” and that Copaxone as a 20 mg daily injection “is an approved therapy for patients  
with [RRMS], including patients who have experienced a first clinical episode”.  
[179] The ‘802 Patent also notes that “[t]he 20mg/day subcutaneous (s.c.) dose has been shown  
to reduce the total number of enhancing lesions in MS patients as measured by MRI” and that  
“[s]afety data accumulated for [glatiramer acetate] in clinical trials shows that the drug product is  
safe and well tolerated”.  
 
Page: 46  
[180] The Summary of the Invention describes a “method of alleviating a symptom of [RRMS]  
in a human patient suffering from [RRMS] or a patient who has experienced a first clinical  
episode and is determined to be at high risk of developing [CDMS] comprising administering to  
the human patient three subcutaneous injections of a therapeutically effective dose of glatiramer  
acetate over a period of seven days with at least one day between every subcutaneous injection  
so as to thereby alleviate the symptom of the patient”.  
[181] The ‘802 Patent describes several embodiments including “the therapeutically effective  
dose of glatiramer acetate is 40mg/ml”.  
[182] Under the Detailed Description of the Invention, the ‘802 Patent again describes its goal  
and sets out the several potential embodiments, including several different schedules of three  
injections per week. Other embodiments describe means of alleviating the symptoms of RRMS,  
for example, reducing the level of disability and reducing the number of different types of  
lesions.  
[183] The ‘802 Patent includes the following definitions:  
Immediate post injection reaction (IRPR)” refers to “a reaction  
such as, palpitations, feeling hot, flushing, hot flushes, tachycardia,  
dyspnoea, chest discomfort, chest pain, and non-cardiac chest pain  
that occurs immediately following injection.  
Injection site reaction (ISR)” refers to “a reaction such as  
erythema, hemorrhage, induration, inflammation, mass, pain,  
pruritus, urticaria, and welt that occurs immediately around the site  
of injection.  
Tolerability” relates to “the level of discomfort associated with  
[glatiramer acetate] treatment” and “is associated with the  
frequency and severity of post injection reactions and injection site  
Page: 47  
reactions” and “influences the period that a patient can follow  
[glatiramer acetate] treatment.  
[184] Other definitions include, “clinically isolated syndrome”, “Gd-enhancing lesions”,  
“single clinical attack”, and reference is made to the Poser criteria for a diagnosis of CDMS.  
[185] The ‘802 Patent notes that the example section is set out to aid in understanding of the  
invention but is not intended to “limit in any way the invention as set forth in the claims”.  
[186] Experimental Details are set out over 16 pages.  
[187] The Discussion notes that a “significant drawback to [glatiramer acetate] therapy is the  
requirement of daily injections, which can be inconvenient”. It adds that “in all clinical trials,  
injection-site reactions were seen to be the most frequent adverse reactions and were reported by  
the majority of patients receiving [glatiramer acetate]” (as compared to placebo).  
[188] The ‘802 Patent has 66 claims. The asserted claims are set out in Annex 2. Note that the  
asserted claims all address the use of 40 mg glatiramer acetate for RRMS patients.  
XII. The Structure of this Judgment  
[189] As noted, Teva alleges infringement by Pharmascience of both the ‘437 and the ‘802  
Patents. Pharmascience disputes that it will infringe and alleges that the ‘437 and ‘802 Patents  
are invalid. The principles from the jurisprudence, set out below, apply to the determination of  
 
Page: 48  
the issues with respect to both patents. There is some evidence that applies to both patents,  
including about the treatment of MS. However, other evidence is specific to the patent at issue.  
The allegations regarding the ‘437 Patent are addressed first, followed by the allegations  
regarding the ‘802 Patent.  
XIII. Overview of the Experts’ Evidence re the ‘437 Patent  
A.  
Pharmascience’s Expert, Dr. Green  
[190] Dr. Green described the POSITA as a medical professional (e.g., a neurologist), with  
experience evaluating and diagnosing patients with MS and administering therapeutic agents for  
the treatment of MS, who would also be a member of a drug development team.  
[191] With respect to the common general knowledge as of November 28, 2007, Dr. Green  
stated that the POSITA would be knowledgeable about MS and its characteristics, the  
classification of MS, brain imaging (including the use of MRI), the evolution of diagnostic  
criteria for MS, CIS, MS therapies (including glatiramer acetate) and CIS therapies (including  
ongoing clinical studies of glatiramer acetate) and, more generally, the treatment of MS. Dr.  
