throbber
UNITED STATES PATENT AND TRADEMARK OFFICE
`
`BEFORE THE PATENT TRIAL AND APPEAL BOARD
`
`
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`
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`MYLAN PHARMACEUTICALS INC. and
`AMNEAL PHARMACEUTICALS LLC
`
`Petitioners
`
`v.
`
`YEDA RESEARCH AND DEVELOPMENT CO. LTD.
`
`Patent Owner
`
`Case IPR2015-00643 (Patent 8,232,250 B2)
`Case IPR2015-00644 (Patent 8,399,413 B2)
`Case IPR2015-00830 (Patent 8,969,302 B2)1,2
`
`PATENT OWNER YEDA’S OBSERVATIONS ON CROSS-
`EXAMINATION OF PETITIONERS MYLAN AND AMNEAL’S REPLY
`WITNESSES
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`1 The word-for-word identical paper is filed in each proceeding identified in the
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`caption.
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`2 Cases IPR2015-01976, IPR2015-01980, and IPR2015-01981 have been joined
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`with IPR2015-00643, IPR2015-00644, and IPR2015-00830, respectively.
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`
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`

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`
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`Dr. Green’s Reply Deposition Transcript (Ex. 1142)
`1. In Ex. 1142 (224:3-5), Dr. Green testified that the Th1-Th2 shift theory of
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`the mechanism of action of glatiramer acetate (“GA”) was “one of the leading
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`theories about one of the features of GA or how GA might contribute in terms of
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`its therapeutic effect” in 2009. This testimony is relevant to Dr. Green’s opinion
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`that GA’s effect on the balance of Th1/Th2 cells in the central nervous system was
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`merely a “narrow” and “unproven” hypothesis regarding GA’s therapeutic
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`mechanism of action in ¶ 49 of Ex. 1085. This testimony is also relevant because
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`it supports Dr. Ziemssen’s testimony (Ex. 2135 at ¶ 58) and contradicts Dr.
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`Green’s assertion that a POSA would not rely on evidence regarding a Th1-Th2
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`shift to account for GA’s therapeutic effect.
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`2. In Ex. 1142 (225:8-23), Dr. Green testified that the prior art he relied on to
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`support his opinions states that “[m]ost investigations have attributed the
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`immunomodulatory effect of GA to its capability to alter T-cell differentiation.
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`Specifically, GA treatment is believed to promote development of Th2-polarized
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`reactive . . . GA-reactive, CD4+ T-cells which may dampen neighboring
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`inflammation within the central nervous system.” This testimony is relevant for
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`the same reasons identified above in ¶ 1.
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`3. In Ex. 1142 (228:15-25), Dr. Green testified that the prior art disclosed that
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`“[t]he clinical effects of glatiramer acetate (GA), an approved therapy for multiple
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`1
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`sclerosis, are thought to be largely mediated by a T-helper 1 (Th1) to T-helper 2
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`(Th2) shift of GA-reactive T lymphocytes.” This testimony is relevant for the
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`same reasons identified above at ¶ 1.
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`4. In Ex. 1142 (278:6-18), Dr. Green testified that the prior art disclosed that,
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`“[t]he GA-reactive T-cells are stimulated to secrete down-modulatory cytokines,
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`like IL-4, which exert a bystander suppressive effect on other T-cells,” and that
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`these GA-reactive T-cells will enter into the central nervous system (“CNS”) and
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`secrete anti-inflammatory cytokines. This testimony is relevant for the same
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`reasons identified above at ¶ 1.
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`5. In Ex. 1142 (241:23-242:7 and 280:7-11), Dr. Green testified that antigen
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`specific T-cells secrete cytokines and proliferate in response to antigens and that
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`the prior art disclosed that “[m]ost investigators of the human immune response to
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`GA found that GA is not cross-reactive with MBP (myelin basic protein) at the
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`level of proliferation.” This testimony is relevant to Dr. Green’s assertion that,
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`based on Hickey 1991A (Ex. 2075), a POSA would believe that GA-specific Th2
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`cells that cross-react with MBP should persist in the CNS for beyond three days
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`based upon Hickey’s reference to antigen specific T-cells in ¶ 58 of Ex. 1085. This
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`testimony clarifies that the portion of GA specific T-cells that cross react with
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`MBP are not specific for MBP as described in Hickey 1991A and thus it
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`contradicts Dr. Green’s contention that a POSA would believe GA-specific T-cells
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`2
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`would persist for beyond three days by equating cross recognition of MBP with
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`MBP specificity.
