`
`
`UNITED STATES PATENT AND TRADEMARK OFFICE
`————————————————
`
`BEFORE THE PATENT TRIAL AND APPEAL BOARD
`————————————————
`
`MYLAN PHARMACEUTICALS INC. and
`AMNEAL PHARMACEUTICALS LLC
`
`Petitioners,
`
`v.
`
`YEDA RESEARCH & DEVELOPMENT CO. LTD.
`
`Patent Owner.
`
`————————————————
`
`Case No. IPR2015-00643 (8,232,250 B2)
`Case No. IPR2015-00644 (8,399,413 B2)
` Case No. IPR2015-00830 (8,969,302 B2)1,2
`————————————————
`
`PETITIONERS’ RESPONSE TO PATENT OWNER’S
`OBSERVATIONS ON REPLY
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`
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`1 Case Nos. IPR2015-01976, IPR2015-01980 and IPR2015-01981 have been
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`joined with these proceedings.
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`2 A word-for-word identical Response is being filed in each proceeding.
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`
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`TABLE OF ABBREVIATIONS
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`CNS ...................................................................................... Central Nervous System
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`FDA ............................................................................ Food and Drug Administration
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`GA ................................................................................................. Glatiramer Acetate
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`ISR ........................................................................................... Injection Site Reaction
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`MBP .......................................................................................... Myelin Basic Protein
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`MOA ......................................................................................... Mechanism of Action
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`OOCE .................................................................. Observation on Cross Examination
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`PK ................................................................................................. Pharmacodynamics
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`POSA .................................................................... Person of Ordinary Skill in the Art
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`SBOA ...........................................................Summary Basis of Approval (Ex. 1007)
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`SEC ................................................................. Securities and Exchange Commission
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`TIW ................................................................................... Three Injections Per Week
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`Yeda .................................... Patent Owner Yeda Research & Development Co. Ltd.
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`
`
`
`
`i
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`
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`Petitioners hereby file their response to Patent Owner’s Observations on
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`Cross Examination (“OOCE”). IPR2105-00643, Paper 71.
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`Response 1-6, 23-24, 26, 31-32, 35: Yeda’s OOCEs misstate the record. These
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`OOCEs are not the “testimony” of Dr. Hay or Dr. Green as asserted by Yeda.
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`Rather, Yeda has repackaged its attorney’s reading of selected passages of
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`documents into the record as the experts’ “testimony.” The question and answer
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`underlying OOCE 35 is illustrative of Yeda’s approach:
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`Q. Okay. And then the second paragraph under that section states,
`“Copaxone revenues in the United States in 2015 increased four
`percent to $3.2 billion.” Do you see that?
`A. Yes.
`Q. And then I want to direct your attention about -- to the last
`paragraph on the page, which states: “Copaxone accounted for 20
`percent of our revenues in 2015 and is significantly higher percentage
`contribution to our profits and cash flow from operations during such
`period.” Do you see that?
`A. Yeah. And that’s exactly the kind of misleading statement that I
`would never be able to rely on to look at the profits or the returns on
`investment associated with Copaxone.
`
`Ex. 1141 at 98:6-25. Yeda states that Dr. Hay testified that “Copaxone revenues in
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`the United States in 2015 increased four percent to $3.2 billion” and “Copaxone
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`accounted for 20 percent of our revenues in 2015 and is [a] significantly higher
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`percentage contribution to our profits and cash flow from operations during such
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`1
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`
`
`
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`period.” Yeda repeated this approach throughout both depositions.3 In view of
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`Yeda’s improper use of these observations, OOCEs 1-6, 23-24, 26, 31-32, 35
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`should be struck.
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`Response 1: Yeda concludes that “testimony” attributed to Dr. Green “contradicts”
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`Dr. Green’s assertion that a POSA would not rely on Yeda’s MOA theory that an
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`increase in Th2 cells counteracted inflammation in the CNS to account for GA’s
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`therapeutic effect. But the cited testimony omits Dr. Green’s testimony that “I
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`think that should be qualified.” Ex. 1142 at 224:2-3. In fact, even the question
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`posed to Dr. Green demonstrates his express qualification:
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`And with the caveat that you stated earlier, that we still don't know
`today exactly all of the details of the mechanism of action of GA in
`2009, this increase in Th2 cells theory was one of the leading theories
`of how glatiramer acetate worked in patients; right?