Green set out the sources of knowledge, including conferences, journals, online resources such as  
PubMed and EMBASE (a subscription literature database) and the articles found therein. Dr.  
Green referred to several reports of studies, suggesting that these were part of the common  
general knowledge.  
   
Page: 49  
[192] Dr. Green stated that generally, the ‘437 Patent relates to the treatment of patients who do  
not yet have CDMS to delay the onset of CDMS (and the progression of MS-related symptoms).  
He stated that, more particularly, the ‘437 Patent relates to the use of glatiramer acetate, which  
was a known treatment for patients suffering CDMS (in particular RRMS), to treat patients who  
had not yet developed CDMS.  
[193] In his written opinion, Dr. Green noted that while all the claims use slightly different  
language to describe the patient groups, the POSITA would understand that the claimed patient  
population for all claims is a CIS patient at risk of developing CDMS (and who has not yet  
developed CDMS) and who presents with at least one lesion consistent with MS.  
[194] In his written report in response to Dr. Morrow’s report on validity, and in his oral  
evidence, Dr. Green opined that the claims also covered patients with MS in accordance with the  
McDonald criteria.  
[195] Dr. Green stated that the inventive concept of the claims of the ‘437 Patent is the same as  
the subject matter defined by the claims. Other experts agreed.  
[196] In Dr. Green’s opinion, the claims of the ‘437 Patent were anticipated. Dr. Green stated  
that Karussis 2006 both disclosed and enabled the subject matter of all the claims of the ‘437  
Patent.  
Page: 50  
[197] In Dr. Green’s opinion, the subject matter of the claims was also obvious. Dr. Green  
stated that there was no difference between the state of the art in 2007 and the subject matter of  
the claims disclosed in the ‘437 Patent.  
[198] Dr. Green stated that, by November 2007, a large Phase III clinical study using glatiramer  
acetate to treat CIS patients was underway (i.e., the PreCISe trial). He also stated that the  
consensus of leaders in the field was that using glatiramer acetate to treat CIS patients was  
reasonable and “should work”, and that the ongoing clinical study (i.e. the PreCISe trial) was  
likely to show that early treatment at the time of the initial CIS would have enhanced efficacy  
compared to later treatment of RRMS.  
[199] Dr. Green added that, to the extent that there was any difference between the state of the  
art and the inventive concept, it would have been easily bridged by the POSITA using the  
common general knowledge. No inventive ingenuity was required.  
[200] Dr. Green explained that the POSITA was aware of the concept of CIS. He added that  
disease-modifying drugs or therapies [DMDs or DMTs] (e.g., interferons) used to treat MS  
including RRMS had been shown to be effective in treating CIS patients by reducing the  
likelihood of progression to CDMS and/or delaying the progression to CDMS. Dr. Green added  
that the POSITA would be motivated to find new treatments, and glatiramer acetate was the  
obvious choice.  
Page: 51  
[201] Dr. Green provided a second written opinion in response to the report on infringement by  
Teva’s expert, Dr. Morrow. Dr. Green’s second report addresses several mandates.  
[202] Dr. Green indicated that he generally agreed with Dr. Morrow’s opinions regarding the  
scientific and clinical overview of RRMS, description of the POSITA and construction of the  
claims.  
[203] Dr. Green criticised Dr. Morrow’s use of the terms “CDMS” and “probable MS” given  
her acknowledgement that these terms were not used after the McDonald criteria were adopted.  
In Dr. Green’s opinion, the McDonald criteria had replaced the Poser criteria by 2005, at the  
latest. However, Dr. Green agreed that practicing neurologists remain familiar with the terms  
CDMS and CIS.  
[204] Dr. Green acknowledged that in 2007 a CIS diagnosis would have been for patients who  
had a single clinical event suggestive of MS.  
[205] Dr. Green offered a revised opinion regarding the patients addressed by the claims. In his  
responding report he stated that “by June 4, 2009, … at least some patients presenting with a  
single clinical attack and at least one lesion would have been categorized as having MS pursuant  
to the 2005 McDonald Criteria” and would be included within the claims.  
[206] Dr. Green’s evidence on this issue is elaborated on in the discussion on the construction  
of the claims in Part XV.  