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`6. In Ex. 1142 (244:15-246:7), Dr. Green testified that he could not point to
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`any evidence that a T-cell that cross-reacts with another antigen for which it is not
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`specific will proliferate. This testimony is relevant for the same reasons described
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`above in ¶ 5.
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`7. In Ex. 1142 (245:1-5), Dr. Green states that “this is not nor do I think I’ve
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`ever presented myself to be an expert in the entire field of human immunology or
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`mammalian immunology.” This testimony is relevant to Dr. Green’s expertise and
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`ability to provide testimony in this matter.
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`8. In Ex. 1142 (253:21-254:2), Dr. Green testified that the prior art in the area
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`of the immunological response to glatiramer acetate does draw distinctions
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`between proliferation and cytokine secretion. This testimony is relevant for the
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`same reasons described above in ¶ 5.
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`9. In Ex. 1142 (254:12-17), Dr. Green testified that in the section of Hickey
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`1991A (Ex. 2075) relied upon for T-cell lifetime in the CNS, that no mention is
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`made of cross-reaction. This testimony is relevant to Dr. Green’s hypothesis that a
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`POSA would equate GA-activated Th2 cells (that cross-react) to MBP-specific T-
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`cells (that specifically react) in ¶ 55 of Ex. 1085. This testimony is relevant
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`because it shows that Dr. Green’s opinion regarding the effect of cross-reaction is
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`not supported by the Hickey 1991A reference itself.
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`10. In Ex. 1142 (292:19-293:5), Dr. Green testified that it is “absolutely right”
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`that it is unknown today how many Th2 reactive activated T-cells have to
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`accumulate in the brain in order for GA therapy to be effective. This testimony is
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`relevant to Dr. Green’s assertion that a POSA would expect less frequent dosing to
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`achieve a similar therapeutic effect to daily dosing in ¶ 59 of Ex. 1085. This
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`testimony is relevant because it shows a POSA would have no mechanistic or
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`pharmacokinetic 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.
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`11. In Ex. 1142 (298:5-9), Dr. Green testified that the Flechter 2002A study
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`was an open label study (i.e. it was unblinded). In Ex. 1142 (341:9-342:9), Dr.
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`Green testified that “an un-blinded study is subject to greater bias than a blinded
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`study” and that given the bias that is part of unblinded studies, the results reached
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`by them are by no means unimpeachable. This testimony is relevant because it
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`corroborates Dr. Ziemssen’s opinion that “[t]he open-label nature of the [Flechter
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`2002A] study, coupled with its attempted cross-study comparison, makes it
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`imprudent to draw any firm conclusions concerning the relative efficacy of
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`alternate-day vs. daily administration.” (Ex. 2135 at ¶155.)
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`12. In Ex. 1142 (301:11-21), Dr. Green testified that a POSA would not have a
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`reasonable expectation of success administering 140 mg of GA once per week.
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`This testimony is relevant because it is inconsistent with his repeated discussion
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`and reliance on “total weekly dose” ranges without regard to the frequency of
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`dosing in the prior art. (See, e.g., Ex. 1085 at ¶¶ 5, 8, 16.)
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`13. In Ex. 1142 (312:7-15), when asked why a POSA would not have thought
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`that once-weekly dosing of GA would work, Dr. Green testified that there was no
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`prior art suggesting once a week dosing of GA and no clinical data at the time that
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`suggested once a week dosing of GA would be efficacious. This testimony is
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`relevant because it is inconsistent with Dr. Green’s interpretation of the prior art he
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`uses to support his argument that there would be a reasonable expectation of
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`success for three times weekly GA dosing. As Dr. Green testified, as of 2009 there
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`was no prior art reference that disclosed three times weekly dosing and no clinical
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`data on three times weekly dosing of GA. (Ex. 1142 at 304:23- 305:3, 306:2-12.)