`
`Id. at 223:20-25 (emphasis added). Yeda also failed to cite to Dr. Green’s
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`qualification immediately following the quoted passage: “So I don’t think people
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`thought in 2009, or around that time, that this was exclusively the mechanism of
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`3 After a series of such questions, Dr. Green pointed out in his deposition (Ex. 1142
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`at 285:21-286:1):
`
`I’m not sure if the exercise here is for you to read parts of papers and
`ask me if you’ve read them correctly. I thought it was to ask me
`questions about how these influenced my opinion and ask questions
`about my opinion. So I think it’s important to provide that context.
`
`2
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`
`
`
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`action.” Id. at 224:6-8. Further, Dr. Green testified that Yeda’s proposed MOA
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`theory was “not the only and perhaps even not the major mechanism of action by
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`which the drug worked.” Id. at 226:9-11. Moreover, the testimony cited by Yeda in
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`no way “contradicts” Dr. Green’s opinion that a POSA would rely on demonstrated
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`clinical evidence over a hypothetical MOA theory. Dr. Green testified that a POSA
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`would first look to the clinical literature, “which was overwhelming.” Id. at
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`273:21-24 (testifying that POSA would not have “necessarily even gone to Hickey
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`in the first place . . . . They would have gone to the existing clinical data, which
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`was overwhelming”); see also id. at 295:7-10 (“So that’s why the POSA relies on
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`clinical information and doesn’t rely on tenuous arguments about animal
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`experiments that I certainly did not bring into the proceedings.”). Dr. Green’s
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`testimony is entirely consistent with the opinions set forth in his reply evidence
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`(Ex. 1085 ¶¶ 43-45, 49-71).
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`Response 2-4: Yeda’s conclusion that the quoted “testimony” is “relevant” for the
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`“same reasons identified above in ¶ 1” is incorrect and not supported by the cited
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`testimony. For example, the quoted testimony in OOCE 2 is of Yeda’s attorney
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`reading into the record a sentence from an article. Ex. 1142 at 225:8-15. Dr. Green
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`was then asked, “Do you see that?” and “Did I read that correctly, other than with
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`that one correction?” Dr. Green answered, “Yes.” Id. at 225:16-23. This is not
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`“testimony” that can be attributed to Dr. Green. Yeda also omits Dr. Green’s
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`3
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`
`
`
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`substantive response at Ex. 1142 at 226:3-16. Yeda used the same uninformative
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`technique in Observations 3-4 as in Observation 1.4
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`Response 5: Yeda’s contention that Dr. Green’s “testimony” regarding T cells
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`contradicts his opinion that “a POSA would believe GA-specific T-cells would
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`persist for beyond three days by equating cross recognition of MBP with MBP
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`specificity” mischaracterizes the record and is not supported by the cited
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`testimony. The quoted testimony is of Yeda’s attorney reading into the record a
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`sentence from an article and asking, “And the next sentence says . . . right?”; Dr.
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`Green answered, “Yes.” Ex. 1142 at 280:7-11. No follow-up question was asked
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`and Dr. Green’s opinion was not solicited. There is no evidence of record that the
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`POSA would find a distinction between proliferation and cytokine secretion to be
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`relevant when comparing GA-specific T cells with MBP-specific T cells; and Dr.
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`Green did not testify to one. Dr. Green’s testimony in fact refuted a POSA would
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`draw such a distinction: “At a theoretical level, yes. Is that what a person who’s
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`skilled in the art would look at when they looked at this reference [Hickey] in
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`thinking about the kinetics of GA-reactive lymphocytes? No.” Id. at 253:15-19.
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`Moreover, Yeda’s reliance on the quoted sentence from Neuhaus is taken out of
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`context. Neuhaus states: “Some of the GA-reactive cells cross-react with MBP or
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`MOG and are therefore stimulated to release anti-inflammatory cytokines . . . and
`
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`4 Petitioner incorporates its Response to OOCE 1 herein.