Page: 52  
[207] In his second report, Dr. Green referred to Pinchasi 2007 (a patent application). Dr. Green  
stated that, as read and understood shortly before November 28, 2007, Pinchasi 2007 directed  
physicians to use glatiramer acetate to treat patients with RRMS, which would include some  
patients who had only experienced a single clinical attack. On cross-examination, Dr. Green  
agreed that a physician would not read Pinchasi 2007 to guide their prescribing practices in 2007  
or now.  
[208] Dr. Green also provided his opinion on product monographs in general and, more  
specifically, on the Copaxone 2001 and 2006 product monographs.  
[209] Dr. Green stated that, prior to November 2007, he and other physicians prescribed  
Copaxone to treat CIS patients (i.e., patients who had only experienced a single clinical attack  
but did not meet the 2005 McDonald criteria to confirm a diagnosis of MS). He acknowledged  
that this was “off-label” use, meaning uses not approved and not indicated in the product  
monograph.  
[210] Dr. Green was challenged on his inconsistent testimony in proceedings in the U.K. where  
he suggested that off-label use should only be done in the context of a research study.  
B.  
Teva’s Expert, Dr. Morrow  
[211] Dr. Morrow provided an overview of the scientific and clinical history of MS, including  
the criteria for its diagnosis, as it relates to the ‘437 Patent. Dr. Morrow explained that the Poser  
 
Page: 53  
criteria for diagnosing MS, which were introduced in the 1980s, used the term CIS for patients  
who had experienced only a single clinical attack, and CDMS for patients who had experienced  
at least two clinical attacks.  
[212] Dr. Morrow noted that the Poser criteria were gradually replaced by the McDonald  
criteria, which do not use the terms CIS or CDMS, and do not draw a clear distinction based  
solely on the number of clinical attacks to make a diagnosis of MS.  
[213] Dr. Morrow explained how MRI demonstrates DIT and DIS and that the increasing use  
of MRI permits the diagnosis of MS without the demonstration of clinical attacks.  
[214] Dr. Morrow stated that the POSITA would understand that the language in the claims  
refers to terms that were used in relation to the Poser criteria (i.e., CDMS), which required the  
confirmation of a second clinical attack. Dr. Morrow stated that the POSITA would understand  
that the ‘437 Patent is directed to using glatiramer acetate to treat patients who have had one  
clinical attack suggestive of MS but have not yet experienced a second clinical attack.  
[215] With respect to infringement, Dr. Morrow stated that in her opinion, if Pharmascience’s  
Glatect product is made, sold, used or constructed in accordance with the Glatect Product  
Monograph she had reviewed, Glatect 20 mg and 40 mg will be used in the manner set out in the  
asserted claims of the ‘437 Patent. Dr. Morrow noted the specific wording of the 20 mg product  
and 40 mg product and the distinctions between them.  
Page: 54  
C.  
Teva’s Expert, Dr. Selchen  
[216] Dr. Selchen agreed with Dr. Morrow and with Dr. Green’s initial opinion regarding the  
construction of the claims of the ‘437 Patent as focussed on the CIS patient.  
[217] Dr. Selchen stated that in 2007, a patient presenting with the profile described in claim 1  
was typically diagnosed as a patient with CIS. He explained that CIS was treated as distinct from  
CDMS, which required the confirmation of a second clinical attack (and ruling out other possible  
non-MS causes for the first attack).  
[218] Dr. Selchen emphasized that the claims of the ’437 Patent are directed to the CIS patient  
and not to a patient who could be diagnosed pursuant to the 2001 or 2005 McDonald criteria  
with MS, including RRMS.  
[219] Dr. Selchen noted that the claims of the ‘437 Patent sets out various modes of efficacy,  
including: delaying the onset of CDMS; reducing progression of MRI-monitored disease activity  
(including a reduction in the rate of accumulating new T2-weighted lesions, a measure of active  
inflammatory process); reducing the progression of symptoms of MS; and, reducing the  
frequency of relapse.  
[220] Dr. Selchen also agreed that the inventive concept of the claims is the subject matter of  
the claims asserted.  
 
Page: 55  
[221] Dr. Selchen did not fully agree with Dr. Green regarding the extent of the common  
general knowledge, particularly articles from less known journals and those that reported on pilot  
studies or case reports.  
[222] With respect to the allegation of anticipation, Dr. Selchen opined that Karussis 2006  
neither disclosed nor enabled a skilled person to practice the subject matter of the claims at issue.  
