` BEFORE THE PATENT TRIAL AND APPEAL BOARD
` MYLAN PHARMACEUTICALS, INC.
` Petitioner
` - vs. -
` YEDA RESEARCH AND DEVELOPMENT CO. LTD.,
` Patent Owner
` Case IPR2015-00643 (8,232,250)
` Case IPR2015-00644 (8,399,413)
` Case IPR2015-00830 (8,969,302)
`
` DEPOSITION OF ARI GREEN, M.D.
` VOLUME II
`
` San Francisco, California
` Wednesday, April 6, 2016
`
`REPORTED BY:
` LORRIE L. MARCHANT
` CSR NO. 10523, RMR, CRR, CCRR, CLR
`
`The Little Reporting Company
` (646) 650-5055 | www.littlereporting.com
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`MYLAN PHARMS. INC. EXHIBIT 1142 Page 1
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` UNITED STATES PATENT AND TRADEMARK OFFICE
` BEFORE THE PATENT TRIAL AND APPEAL BOARD
`
`197
`
` MYLAN PHARMACEUTICALS, )
` INC., )
` )
` Petitioner, )
` )
` vs. ) Case No. IPR2015-00643
` ) (8,232,250), et al.
` )
` YEDA RESEARCH AND )
` DEVELOPMENT CO. LTD., )
` )
` Patent Owner. )
` _________________________ )
`
` Deposition of ARI GREEN, M.D., taken on
` behalf of the Patent Owner Yeda,
` commencing at 9:55 a.m., Wednesday, April
` 6, 2016, at Three Embarcadero Center, 24th
` Floor, San Francisco, California, before
` Lorrie L. Marchant, CSR No. 10523, RMR,
` CRR, CCRR, CLR, a Certified Shorthand
` Reporter in and for the County of Sonoma,
` State of California.
`
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` A P P E A R A N C E S:
`
`FOR THE PATENT OWNER YEDA:
` GOODWIN PROCTOR LLP
` BY: WILLIAM G. JAMES, Esq.
` 901 New York Avenue, NW
` Washington, D.C. 20001
` (202) 346-4000
` wjames@goodwinprocter.com
` BRIAN DRUMMOND, Esq.
` DARYL L. WIESEN, Esq.
` 53 State Street
` Exchange Place
` Boston, Massachusetts 02109
` (617) 570-1000
` Bdrummond@goodwinproctor.com
` Dwiesen@goodwinproctor.com
`FOR MYLAN & THE DEPONENT:
` PERKINS COIE
` BY: DAVID L. ANSTAETT, Esq.
` One East Main Street, Suite 201
` Madison, WI 53703
` (608) 663-5408
` Danstaett@perkinscoie.com
` SHANNON M. BLOODWORTH, Esq.
` 700 13th Street, NW
` Suite 600
` Washington, DC 20005-3960
` (202) 654-6206
` Sbloodworth@perkinscoie.com
` COURTNEY M. PROCHNOW, Ph.D., Esq.
` 1888 Century Park East, Suite 1700
` Los Angeles, CA 90067
` (310) 788-3284
` Cprochnow@perkinscoie.com
`and
` WILSON SONSINI GOODRICH & ROSATI
` BY: LORELEI P. WESTIN, Ph.D., Esq.
` 12235 El Camino Real, Suite 200
` San Diego, CA 92130
` (858) 350-2300
` lwestin@wsgr.com
`
`The Little Reporting Company
` (646) 650-5055 | www.littlereporting.com
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` A P P E A R A N C E S:
`
`FOR AMNEAL PHARMACEUTICALS:
` DUANE MORRIS
` BY: CHRISTOPHER S. KROON, Esq.
` 100 High Street
` Suite 2400
` Boston, MA 02110
` (857) 488-4250
` Cskroon@duanemorris.com
`
`ALSO PRESENT:
` Matthew Greinert, Esq., of Mylan
` Lori Wolfe, Esq., of Teva
` ---oOo---
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`200
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` I N D E X
`EXAMINATION: PAGE
` MR. JAMES 201
` MR. ANSTAETT 392
` MR. JAMES 400
` ---oOo---
` E X H I B I T S
` EXHIBIT DESCRIPTION PAGE
` Exhibit 1140 Redacted copy of the 396
` deposition transcript of Jerry
` S. Wolinsky, M.D., taken on
` February 15th, 2016
`
` ---oOo---
` INFORMATION REQUESTED
` (NONE)
` ---oOo---
` QUESTIONS MARKED
` (NONE)
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`201
` SAN FRANCISCO, CALIFORNIA; WEDNESDAY, APRIL 6, 2016
` 9:55 A.M.
` ARI GREEN, M.D.