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`14. In Ex. 1142 (304:23- 305:3), Dr. Green testified that Flechter 2002A does
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`not “specifically suggest administering Copaxone three times a week.” Dr. Green
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`also testified that there is no prior art that discusses any dose of GA dosed three
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`times weekly. (Ex. 1142 at 306:2-12.) This testimony is relevant because it
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`further supports the Patent Owner’s position that there is no prior art that teaches
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`GA dosed three times per week and that a POSA would not be motivated to
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`administer GA three times a week, as required by the claims.
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`15. In Ex. 1142 (322:12-24), when explaining why a 140 mg total weekly dose
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`of GA, administered twice weekly as 70 mg injections would not have had a
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`reasonable expectation of success, Dr. Green testified that one reason was the “gap
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`between the doses.” This testimony is relevant because it highlights the
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`inconsistency in Dr. Green’s opinion regarding what “time gaps” a POSA would
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`have thought were permissible to maintain efficacy in 2009. The three times
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`weekly dosing regimen claimed in the patent has a “time gap” of 72-96 hours.
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`(See Paper 58 [Petitioners’ Reply to Patent Owner’s Response] at 2.) A twice
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`weekly dosing regimen would have “time gaps” of about 72 and 96 hours. The
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`“time gap” Dr. Green expressed concern about during his deposition regarding the
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`twice weekly dose, is the same “time gap” that is part of the three times a week
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`dosing regimen claimed in the patent.
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`16. In Ex. 1142 (323:14-20 and 325:14-24), Dr. Green testified that part of his
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`understanding of why a 96-hour “time gap” between GA doses would be
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`acceptable to a POSA in 2009 was an understanding of “how the drug may work.”
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`Dr. Green testified that a POSA would have the “understanding that the potential
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`mechanisms of action or the likely mechanisms of action of the drug include that
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`the drug is acting on the immune system and lead to downstream effects in
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`immune cells that are likely not limited in their kinetics in terms of time periods
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`like a day.” (Ex. 1142 at 325:14-24.) This testimony is relevant because it is
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`inconsistent with Dr. Green’s opinions provided in his previous deposition where
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`he stated:
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`But, again, the important thing to note here is whether or
`not the precise mechanism of action is known may not be
`-- or is not of any importance in trying to figure out how
`to dose the drug or the dosing regimen, which are the
`issues I was asked to opine on in this proceeding.
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`(Ex. 1065 at 38:10-19.)
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`17. In Ex. 1142 (323:14-20), Dr. Green testified that part of his understanding
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`why a 96-hour “time gap” between GA doses would be acceptable to a POSA in
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`2009 was based on his assumption that some patients in the Flechter 2002A trial
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`skipped doses and had 96-hour “time gaps” between doses. Dr. Green further
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`testified that Flechter 2002A does not report that any patients skipped doses. (Ex.
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`1142 at 324:15-17.) This testimony is relevant because it reflects a lack of
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`evidence supporting Dr. Green’s opinions regarding obviousness.
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`18. In Ex. 1142 (357:24-358:4), Dr. Green testified that as of 2009 there was
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`no known pharmacokinetic-pharmacodynamic relationship for GA. Despite this,
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`Dr. Green testified that his obviousness opinions, at least in part, depend on on the
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`iodinated radio-labeled GA pharmacokinetic monkey data found in the SBOA (Ex.
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`1007). (Ex. 1142 at 334:24-335:15.) This testimony is relevant because it
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`supports Dr. Ziemssen’s opinion that a POSA would not rely on pharmacokinetic
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`properties to predict the behavior of GA. (Ex. 2135 at ¶ 120-124.)
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`19. In Ex. 1142 (337:14-17), Dr. Green admits that intact GA has never been
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`measured in the systemic circulation of humans. This testimony is relevant
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`because it is consistent with Dr. Ziemssen’s opinion that GA does not exert its
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`therapeutic effect by passage through systemic circulation, instead acting locally in
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`the periphery, which means that classical pharmacokinetic data cannot be used to
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`predict the activity of GA in humans, and accordingly cannot be used to predict the
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`effect of varying dosage amounts or frequencies. (See Ex. 2135 at ¶ 68-69.)
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`20. In Ex. 1142 (343:7-345:25), Dr. Green testified that “Flechter does not
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`state, unconditionally, that daily injections are unnecessary.” This testimony is
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`relevant because it contradicts Dr. Green’s declaration where he stated that
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`“Flechter 2002A concludes that ‘daily injections are unnecessary.’ ” (Ex. 1085 at ¶
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`81.)