[223] Dr. Selchen noted that the Karussis Working Group was tasked with developing  
evidence-based recommendations. Karussis 2006 clearly stated that their proposed  
recommendation for using glatiramer acetate (among other therapies) to treat patients with CIS  
was not evidence-based. Dr. Selchen stated that the suggestion in Karussis 2006 that the  
approved therapies “should” work did not single out glatiramer acetate. He stated that the  
suggestions and opinions would not enable a skilled person to achieve the claimed outcomes of  
the ‘437 Patent.  
[224] Dr. Selchen acknowledged that in November 2007 the POSITA would have known only  
that a clinical study had been commenced (i.e., the PreCISe trial). Dr. Selchen also noted that  
several other clinical trials studying drugs for use in treating MS had failed to meet their  
objectives and the POSITA would not have assumed the successful outcome of the PreCISe trial  
simply because the trial had been started.  
[225] Dr. Selchen stated that, in 2007, the POSITA would not and could not have treated CIS  
patients with glatiramer acetate, noting that it was not approved for this use, it would not have  
Page: 56  
been covered by any drug plan and, more importantly, there was no evidence to support its  
effectiveness.  
[226] Dr. Selchen did not agree with Dr. Green that it would be obvious to the POSITA that  
glatiramer acetate would be useful to treat CIS as claimed in the ‘437 Patent. Dr. Selchen again  
noted that there was no evidence that glatiramer acetate had been used to treat patients with CIS,  
and no evidence of any effect of that treatment, not even from uncontrolled studies or patient  
case reports.  
D.  
Teva’s Expert, Dr. Kreitman  
[227] Dr. Kreitman described the PreCISe trial, which demonstrated that 20 mg daily of  
glatiramer acetate was efficacious in delaying the onset of CDMS in CIS patients. Dr. Kreitman  
confirmed that the PreCISe trial did not test a 40 mg dose of glatiramer acetate.  
[228] Dr. Kreitman also described Teva’ activities leading up to the development of Copaxone  
40 mg three times a week and the ‘802 Patent.  
[229] Dr. Kreitman noted other trials conducted by Teva, including to test a higher  
concentration formulation of glatiramer (i.e., 20 mg/0.5 mL), which were abandoned or not  
successful.  
 
Page: 57  
[230] Dr. Kreitman explained that around 2002 Teva began to explore the development of  
glatiramer acetate 40 mg daily. Teva conducted a Phase III clinical trial, the FORTE trial, which  
compared 40 mg daily to 20 mg daily of glatiramer acetate. The study failed to show that the  
40 mg dose improved efficacy compared to the 20 mg dose.  
XIV. The POSITA for the ‘437 Patent  
A.  
The Principles from the Jurisprudence  
[231] The jurisprudence refers to this mythical person as the person of skill or the skilled  
person or as noted above, the POSITA.  
[232] The POSITA is not one real person, rather a fictitious person or team of persons with an  
amalgamation of different skills. The POSITA provides the lens through which the patent is  
construed, the prior art is considered, and other issues are assessed (Pfizer Canada Inc v  
Pharmascience Inc, 2013 FC 120 at para 28; Teva Canada Limited v Janssen Inc, 2018 FC 754  
at para 66, aff’d 2019 FCA 273).  
[233] In Valeant Canada LP/Valeant Canada SEC v Generic Partners Canada Inc, 2019 FC  
253 at para 44 [Valeant], Justice Fothergill described the POSITA as follows:  
44.  
The PSA is unimaginative and uninventive, but reasonably  
diligent in keeping up with advances (Pfizer Canada Inc v Teva  
Canada Ltd, 2017 FC 777 at para 185). The PSA is not  
incompetent, and brings background knowledge and experience to  
the workbench (AstraZeneca Canada Inc v Apotex Inc, 2015 FC  
322 at para 276). The PSA is not stripped of the ability to pursue  
   
Page: 58  
reasonable and logical enquiries, and can make deductions based  
on the information available (Jay-Lor International Inc v Penta  
Farms Systems Ltd, 2007 FC 358 at para 75 [Jay-Lor], citing Beloit  
Canada Ltd v Valmet Oy (1986), 8 CPR (3d) 289 at 294 (FCA)  
[Beloit]).  
B.  
Who is the POSITA for the ‘437 Patent?  
[234] Teva submits that the POSITA is a neurologist with experience in the diagnosis and  
management of MS.  