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`4
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`
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`
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`even neurotrophic factors.” Ex. 2065 at 5 (Fig. at 3). Dr. Green’s testimony that
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`GA-specific T cells persist in the CNS for days is supported by Aharoni 2000 (Ex.
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`2044) and 2003 (Ex. 1084), and Dr. Ziemssen (Ex. 2009), as is stated in Dr.
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`Green’s reply declaration. See Ex. 1085 ¶¶ 57-62 (citing, e.g., Ex. 2044 at Abstract,
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`4; Ex. 1084 at Abstract, 5; Ex. 2009 at 4 (“[s]o it can be concluded that activated
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`TH2 cells are able to cross the bloodbrain barrier [], accumulate in the CNS and
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`express in situ anti-inflammatory cytokines”)); Ex. 1085 ¶¶ 52-58 (emphasizing
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`that if a POSA were to rely on Hickey, which does not discuss GA-specific Th2
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`cells, the POSA would look to the more relevant activated MBP-specific T cells
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`that bind to an antigen in the CNS rather than the other activated T cells that do not
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`bind to antigens in the CNS because GA-specific Th2 cells were known to bind
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`antigens in the CNS). Fourth, Yeda failed to account for Dr. Green’s testimony
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`refuting the OOCE’s conclusion (Ex. 1142 at 259:16-260:7; 253:2-8):
`
`[A] person of ordinary skill in the art would look at this and recognize
`that although these were T-cells that have a high affinity for the
`antigen MBP, the whole concept of cross-reactivity and the whole
`concept of bystander suppression would be dependent on the notion
`that there was the potential to interact with other antigens that either
`looked similar or maybe even were identical that came up from--in
`response to GA.
`
`* * *
`There’s no--you can’t make an argument that there’s bystander
`suppression unless you give the capacity for those lymphocytes to
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`5
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`
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`
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`encounter or be restimulated once they’ve crossed the CNS by an
`antigen.5
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`Response 6: Dr. Green objected to answering a question premised on “any
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`evidence” in the field of immunology, rather than a question directed to GA and its
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`MOA. Id. at 245:5-9; 245:17-246:7 (“[Y]ou asked me a question about any
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`evidence. I’m not willing to say anything about a statement about any evidence.
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`The medical literature is broad and deep. So, again, I think the important thing here
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`is can I posit opinions specifically on the topics of the proceedings here related to
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`glatiramer acetate and its mechanism of action. I feel very comfortable there.”).
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`Yeda’s counsel then changed topics. Id. at 245:17-246:9. Dr. Green’s cited
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`testimony is not relevant to and does not support OOCE 6.6
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`Response 7: OOCE 7 omits Dr. Green’s full testimony. See id. at 245:22-246:5;
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`261:8-14. Dr. Green is eminently qualified to testify as a POSA here. See Ex. 1004
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`¶¶ 2-12, Ex. A; Ex. 1085 ¶¶ 41-42. The cited testimony is irrelevant as the POSA
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`definition does not require an expert in immunology, much less in the entire field
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`of immunology. IPR2015-0063, Paper 13 at 8-9; IPR-00644, Paper 14 at 4-5; IPR-
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`00830, Paper 8 at 5.
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`Response 8: There is no evidence that the POSA would find a distinction between
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`proliferation and cytokine secretion to be relevant. Further, this OOCE omits Dr.
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`5 Petitioner incorporates its Response to OOCEs 1, 6 and 8-10 herein.
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`6 Petitioner incorporates its Response to OOCEs 1, 5 and 8-10 herein.