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`21. In Ex. 1142 (347:15-24), Dr. Green testified that in a clinical trial, when
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`evaluating efficacy, an investigator tries to account for dropouts. Dr. Green also
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`testified that Flechter 2002A failed to account for 27 out of the 68 total patients in
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`the trial because they dropped out, some because of disease progression and that
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`this was a “weakness” in the Flechter study. (Ex. 1142 at 351:1-4, 355:9-12.) This
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`testimony is relevant because it supports Dr. Ziemssen’s opinion that “Flechter’s
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`high drop-out rate for every other day administration [is] potentially skewing the
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`results.” (Ex. 2135 at ¶ 158.)
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`22. In Ex. 1142 (358:6-21), Dr. Green stated that as of 2009:
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`But one could – given that the mechanism of action is not
`understood or not known, one would have to theorize
`about what the presumed mechanisms might be and think
`about how that pharmacokinetic information or data
`would influence one’s understanding. That's what a
`person of ordinary skill in the art would have done at the
`time when they first considered could you give a dosing
`regimen that was less frequent.
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`This testimony is relevant because it is consistent with Dr. Ziemssen’s opinion that
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`without a known pharmacokinetic-pharmacodynamic relationship, a POSA would
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`rely upon what was known about GA’s mechanism of action in determining
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`whether or not less frequent dosing would be efficacious. (See Ex. 2135 at ¶ 53-
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`69, 120-124.) This testimony is also relevant because it is inconsistent with Dr.
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`Green’s previous deposition testimony where he stated that the mechanism of
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`action was “not of any importance in trying to figure out how to dose the drug.”
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`(Ex. 1065 at 38:10-19.)
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`23. In Ex. 1142 (372:5-24), Dr. Green testified that the SBOA (Ex. 1007)
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`states:
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`
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`Additionally, the sponsor demonstrated that Copolymer 1
`directly
`induced histamine release from basophils
`isolated from healthy volunteers and MS patients, and
`that the anti-Copolymer 1 antibodies taken from patients
`receiving the drug were IGG and not IGE, they
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`concluded from these studies that skin reactions from
`skin testing with Copolymer 1 done in patients receiving
`the drug were probably due to Copolymer 1 directly
`inducing histamine
`release and not due
`to an
`immunological reaction involving IGE.
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`This testimony is relevant because while Dr. Green relied on the SBOA for the
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`reviewer comment regarding dosing frequency and pharmacokinetic monkey data,
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`he rejected the data related to histamine release caused by GA injections.
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`24. In Ex. 1142 (374:11-376:12), Dr. Green testified that Levi-Shaffer (Ex.
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`2054) reports that wheal and flare injection site reactions were lessened by the
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`administration of terfenadine, an antihistamine drug. This testimony is relevant
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`because it contradicts Dr. Green’s opinion that GA injection site reactions are not
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`related to histamine release.
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`25. In Ex. 1142 (379:10-380:10 and 387:25-388:4), Dr. Green testified that the
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`Zwibel and Pardo abstracts (Ex. 1069) that he relied on in his Reply Declaration
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`(Ex. 1085), do not disclose what antihistamine drug was given to patients. This
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`testimony is relevant because without knowing what antihistamine was
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`administered to patients, a POSA could not evaluate the extent to which
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`antihistamines would not be effective in lessening GA injection site reactions,
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`especially considering terfenadine was successful in lessening GA injection site
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`reactions in the Levi-Shaffer trial (Ex. 2054).
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`26. In Ex. 1142 (381:20-383:16), Dr. Green testified that even though the
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`Pardo abstract (Ex. 1069) reported that anti-histamines were modestly effective, a
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`POSA would not think anti-histamines were useful for treating GA injection site
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`reactions because the results were not statistically significant. This testimony is
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`relevant because it is inconsistent with Dr. Green’s interpretation of other prior art
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`references. For example, Flechter 2002A (Ex. 1008), Khan (Ex. 1010), Caon (Ex.
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`1011) and Pinchasi (Ex. 1005) all either fail to meet statistical significance, do not
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`disclose data from which statistical significance can be assessed, or are not
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`powered to achieve statistical significance.