[235] Pharmascience submits that the POSITA would include a neurologist with several years  
of experience, including direct experience evaluating and diagnosing patients with MS and  
administering therapeutic agents for the treatment of MS (including familiarity with their dosing  
schedules and frequencies of administration). Pharmascience adds that the POSITA would also  
be part of a drug development team with experience developing clinical studies.  
[236] Dr. Green described the POSITA as a medical professional, particularly a neurologist  
with several years of experience, including direct experience evaluating and diagnosing patients  
with MS and administering therapeutic agents for the treatment of MS. This would include  
familiarity with the dosing schedules and frequencies of the different therapeutic agents available  
for MS treatment, as well as side effects or adverse events that occur with these treatments. Dr.  
Green added that the POSITA would also be part of a drug development team and have  
experience with the design of clinical studies. Dr. Green disagreed with Dr. Morrow that the  
POSITA would also include a biochemist, but agreed that a biochemist could be consulted by the  
POSITA.  
 
Page: 59  
[237] Dr. Selchen agreed that the POSITA would be a medical professional such as a  
neurologist, with at least a few years’ experience evaluating and diagnosing patients with MS  
and administering therapeutic agents for the treatment of MS. Dr. Selchen did not agree with  
Dr. Green that the POSITA or team should include a member of a drug development team, or  
that the POSITA would have experience with the design of studies necessary for drug  
development. Dr. Selchen opined that this would be too specialized.  
[238] The experts all agree on the basic qualifications of the POSITA but disagree on the  
additional special attributes argued by Pharmascience.  
[239] Pharmascience appears to advocate for the POSITA to be part of a drug development  
team and with experience in the design of clinical studies to later argue that the POSITA would  
conduct patent searches and would have the skill to conduct clinical studies to the extent that this  
would be “routine” work.  
[240] In my view, the POSITA – through whose eyes the ‘437 Patent is understood and  
directed is a practicing neurologist with several years of experience evaluating, diagnosing and  
treating patients with MS. This POSITA would be familiar with the therapeutic agents available  
for the treatment of MS (i.e., the DMTs), their dosing schedules and side effects or adverse  
events that occur with the various DMTs. The POSITA would have some knowledge of and  
familiarity with clinical studies and their interpretation but would not be a member of a drug  
development team. The POSITA is also referred to herein as a practicing neurologist.  
Page: 60  
XV.  
A.  
The Construction of the Claims  
The Principles from the Jurisprudence  
[241] Claims construction is for the court to determine guided by expert evidence if needed.  
The construction of the claims precedes consideration of the allegations of invalidity. The claims  
are construed as of the publication date; for the ‘437 Patent it is June 4, 2009 and for the ‘802  
Patent it is February 24, 2011.  
[242] In Biogen Canada Inc v Taro Pharmaceuticals Inc, 2020 FC 621 [Biogen], the Court  
summarized the principles of claim construction at paras 76-78, noting at para 78:  
[78] The principles of claim construction were laid out by the  
Supreme Court of Canada in Whirlpool and Free World  
Trust (Whirlpool at paras 49-55; Free World Trust v Électro Santé  
Inc, 2000 SCC 66 at paras 44-54 [Free World Trust]). Claims are  
to be read in an informed and purposive way, with a mind willing  
to understand and viewed through the eyes of a POSITA having  
regard to the common general knowledge. The entire patent  
specification should be considered in order to ascertain the nature  
of the invention, however adherence to the claim language allows  
the claims to be read in the way in which the inventor is presumed  
to have intended, promoting fairness and predictability.  
[243] In Valeant, the Court reiterated the “canons of claim construction” at para 42:  
[42] The canons of claims construction are found in the  
Supreme Court of Canada’s decisions in Whirlpool at paragraphs  
49 to 55 and Free World Trust v Électro Santé Inc, 2000 SCC 66  
[Free World Trust] at paragraphs 44 to 54. They are the following:  
(a) claims are to be read in an informed and  
purposive way with a mind willing to understand,  
viewed through the eyes of the person skilled in the  
   
Page: 61  
art as of the date of publication having regard to the  
common general knowledge;  
(b) adherence to the language of the claims allows  
them to be read in the manner the inventor is  
presumed to have intended, and in a way that is  
sympathetic to accomplishing the inventor’s  
purpose, which promotes both fairness and  
predictability; and  
I the whole of the specification should be  
considered to ascertain the nature of the invention,  
and the construction of claims must be neither  
benevolent nor harsh, but should instead be  
reasonable and fair to both the patentee and the  
public.  