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`6
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`
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`Green’s testimony immediately preceding: “Q: Well, it could be that the cells are
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`stimulated to produce cytokines by a cross-reactive antigen but not to proliferate,
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`correct? A: At a theoretical level, yes. Is that what a person who’s skilled in the art
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`would look at when they looked at this reference in thinking about the kinetics of
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`GA-reactive lymphocytes? No.” Ex. 1142 at 253:10-19.7
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`Response 9: The cited text is irrelevant and the conclusions not supported by the
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`cited testimony. Dr. Green testified that the POSA would not interpret Hickey the
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`same way Yeda does. See id. at 259:22-260:7. Hickey was brought into the
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`proceedings by Dr. Ziemssen, who in doing so made no distinctions between “Th2
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`cells (that [purportedly] cross-react)” and “Th2 cells (that [purportedly]
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`specifically react).” Thus, there is no record citation to support that the POSA
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`would make the distinction drawn in this OOCE. Further, in rebutting Dr.
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`Ziemssen’s introduction of Hickey, Dr. Green testified that the POSA would first
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`look to the clinical evidence and if a POSA were to look to Hickey, Hickey teaches
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`that activated T-cells that bind MBP persist for beyond three days. Id. at 272:1-10,
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`272:24-274:4. This is consistent with Dr. Green’s opinion that if a POSA were to
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`rely on Hickey, which does not discuss GA-specific Th2 cells, the POSA would
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`look to the more relevant activated MBP-specific T cells that bind to an antigen in
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`the CNS rather than the other activated T cells that do not bind to antigens in the
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`7 Petitioner incorporates its Response to OOCEs 1, 5, 6 and 9 herein.
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`7
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`CNS.8 See Ex. 1085 ¶¶ 52-58.
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`Response 10: In this OOCE, Yeda argues that “a POSA would have no
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`mechanistic . . . basis upon which to form a reasonable expectation regarding
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`whether GA would maintain its efficacy when used on a three times per week
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`dosing regimen.” In general, Petitioners agree—the available clinical data supports
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`a three times weekly dosing regimen, and nothing related to GA’s still-unknown
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`MOA teaches otherwise. A POSA would therefore rely on the clinical data and
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`discard unproven MOA theories. See Ex. 1142 at 293:2-3 (MOA data would be “of
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`limited importance”); id. at 295:7-10 (“[T]hat’s why the POSA relies on clinical
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`information and doesn’t rely on tenuous arguments about animal experiments[.]”);
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`Ex. 1085 at ¶ 43-44, 49.
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`Response 11: Dr. Green refers to GLACIER being unblinded as a flaw because
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`GLACIER measured a purely subjective endpoint, so that failing to blind the study
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`introduced sufficient bias so that its results “are by no means unimpeachable.” Id.
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`at 342:8-9; see Ex. 1085 ¶¶ 84-89; Ex. 1065 at 180:23-182:22. By contrast,
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`Flechter examined inter alia relapse rate. Ex. 1004 ¶¶ 65-66. Yeda’s attempt to
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`draw parallels between GLACIER and Flechter is also not supported by the record.
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`Dr. Ziemssen’s opinion that no “firm conclusions” can be drawn “concerning the
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`relative efficacy of alternate-day vs. daily administration” is irrelevant—Petitioner
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`8 Petitioner incorporates this Response into its Response to OOCEs 8-10.
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`8
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`must only show a reasonable expectation that the claimed regimen is efficacious.
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`Finally, Dr. Green testified that Khan 2008 (Ex. 1010) and Caon (Ex. 1011)
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`corroborate Flechter 2002A’s results with a rater-blinded study. See Ex. 1085 ¶32.
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`Response 12-14: Whether a POSA would have reasonably expected a once-per-
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`week regimen to succeed is irrelevant—the patents at issue do not cover once-
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`weekly dosing. In testimony omitted by Yeda, Dr. Green explained that the
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`average total weekly dose informs the dose a POSA would choose, while the prior
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`art clinical evidence informs the dosing regimens likely to be safe and effective.