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`Dr. Hay’s Reply Deposition Transcript (Ex. 1141)
`27. In Ex. 1141 (13:18-21), Dr. Hay testified “[w]ell, I couldn’t even look at
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`the IMS data because it wasn’t made available to me. So I don’t know what was
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`said about IMS data in this case because I didn’t see any IMS data.” Dr. Hay also
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`testified that he “didn’t get any data” despite asking counsel for “any data they had,
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`including IMS data.” (Id. at 14:14-15.) This testimony is relevant to Petitioners’
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`position that Dr. Grabowski’s analysis of commercial success is unreliable due to
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`its reliance on IMS data because Dr. Hay’s criticisms of the IMS data upon which
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`Dr. Grabowksi relied were not based on any evaluation of that data or on an
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`evaluation of any alternative datasets, despite the IMS data having been made
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`available to Petitioners’ counsel for use in these proceedings. (See Paper 58 at 21;
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`Ex. 1099 at ¶¶ 39-46, 59, 78; Ex. 1075 (Mitrokostas Letter to White 1/19/16).)
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`28. In Ex. 1141 (39:7-10), Dr. Hay testified that “Glatopa offered a zero dollar
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`copay for its generic alternative to Copaxone 20 mg.” This is relevant to Dr. Hay’s
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`assertion that “[r]educing patient payments or co-payments through coupons,
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`rebates and discounts will certainly drive Copaxone 40 mg/mL sales” and
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`Petitioners’ contention that a more favorable copay drove Copaxone® 40 mg/mL
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`sales rather than the claimed subject matter of the patent at issue. (See Ex. 1099 at
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`¶ 69; Paper 58 at 20-21.) This testimony is relevant because it shows that the
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`Copaxone 40 mg/mL co-payment program did not offer any incentive for patients
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`to select that product over the generic 20 mg/mL daily competitor, Glatopa.
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`29. In Ex. 1141 (43:4-9), when asked whether he knew “by how much the
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`copay differential that [he] reference[s] in [his] declaration would impact the sales
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`of Copaxone 40,” Dr. Hay testified that he “wasn’t asked to provide that opinion”
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`and that a “careful econometric analysis” would be required to provide that
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`opinion. This is relevant to Dr. Hay’s assertion that “[r]educing patient payments
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`or co-payments through coupons, rebates and discounts will certainly drive
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`Copaxone 40 mg/mL sales . . .” and Petitioners’ contention that a more favorable
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`copay drove Copaxone® 40 mg/mL sales rather than the claimed subject matter of
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`the patent at issue. (See Ex. 1099 at ¶ 69; Paper 58 at 20-21.) This testimony is
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`relevant because it indicates that Dr. Hay did not conduct the necessary
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`econometric analysis to support his assertion and Petitioners’ position.
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`30. In Ex. 1141 (56:11-12, 56: 16-21), Dr. Hay testified that, “my
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`understanding as a health economist is that the claims of the patents or at least
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`some of the claims relate to three times weekly administration. So to that extent, I
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`think Copaxone at least has that route of administration.” This is relevant to Dr.
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`Hay’s statement at ¶ 66 of Ex. 1099 that he “understand[s] that it is the Patent
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`Owner’s burden to show that there is a nexus between the promotion and sales of
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`the product and the claims of the patent at issue.” This testimony is relevant
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`because it demonstrates Dr. Hay applied the wrong legal standard in his analysis of
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`whether the commercial success of Copaxone 40 mg/mL has a nexus to the claims
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`of the patent issue.
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`31. In Ex. 1141 (59:7-25), Dr. Hay testified that “branded drugs compete
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`primarily on their perceived and actual clinical attributes, not their prices.” This
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`testimony is relevant because it contradicts Dr. Hay’s contention and Petitioners’
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`position that price differences, patient copayment assistance programs, rebates, and
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`discounts generated Copaxone 40 mg/mL sales. (See Paper 58 at 20-21; Ex. 1099
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`at ¶¶ 53-59, 66-72.)