B.  
The Claims of the ‘437 Patent  
[244] The ‘437 Patent includes definitions of some of the terms used in the patent and in the  
claims.  
[245] The ‘437 Patent defines a “patient at risk of developing MS (i.e. CDMS)” as a patient  
presenting any of the known risk factors for MS. The risk factors noted include a CIS, a single  
attack suggestive of MS without a lesion, the presence of a lesion without a clinical attack, and  
environmental and genetic factors.  
[246] CIS is defined as referring to “a single clinical attack (used interchangeably herein with  
‘first clinical event’ and ‘first demyelinating event’) suggestive of MS, which, for example,  
presents as an episode of optic neuritis, blurring of vision, … loss of balance, tremors…[and  
several other indicators], and “at least one lesion suggestive of MS”.  
 
Page: 62  
[247] The ‘437 Patent states that “the criteria as defined by Poser … used to determine if a  
subject meets the condition consistent with [CDMS] are:  
Two attacks and clinical evidence of two separate lesions or  
Two attacks; clinical evidence of one lesion and paraclinical evidence of another separate  
lesion.”  
[248] An “attack” or “exacerbation, flare, or relapse” are defined clinically as the sudden  
appearance or worsening of a symptom or neurological dysfunction, with or without objective  
confirmation.  
[249] The ‘437 Patent defines both clinical and paraclinical evidence. Clinical evidence of a  
lesion is defined as “signs of neurological dysfunction demonstrable by neurological  
examination” and this includes signs that are no longer present if the sign was recorded by a  
“competent examiner”. Paraclinical evidence of a lesion that has not produced clinical signs and  
may or may not have caused symptoms includes evidence from various tests, including  
neuroimaging.  
[250] There are 50 claims in the ‘437 Patent of which 13 are asserted. As noted, the claims are  
set out in full at Annex 1.  
[251] Claim 1 provides:  
A pharmaceutical composition comprising a pharmaceutically  
acceptable carrier and a therapeutically effective amount of  
Page: 63  
glatiramer acetate for use in delaying the onset of clinically  
definite multiple sclerosis in a patient who experienced a single  
clinical attack suggestive of multiple sclerosis, who presents with  
at least one lesion consistent with multiple sclerosis and who is at  
risk of developing clinically definite multiple sclerosis and prior to  
development of clinically definite multiple sclerosis.  
[252] The claim describes the pharmaceutical composition of glatiramer acetate. Subsequent  
claims make it clear that this is administered as a subcutaneous injection, administered daily in a  
20 mg or 40 mg dose.  
[253] The claims that address the effects of treatment are not in dispute. These are claims 2  
(reducing progression of… (MRI)-monitored disease activity), 3 (reducing the progression of  
symptoms of [MS]), 4 (reducing the frequency of relapse), 19 and 24 (the relapse rate and the  
mean number of new T2 lesions) and 33 (the reduction by at least 50% in the rate of  
accumulating new T2-weighted lesions) and all relate to the patient population described in  
claim 1.  
[254] Claims that describe how glatiramer acetate is administered are also not in dispute:  
claims 13 (use is once-a-day), 14 (use is subcutaneous), 15 (the therapeutically effective amount  
of glatiramer acetate is 20 mg) and 16 (the therapeutically effective amount of glatiramer acetate  
is 40 mg).  
[255] Claims 47 and 50 relate to the use of glatiramer acetate in the manufacture of a  
medicament for the treatment of the patient population set out in claim 1.  
Page: 64  
[256] The experts all construed the claims in a similar way noting the independent and  
dependant claims and grouping them according to their similar features. Although all the experts  
construed claim 1 in the same manner basically, it means what it says. Teva and Pharmascience  
interpret the scope of the patient population described in claim 1 differently, which in turn  
impacts all the claims.  
C.  
The Dispute regarding the Patients Included in the Claims  
(1)  
Pharmascience’s Submissions  
[257] Pharmascience submits that the ‘437 Patent is clear that its invention, defined in terms of  
the Poser criteria, is the delay in onset of CDMS in a patient that has suffered a single clinical  
attack and is at risk of having a second clinical attack (i.e., a CIS patient in accordance with the  
definition of CIS provided in the ‘437 Patent).  