`having declared under penalty of perjury to tell the
` truth, was examined and testified as follows:
` ARI GREEN, M.D.,
` FIRST DULY SWORN/AFFIRMED, TESTIFIED AS FOLLOWS:
` EXAMINATION BY MR. JAMES
` BY MR. JAMES:
` Q. Good morning.
` A. Good morning.
` Q. Could you state and spell your name for the
` record, please.
` A. Sure. So my name is Ari, spelled A-R-I,
` Green, just like the color.
` Q. And you hold an M.D.?
` A. I do.
` Q. When did you start treating patients?
` A. You mean patients of any sort?
` Q. Yes.
` A. After I finished medical school in 2001.
` Q. When did you start treating MS patients?
` A. I've been involved in the care of MS
` patients for many years, but do you mean
` independently, or do you mean as a physician?
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` Q. As a physician.
` A. As a physician, in around 2001 or 2002.
` Q. And when you began practicing medicine and
` began treating patients for MS, Copaxone was on the
` market; right?
` A. It was.
` Q. And when you began treating patients for
` MS, you were aware of all the prior art literature
` at the time; right?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: So maybe you can clarify what
` your question is one more time.
` BY MR. JAMES:
` Q. Which part of my question don't you
` understand?
` A. I don't understand the question in general,
` so if you would state it again, it would help.
` Q. Do you know what prior art is?
` A. I do.
` Q. So at the time you started practicing
` medicine and treating patients for MS, were you
` aware of the prior art available at the time about
` treating MS?
` MR. ANSTAETT: Objection. Objection to
` form.
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` THE WITNESS: So do you mean the first time
` that I ever saw a patient with MS, was I aware of
` all the prior art that existed?
` BY MR. JAMES:
` Q. At the time, yes.
` A. No.
` Q. When did you become aware of the paper by
` Flechter?
` A. The paper by Flechter --
` Q. That you relied on in your expert report.
` A. There's two papers by Flechter.
` Q. Well, there's only one Flechter paper that
` is the subject of the IPR institution decision;
` correct?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: I would have to look at my
` report to know, but I think I know which paper
` you're talking about.
` So I became aware of that Flechter paper
` when I was -- as I was preparing my response in this
` case.
` BY MR. JAMES:
` Q. Not before then?
` A. No.
` Q. And is the same true of the SBOA? Do you
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`
` know what I mean when I say "SBOA"?
` A. I do.
` Q. The summary basis of approval for the
` 20-milligram Copaxone product?
` A. Yes.
` Q. You only became aware of that when you
` start working on this litigation; correct?
` A. So if you can clarify what you mean by
` "this litigation."
` Do you mean this specific case, or do you
` mean earlier cases related to Copaxone?
` Q. When did you first become aware of the
` SBOA?
` A. I don't know the exact date, but sometime
` in the proceedings between -- between Mylan and
` Teva, but I don't know which specific case it was.
` Q. Do you recall about how long ago it was
` that you became aware of the SBOA?
` A. Sometime in the last number of years. I
` don't remember exactly.
` Q. What does that mean, Dr. Green, "the last
` number of years"? Ten years?
` MR. ANSTAETT: Objection to form.
` BY MR. JAMES:
` Q. Two years?
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` MR. ANSTAETT: Objection to form.
` Argumentative.
` THE WITNESS: Probably three or four, but I
` don't know.
` BY MR. JAMES:
` Q. Okay. After 2011; right?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: Yes.
` BY MR. JAMES:
` Q. Now, when you treat MS patients, do you
` measure EDSS?
` A. Yes.
` Q. What does that stand for?
` A. It stands for the expanded disability
` score, and that's a score that's established to
` estimate or to try and put a numerical value on the
` amount of disability that a patient suffers from.
` Q. What do you mean by "disability"?
` A. So disability in this context means
` difficulty with some neurological function, some
` impairment of neurological function.
` Q. So the EDSS score is a way of quantifying a
` patient's neurological function; is that fair?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: No.
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` BY MR. JAMES:
` Q. Okay. What's wrong with that?
` A. It's quantifying their neurological
` dysfunction.
` Q. Okay. And do I understand correctly that
` if the number gets higher in the quantification for
` EDSS, that the patient's dysfunction is worse, if
` you will?
` A. That's correct.
` Q. So a higher number is bad, so to speak?
` A. That's right.
` Q. All right. And is EDSS something that you
` measure in treating your patients?
` A. Yes.
` Q. So an increase in EDSS score means that the
` therapy that you are using in a patient is not
` maintaining their disease; is that correct?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: No. I think that's an
` oversimplification.
` BY MR. JAMES:
` Q. Okay. Would it be fair to say that an
` increase in the EDSS score means that the patient's
` dysfunction is increasing?
` MR. ANSTAETT: Objection to form.