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`Ex. 1142 at 302:24-303:10, 309:14-311:20. That is, a POSA would have a
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`reasonable expectation of success with a 40 mg dose TIW, in part because the
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`average total weekly dose (120 mg) falls within a known range of likely
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`efficacious doses (70 mg to 280 mg) and is similar to that of the FDA-approved 20
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`mg daily regimen (140 mg). Id. Similarly, a POSA would have a reasonable
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`expectation of success that a three-times-per-week dosing regimen would be
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`successful in view of (1) substantial pre-2009 clinical evidence for nearly identical
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`every other day regimen (Ex. 1008, 1010, 1011), and (2) patient preference for a
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`convenient TIW regimen (Ex. 1004 ¶¶ 54-59, 1085 ¶¶ 23-28, 2129 ¶¶ 37-39). Ex.
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`1142 at 299:5-19, 302:24-303:10, 305:9-22, 312:17-313:15, 403:14-404:4. Yeda’s
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`attempt to analogize once weekly dosing to thrice weekly dosing is misleading.
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`Response 15, 17: Whether a POSA would have had a reasonable expectation of
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`9
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`
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`success with a 70 mg regimen administered twice weekly is irrelevant to the
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`patents at issue. A twice weekly regimen includes both 72-hour and 96-hour gaps
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`between doses, whereas a TIW regimen is identical to prior art every other day
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`dosing, save one less injection every two weeks—a single 72-hour gap. Dr. Green
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`did not testify that “a 140 mg total weekly dose of GA, administered twice weekly
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`as 70 mg injections would not have had a reasonable expectation of success.”
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`Rather, Dr. Green explained that the prior art gives an indication that twice weekly
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`dosing might work. Id. at 322:4-8. Dr. Green also testified that Flechter 2002A
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`supports a 96-hour gap between doses. Id. at 323:7-12. Dr. Green testified that a
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`POSA would know that patients on Copaxone miss doses. Id. at 324:7-325:13. A
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`POSA would read the absence of compliance information in Flechter 2002A to
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`mean that patients missed doses. Id. A POSA would know that patients in Flechter
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`2002A often had 96-hour “time gaps” between doses. Id. at 322:25-323:12.
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`Response 16: Dr. Green has not relied upon any alleged MOA for GA as the basis
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`of his opinion. See Response to OOCE 1. In his declaration, Dr. Green explained:
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`In general, claims about a therapeutic agent’s purported mechanism of
`action derived from in vitro models and/or animal data are subordinate
`to patient-derived, real-world clinical data. In 2009, a POSA
`considering the uncertainty surrounding GA’s mechanism of action
`and the available clinical data would have recognized the clinical data
`to be the most relevant information.
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`10
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`
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`
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`Ex. 1085 ¶ 43. Dr. Green stated that “[i]f anything, the uncertainty surrounding
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`GA’s [MOA] would motivate a POSA to investigate dosing regimens with existing
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`and even preliminary clinical support.” Id. ¶ 44. Yeda takes Dr. Green’s comments
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`out of context. Dr. Green referred to the fact that immunological processes
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`“occur[] over the period of time, over the period of days” when asked about a 96-
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`hour gap between doses. Ex. 1142 at 327:23-24. A 96-hour gap between doses is
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`not at issue here. Dr. Green cautioned Yeda at the time that “I think you’re
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`mischaracterizing what I’m saying.” Id. at 327:19-20. In fact, Dr. Green concluded
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`that discussion by underlining that the clinical data is paramount (id. at 332:2-11):
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`I think we’ve established that we don’t know which of these are
`driving the clinical effect of the drug. That’s why we are going to
`make assessments based on a combination of the clinical data with our
`understanding of the biological processes that underlie the mechanism
`of action of the drug. And it’s that thinking about the data in that way
`that guides one towards an understanding of the likely dosing
`regimens that are going to work.
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`Response 18: Dr. Green testified that the PK data provided to FDA to support
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`Copaxone’s approval was not an “absolutely necessary part of [his] argument” but
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`that “it supports the opinion that [he has].” Ex. 1142 at 335:21-25. Yeda omits the
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`prior art that relies on the SBOA’s PK data. See Ex. 1085 ¶ 48 n.2; Ex. 1022 at 2.
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`Dr. Ziemssen’s publication relied on Lobel (Ex. 1022) and the Teva radiolabeled
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`PK data for the PK properties of GA. Ex. 2021 at 4 n.51.