[258] Pharmascience argues that the claims cover two groups of patients who have experienced  
a single clinical attack:  
A patient who does not yet meet the MRI criteria to be diagnosed with MS under the  
2005 McDonald criteria; and  
A patient who does meet the MRI criteria and is diagnosed or can be diagnosed with MS  
under the 2005 McDonald criteria.  
   
Page: 65  
[259] Pharmascience argues that using the words of the claim and the definitions set out in the  
‘437 Patent, the key terms are “single attack” and “prior to the onset of CDMS”, which is  
specifically defined as a second clinical attack. Pharmascience relies on the McDonald criteria  
which would result in a diagnosis of MS, based on MRI evidence demonstrating DIS and DIT of  
lesions, for some patients who experienced only a single clinical attack.  
[260] Pharmascience argues that CDMS as defined is not the same as MS or RRMS.  
Pharmascience submits that a patient could be diagnosed with MS or RRMS pursuant to the  
McDonald criteria after having only one clinical attack and that this “McDonald MS” patient  
falls in the claims of the ‘437 Patent because the patient has not yet had a second clinical attack  
and does not meet the definition of CDMS.  
[261] Pharmascience submits that the experts agreed that, due to the use of the “out of date”  
Poser criteria, the claims cover two groups of single attack patients.  
[262] Pharmascience notes that, although its expert, Dr. Green, described the claimed patient  
population for all claims as being a “CIS patient at risk of developing CDMS (and who has not  
yet developed CDMS) and presenting with at least one lesion consistent with MS”, Dr. Green  
repeatedly advised counsel to Teva on cross-examination that he was simply using the definition  
offered by the patentee, Teva.  
[263] Pharmascience also relies on the evidence of Teva’s expert, Dr. Morrow, who described  
the claims of the ‘437 Patent as relating to “use in patients who meet the diagnostic criteria for  
Page: 66  
CIS, but do not meet the Poser criteria for CDMS . . . in order to delay the onset of CDMS”.  
Pharmascience suggests that Dr. Morrow’s description must be read in light of her opinion on  
infringement where she stated that the indication for Glatect 40 mg includes within its scope  
single-attack patients who meet the McDonald criteria.  
[264] Pharmascience disputes Teva’s proposed narrow construction of the claims.  
Pharmascience argues that Teva is bound by its choice to use the Poser criteria to draft the claims  
of the ‘437 Patent despite that the McDonald criteria were widely accepted and used well before  
2007. Pharmascience argues that Teva cannot seek to rewrite the claims with new definitions.  
Pharmascience adds that if Teva intended to limit the claims it could have drafted the patent  
clearly to do so.  
[265] Pharmascience says that Teva’s narrow construction should be rejected as it relies on a  
construction of the claim language that was rejected by Drs. Green, Selchen and Morrow when  
they were “properly oriented”.  
(2)  
Teva’s Submissions  
[266] Teva submits that claims 1-4 address the treatment of a patient who experienced a single  
clinical attack suggestive of MS, presents with at least one lesion consistent with MS, and is at  
risk of developing CDMS. Teva submits that this is a CIS patient not a patient who has already  
been diagnosed or met the criteria of CDMS. Nor is it a patient who has met the criteria of MS  
pursuant to the application of the McDonald criteria.  
 
Page: 67  
[267] Teva submits that all the experts agree that the claims are directed to the treatment of a  
CIS patient who experienced a single clinical attack suggestive of MS. Teva disputes  
Pharmascience’s interpretation that this includes a CIS patient who meets the McDonald criteria  
for MS but who has not yet experienced a second clinical attack.  
[268] Teva submits that the claims should be construed through the eyes of the POSITA with  
the common general knowledge as of the claim date, June 4, 2009, which included knowledge of  
the criteria for diagnosing MS, pursuant to both the Poser criteria and the McDonald criteria.  
[269] Teva notes that the McDonald criteria do not require two distinct clinical attacks for a  
diagnosis of MS. Teva also notes that the experts agreed that reliance on the McDonald criteria  
led to more CIS patients being diagnosed with MS (typically RRMS) based on the MRI evidence  
of new lesions regardless of whether new clinical symptoms developed. Teva relies on the  
evidence of Dr. Morrow who explained that the Poser terms continue to be used and that CIS is  
understood to be a patient that does not yet meet the diagnostic criteria for MS.  
[270] Teva also notes that Dr. Green stated (in his report on validity) that there are several  
forms of CDMS, including RRMS and that the POSITA would understand that these do not  
include CIS patients.  