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`207
` THE WITNESS: No. Because the EDSS is well
` known to be highly subjective. So it depends on
` who's making the assessment, whether or not they're
` appropriately trained and whether or not you have
` different observers making the assessment.
` In general, same observer, same patient,
` you would think that an increase in the EDSS
` generally is a sign of worsening of disease. But it
` still has to be qualified by the fact that with
` small changes in EDSS, even with the same observer,
` sometimes it's just day-to-day variation for the
` patient.
` BY MR. JAMES:
` Q. If you're treating a patient for MS with
` whatever therapeutic agent that they happen to be on
` and their EDSS score is increasing, do you see that
` as a sign that the therapy is not working
` adequately?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: So it depends on what
` therapies we're talking about. So it depends on --
` because the principal basis of approval for
` medications from the FDA for MS treatments is based
` on relapse rate and not necessarily based on EDSS.
` So while, in general, I think the thing
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`208
`
` that you are saying is true, it is true that
` worsening EDSS would be seen as a sign of a patient
` having progression of disease, which would be seen
` as a potential sign that the therapy that they're on
` isn't working.
` The challenge is you have to think about
` the underlying biological basis of progression, and
` the biological basis of progression is not strictly
` based upon inflammatory disease per se. So there
` may be neurodegeneration, there may be things
` written in the cards before you initiated the
` therapy that progress onwards despite the fact that
` you're treating the patient with the therapy.
` BY MR. JAMES:
` Q. Copaxone is injected subcutaneously;
` correct?
` A. Yes.
` Q. And after it's injected into the
` subcutaneous tissue, the polypeptide molecules are
` hydrolyzed in the subcutaneous tissue; right?
` A. So there's a literature that suggests that
` there's local hydrolysis of the polypeptides after
` injection -- after injection of the drug, yes.
` Q. And are there antigen-presenting cells in
` the subcutaneous tissue?
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`
` A. There are.
` Q. There are antigen-presenting cells in the
` lymph nodes?
` A. There are.
` Q. When the Copaxone is injected
` subcutaneously, it will elicit an immunological
` response in the patient; right?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: Yes.
` BY MR. JAMES:
` Q. And at least one of the immunological
` responses that it elicits will be a T-cell response;
` right?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: As far as we understand the
` mechanism of action of the drug. It still has to be
` clarified that the mechanism of action of the drug
` is far from settled.
` BY MR. JAMES:
` Q. Okay. I hear that.
` But at least one of the theories of the
` mechanism of action of Copaxone is that it will
` elicit a T-cell response in patients; right?
` A. Yes.
` Q. Now, because the drug is thought to be
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`210
`
` hydrolyzed in the subcutaneous tissues, we don't
` know precisely what is presented to the
` antigen-presenting cells; correct?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: Yes.
` BY MR. JAMES:
` Q. It could be that it's intact polypeptide
` molecules; right?
` A. Yes.
` Q. It could also be that it is fragments of
` the polypeptides?
` A. Yes.
` Q. But whatever it is, whether it's a fragment
` of the molecules or the molecules themselves,
` they're taken up by these antigen-presenting cells
` in the subcutaneous tissue or the lymph node and
` presented to T-cells; right?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: No. Not necessarily. So an
` argument has been made that they directly interact
` with the MHC Class II molecule without necessarily
` needing to be processed by antigen-presenting cells.
` BY MR. JAMES:
` Q. Do we know for sure whether they are
` processed by antigen-presenting cells or not?
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` MR. ANSTAETT: Objection to form.
` THE WITNESS: We don't. The argument
` against the notion that they wouldn't need to --
` they wouldn't need to be processed by
` antigen-presenting cells is that if you give a
` dextroversion of the drug, so you give a drug in
` which the chirality of the molecule is reversed, so
` dextro GA, although it seems to -- it seems to still
` bind to the MHC class II, it doesn't seem to
` suppress the AE.
` So that would be an argument that, in fact,
` the antigen-presenting cells probably have to
` process GA. But it's still not clear, because it
` could still be that GA is acting on other cells
` without necessarily needing to be processed as
` antigen. So none of the mechanisms are conclusive
` about exactly how the molecules are processed or
` taken up or where they're processed or taken up.
` BY MR. JAMES:
` Q. But there's some evidence that the
` glatiramer acetate molecules are taken up and
` processed by antigen-presenting cells; correct?
` MR. ANSTAETT: Objection. Form.
` THE WITNESS: When you say "some evidence,"
` it just seems rather loose. It might help me if
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` you'd characterize for me what type of evidence
` you're asking me about. Are you asking me about
` animal evidence? Are you asking me about human
` evidence?
` BY MR. JAMES:
` Q. I think you just recited some evidence to
` that effect; right? The dextro --
` A. GA.
` Q. -- GA testing; correct?