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`11
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`
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`
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`Response 19: Yeda omits Dr. Green’s testimony that a POSA must account for
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`GA acting systemically. Ex. 1142 at 337:24-338:9. Yeda omits that the Copaxone
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`label states: “Some fraction of the injected material . . . may enter the systemic
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`circulation intact.” Ex. 1047 at 1. Yeda omits that Dr. Gristwood testified that “[a]
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`responsible pharmaceutical company would not leave information known to be
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`incorrect [in] prescribing information.” Ex. 2145 at 65:19-24.
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`Response 20: In his reply declaration (Ex. 1085 ¶ 81), Dr. Green explains his
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`testimony, which he reiterated at deposition (Ex. 1142, 343:7-345:25). Yeda omits
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`Dr. Green’s discussion of the teachings of Flechter 2002A. E.g., Ex. 1004 at 65-66.
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`Response 21: Dr. Green did not testify that the dropout rate was a “weakness” in
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`Flechter. Ex. 1142 at 350:15-351:14. Dr. Green explained that the lower dropout
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`rate for patients on alternate day dosing suggests that patients tolerated alternate
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`day dosing better than daily dosing. Id. at 352:18-353. Dr. Green explained that it
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`is the skilled artisan’s job to interpret data as presented. Id. at 351:1-14.
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`Response 22: Dr. Green was asked generally whether “[i]n 2001 there was no way
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`to predict a pharmacodynamics outcome from a [PK] measurement?” Id. at 358:6-
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`8. The beginning of Dr. Green’s response, omitted by Yeda, shows that Dr. Green
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`was explaining that a POSA could theorize about how PK data might “predict” a
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`pharmacodynamics outcome, not that a POSA would rely on a MOA theory. Id. at
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`12
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`
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`
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`358:11-21. As explained in responses to OOCE 1 and16, Dr. Green has not relied
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`upon any alleged MOA for GA as the basis for any opinion in this case.
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`Response 23: Yeda’s assertion that its quotation is Dr. Green’s testimony is false.
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`Yeda’s OOCE is an improper reply as the SBOA (Ex. 1007) was a Petition exhibit.
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`Yeda was obligated to address its criticisms of Ex. 1007 in its Response. No
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`substantive questions were asked as to this passage. See Ex. 1142 at 372:18-374:9.
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`Response 24: Yeda states the question as testimony. Dr. Green’s answer confirms
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`that Ex. 2054 does not contain information necessary to determine whether the
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`conclusion suggested in the question could be reached. Id. at 376:2-4.
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`Response 25: Yeda omits Dr. Green’s answer explaining that at no time have
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`physicians used antihistamines to address Copaxone’s ISRs, nor has Teva
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`encouraged the use of antihistamines. Id. at 380:10-381:18. This refutes the
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`unsupported suggestion that GA’s ISRs are related to histamine release.
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`Response 26: Dr. Green did not testify that Ex. 1069 “reported that anti-histamines
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`were modestly effective.” Rather, in his answer, Dr. Green explained “why the
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`authors conclude antihistamine use as a strategy to reduce local injection site
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`reactions in patients on GA therapy cannot be recommended.” Id. at 282:4-20.
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`Response 27: The IMS data referenced is not of record and is not admissible for
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`any purpose. 37 C.F.R. 42.61(a). Dr. Hay cannot be criticized for Yeda’s decision
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`not to file evidence. Dr. Hay’s criticisms of the IMS data do not require analysis of
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`13
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`
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`this particular data set. Dr. Hay stated (Ex. 1099 ¶¶ 40-41) that IMS admits it fails
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`to capture sales of specialty products (Ex. 1111, 1112), which is corroborated in
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`Ex. 1113. IMS data is not relevant to the issue of commercial success as it does not
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`reflect actual revenue to Yeda. Ex. 1099 ¶¶ 55, 57-58, 62; Ex. 2148 at 21:13-22:15.
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`Response 28: Glatopa’s co-pay is irrelevant to the issue of whether sales of
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`Copaxone 40 mg were driven by its more favorable pricing and co-pay support.