[271] Teva also points to Dr. Green’s opinion, which was echoed by Dr. Selchen, “[t]hough the  
claims use slightly different language to describe the patient groups, the skilled person would  
understand that the claimed patient population for all claims is a CIS patient at risk of developing  
Page: 68  
CDMS (and who has not yet developed CDMS) and presenting with at least one lesion consistent  
with MS.”  
[272] Teva notes that Dr. Selchen clearly explained that “a CIS patient by definition is different  
than a McDonald patient” and that a single attack patient who meets the McDonald criteria does  
not fall within the claims.  
[273] Teva notes that Dr. Green revised his opinion in response to Dr. Morrow’s infringement  
report but could not explain why he did not state this opinion in his validity report.  
[274] Teva submits that Dr. Green’s revised opinion is inconsistent with his description of the  
common general knowledge as reflecting that the patient population was “CIS patients at high  
risk for developing MS”. Teva also notes that the papers cited by Dr. Green, including Comi  
2001 and Kappos L et al, “Treatment with interferon beta-1b delays conversion to clinically  
definite and McDonald MS in patients with clinically isolated syndromes” 2006 Neurology 67:  
1242-1249 [Kappos 2006], distinguish CIS patients from patients diagnosed with MS under the  
McDonald criteria. For example, Dr. Green cited Kappos 2006 which reported on the use of an  
interferon (i.e., Betaseron® [Betaseron]) in CIS patients (at the time of the initial attack) to  
prevent future relapses.  
Page: 69  
D.  
What do the Experts Say regarding the Patients Included in the Claims?  
(1)  
Dr. Green  
[275] Dr. Green explained that by 2001, pursuant to the McDonald criteria, there was no longer  
the requirement for two attacks to confirm the diagnosis and the term CDMS was no longer  
used rather the term MS was used. A patient could have one attack yet meet the other  
McDonald criteria for a diagnosis of MS. If the “one attack” patient did not meet that criteria,  
they were considered to be a CIS patient.  
[276] Dr. Green acknowledged that in 2007 a CIS diagnosis would have been for patients who  
had a single clinical event suggestive of MS.  
[277] He explained that MRI scans of CIS patients did not meet the McDonald criteria, at para  
104 of his report:  
MRI scans of such CIS patients, while consistent with MS, did not  
fulfill the McDonald criteria to enable a confirmed diagnosis of  
MS. CIS was defined somewhat differently depending on the  
setting but was generally used to apply to patients who had a single  
episode of clinical neurological worsening that was suspicious for  
demyelination (i.e., subacute onset of neurological dysfunction,  
especially in a young or middle-aged person) with MRI evidence  
of other lesions (at least 1 or 2 depending on the investigator). Dr.  
Green acknowledged that in 2007 a CIS diagnosis would have  
been for patients who had a single clinical event suggestive of MS.  
[278] In his validity report, Dr. Green explained that the Summary of the Invention set out in  
the ‘437 Patent would be understood by the POSITA as the use of glatiramer acetate to treat CIS  
   
Page: 70  
patients and to produce various results, such as delaying the onset of CDMS, delaying  
progression to CDMS, reducing the progression of MRI-monitored disease activity, reducing the  
progression of MS symptoms, and reducing the frequency of relapses, among others.  
[279] In his second report, which was for the purpose of responding to Dr. Morrow’s report on  
infringement, Dr. Green stated that he generally agreed with Dr. Morrow’s interpretation of the  
claims. Dr. Green then added “by June 2009 (and earlier), which is the date that I was instructed  
to interpret the claims from the perspective of the skilled person, at least some patients  
presenting with a single attack and at least one lesion would have been categorized as having MS  
pursuant to the McDonald criteria”.  
[280] Dr. Green reiterated this view in his oral testimony, to indicate that the POSITA would  
understand that the claims include a McDonald MS patient, despite the definition of CIS  
included in the ‘437 Patent.  
[281] On cross-examination, Dr. Green was directed to para 269 of his validity opinion, where  
he summarized the claims and stated that the “skilled person would understand that the claimed  
patient population for all claims is a CIS patient at risk of developing CDMS and presenting with  
at least one lesion consistent with MS”.  
[282] Dr. Green acknowledged that he did not explicitly state that his reference to a CIS patient  
means CIS patients plus “McDonald MS” patients because he had explained this in his opinion  
on claims construction and he was working from the definitions in the patent. Dr. Green added