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`32. In Ex. 1141 (62:16-63:4), Dr. Hay testified that “if for a particular
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`treatment episode a treatment decision is irreversible,” then “the last thing on the
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`doctor's mind in those situations is saving a few dollars by using drug A rather than
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`drug B. They will choose the drug that they personally believe is the most likely to
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`produce the best clinical outcomes for their patients.” In Ex. 1142 (361:25-363:2),
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`Dr. Green testified that “it is important when you prescribe a drug for an MS
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`patient that you do the best you can to pick a drug that’s going to stop the disease
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`progression,” “or do its best to stop the disease activity in the hopes that that [sic]
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`stops progression,” and that “Copaxone does not reverse the effects of MS.” This
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`testimony is relevant because it contradicts Dr. Hay’s contention and Petitioners’
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`position that price differences between Copaxone 40 mg/mL and Copaxone 20
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`mg/mL or Glatopa 20 mg/mL drove the sales of Copaxone 40 mg/mL. (See Paper
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`58 at 20-21; Ex. 1099 at ¶¶ 53-59, 66-72.)
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`33. In Ex. 1141 (66:3-9 and 68:17-19), Dr. Hay testified that the list prices
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`disclosed the Missouri Medicaid Program Report (Ex. 1123), “fail to capture the
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`confidential rebates that the Missouri Medicaid program receives,” and “that there
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`are substantial rebates off of these prices,” and that the price “is not the true price”
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`and “does not account for rebates and discounts.” This is relevant to Dr. Hay’s
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`reliance on Ex.1123 in ¶ 56 of Ex.1099 to show that Copaxone 20 mg/mL is more
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`expensive than Copaxone 40 mg/mL. This testimony is relevant because it
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`indicates the prices upon which Dr. Hay relied in this paragraph do not reflect the
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`true prices of Copaxone 20 mg/mL and Copaxone 40 mg/mL.
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`34. In Ex. 1141 (70:1-71:2), Dr. Hay testified that the administrative price for
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`Glatopa in the Missouri Medicaid Program Report (Ex. 1123) is $63,824.63. This
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`is relevant to Dr. Hay’s statement in ¶ 56 of Ex. 1099 that “Copaxone 40 mg/mL
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`($71,409 per year) is significantly less expensive than Copaxone 20 mg/mL
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`($81,017 per year),” and that “Glatopa was priced higher than Copaxone 40
`
`mg/mL.” This testimony is relevant because it demonstrates that Glatopa is not
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`always priced higher than Copaxone 40 mg/mL.
`
`35. In Ex. 1141 (96:7-12, 97:9-19, 98:6-22), Dr. Hay testified that “Copaxone
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`revenues in the United States in 2015 increased four percent to $3.2 billion” and
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`“Copaxone accounted for 20 percent of our revenues in 2015 and is [a]
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`significantly higher percentage contribution to our profits and cash flow from
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`operations during such period.” This testimony is relevant because it contradicts
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`Dr. Hay’s and Petitioners’ contention that Copaxone 40 mg/mL was not a
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`commercial success because it may not have been profitable. (Ex. 1099 at ¶ 60;
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`Paper 8 at 21.)
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`Dated: April 13, 2016
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`Respectfully submitted,
`
`/Elizabeth J. Holland/
`Elizabeth J. Holland
`Registration No. 47,657
`GOODWIN PROCTER LLP
`The New York Times Building
`620 Eighth Avenue
`New York, NY 10019-1405
`Tel: 212-813-8800
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`CERTIFICATE OF SERVICE
`
`The undersigned hereby certifies that I caused the PATENT OWNER
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`YEDA’S OBSERVATIONS ON CROSS-EXAMINATION OF
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`PETITIONERS MYLAN AND AMNEAL'S REPLY WITNESSES to be
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`served electronically via e-mail on April 13, 2016 on the following:
`
`Jeffrey W. Guise
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`jguise@wsgr.com
`
`Brandon M. White
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`BMWhite@perkinscoie.com
`
`Shannon Bloodworth
`
`sbloodworth@perkinscoie.com
`
`David Anstaett
`
`DAnstaett@perkinscoie.com
`
`Richard Torczon
`
`rtorczon@wsgr.com
`
`Vince Capuano
`
`vcapuano@duanemorris.com
`
`Christopher Kroon
`
`CSKroon@duanemorris.com
`
`/April E. Weisbruch/
`April E. Weisbruch
`
`Dated:
`
`April 13, 2016

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