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`Response 29: Dr. Hay had no burden to demonstrate the degree to which
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`Copaxone 40 mg’s more favorable pricing and co-pay support drove sales. Dr.
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`Grabowski’s declaration was unsupported by record evidence and failed to address
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`the impact of Copaxone 40 mg’s more favorable pricing.
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`Response 30: Yeda appears to argue that because Copaxone 40 mg is administered
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`three times per week, there is a nexus to the patents in suit. This argument is
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`legally incorrect. If commercial success is due to an unclaimed feature of a
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`product, or if that feature was known in the art, the commercial success is not
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`relevant. See, e.g., Ormco Corp. v. Align Tech., Inc., 463 F. 3d 1299, 1312 (Fed.
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`Cir. 2006); see also Ex. 1141 at 57:1-5, 58:7-13.
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`Response 31-32: Both OOCEs relate to questions concerning an article that is not
`
`of record. Yeda omits Dr. Hay’s testimony that the quotations are taken out of the
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`context of the article (Ex. 1141 at 59:11-14, 17) and that any statements in the
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`article were qualified within the article (id. at 59:23-25, 60:8-14). Yeda omits Dr.
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`14
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`
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`Hay’s testimony that Copaxone 40 mg is priced lower than the 20 mg product,
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`refuting the suggestion that Copaxone 40 mg does not compete on price.
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`Response 33: Dr. Hay reviewed publicly available comparative pricing of
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`Copaxone 20 mg and 40 mg, including Missouri Medicaid pricing, in the absence
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`of pricing data in Yeda’s Response. Id. at 66:13-22. Dr. Hay testified that there is
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`no true pricing data available in the record of this proceeding, which is a fatal flaw
`
`in Yeda’s commercial success theory. Id. at 66:13-22, 67:1-18.
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`Response 34: Yeda omits portions of Dr. Hay’s answer. Dr. Hay testified as to the
`
`substantial evidence establishing that Copaxone 40 mg is priced higher than
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`Glatopa. Id. at 71:3-71:23; Ex. 1099 ¶¶ 55-56; Ex. 1104, 1122, 1124.
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`Response 35: The quoted testimony is not the witness’s, but is the question of
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`Yeda’s attorney reading from a document not of record. Ex. 1141 at 96:10-12,
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`97:14-16; see Response at p. 1, supra. Yeda omits the witness’s answer.
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`15
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`Dated: April 22, 2016
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`
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`
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`
`
`/Brandon M. White/
`Brandon M. White
`Reg. No. 52,354
`Perkins Coie LLP
`700 13th St., NW, Suite 600
`Washington, D.C. 20005
`Telephone: (202) 654-6206
`E-mail: bmwhite@perkinscoie.com
`
`Attorney for Mylan Pharmaceuticals Inc.
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`16
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`
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`CERTIFICATE OF SERVICE
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`The undersigned hereby certifies that the foregoing Petitioners’ Response to
`
`Yeda’s Observation on Reply was served electronically via email as follows:
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`Patent Owners:
`
`Elizabeth Holland
`Goodwin Procter LLP
`eholland@goodwinprocter.com
`
`William James
`Goodwin Procter LLP
`wjames@goodwinprocter.com
`
`Eleanor Yost
`Goodwin Procter LLP
`eyost@goodwinprocter.com
`
`Petitioner Amneal Pharmaceuticals LLC:
`
`
`Nicholas Mitrokostas
`Goodwin Procter LLP
`nmitrokostas@goodwinprocter.com
`
`Daryl Wiesen
`Goodwin Procter LLP
`dwiesen@goodwinprocter.com
`
`John Bennett
`Goodwin Procter LLP
`jbennett@goodwinprocter.com
`
`Vincent L. Capuano
`Duane Morris LLC
`VCapuano@duanemorris.com
`
`Christopher S. Kroon
`Duane Morris LLC
`CSKroon@duanemorris.com
`
`
`Dated: April 22, 2016
`
`
`
`/Brandon M. White/
`Brandon M. White
`
`Attorney for Mylan Pharmaceuticals Inc.
`
`
`
`1