` A. Sure. That's done in animals. So we
` understand some of the immunological effects of GA
` in animals. The way in which we understand the --
` the effect in humans is largely based on clinical
` research.
` Q. To the extent that antigen-presenting cells
` present these antigens to T-cells, which is,
` again -- well, let me strike that and say there --
` there is a theory of the mechanism of action of GA
` that antigen-presenting cells do present GA
` molecules or their fragments to T-cells; correct?
` A. Yes.
` Q. And in that presentation process, the
` T-cells are activated; is that right?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: They have a response. I'm
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`213
` not sure -- the word "activated" is a loaded word in
` that context.
` BY MR. JAMES:
` Q. Well, in your own words, then, what happens
` to those T-cells when they respond?
` A. So they may proliferate, so you may get a
` subclass of T-cells that recognizes that antigen
` that proliferates. You may have other changes in
` the cell in terms of releasing certain cytokines,
` and some of those -- the reason I'm giving pause to
` the use of the word "activation" is I would want to
` make sure we're talking about distinguishing between
` cells that are pro-inflammatory and cells that are
` anti-inflammatory.
` And so it's important to make that
` distinction. Some of those cells may have
` pro-inflammatory effect and some may have an
` anti-inflammatory effect.
` Q. Well, one of the theories behind the
` mechanism of action of glatiramer acetate is that
` the presentation of the glatiramer acetate molecules
` to the T-cells will actually influence the T-cells
` to be less inflammatory; correct?
` A. Yes.
` Q. And that is -- it's referred to as the
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`
` Th1-to-Th2 shift; correct?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: That's -- I think to create
` exact symmetry between those two is not correct. It
` is one of the potential ways in which T-cells may be
` having an anti-inflammatory effect is the switch
` from Th1 to Th2, but I don't think that Th1 to Th2
` switch would cover all the ways in which cells may
` be having an anti-inflammatory effect.
` BY MR. JAMES:
` Q. Okay. That's fair.
` Just so we're on the same page, can you
` explain what a Th1 cell is?
` A. Sure.
` So these are classes of lymphocytes that
` are CD4-positive, and Th1 cells are ones that are --
` the class of cells that are CD4-positive are thought
` of as helper T-cells. And these helper T-cells, at
` least canonically, have two major subtypes.
` Additional subtypes have been identified since
` earlier research was performed.
` But the Th1 subtype secretes cytokines that
` are thought of as pro-inflammatory. The Th2,
` sometimes in a simplistic fashion, are called
` anti-inflammatory, although they're -- more
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` accurately, they're involved in humoral immunity,
` which is spelled H-U-M-O-R-A-L.
` Q. What are these pro-inflammatory -- let me
` strike that.
` The Th1 cells and the Th2 cells both will
` release something called cytokines; right?
` A. Correct.
` Q. Cytokines are chemicals; is that right?
` A. Sure.
` Q. Okay. And Th1 cells release
` pro-inflammatory cytokines?
` A. Again, with the qualifications I said
` before, I think a qualified "yes."
` Q. Th2 cells, in general, are thought to
` release anti-inflammatory cytokines?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: With the same qualification,
` yes.
` BY MR. JAMES:
` Q. Can you tell me what the pro-inflammatory
` Th1 cytokines are?
` A. Well there's a number of them, but
` interferon gamma would be one. IL-4, IL-5. I think
` IL-6. These are interleukins.
` Q. And what are the anti-inflammatory
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` cytokines that are released by Th2 cells?
` A. TGF-beta. IL-10.
` Q. Any others?
` A. Yeah. I mean, there are other
` anti-inflammatory cytokines that -- off the top of
` my head, those are the ones I think of principally
` as the ones secreted by Th1 cells.
` Q. Now, when these -- let me strike that.
` When Th -- strike that.
` When a T-cell is activated -- I know you
` didn't like the term. I can't remember what the
` term was that you liked, but let's say activated for
` a moment -- by presentation of an antigen, are they
` able to cross the blood-brain barrier?
` A. Once activated?
` Q. Correct.
` A. Yes.
` Q. And they have to be activated in order to
` cross the blood-brain barrier; right?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: There's evidence to suggest
` that that is the case.
` BY MR. JAMES:
` Q. And the blood-brain barrier, just so the
` record is clear, is a structure that surrounds and
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` protects the central nervous system; right?
` A. It is not a structure. It's actually a set
` of different systems that help to provide the brain
` immune privilege, to prevent immune cells from just
` gaining free access to the central nervous system.
` Q. But it doesn't just protect the CNS from
` immune cells; right?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: Yes. It doesn't just protect
` from immune cells.
` BY MR. JAMES:
` Q. It has other functions besides that?
` A. It does, but not just -- it's not a
` structure. Right. There's multiple systems that
` make up the blood-brain barrier.
` Q. And the Th1 cells, are they found in a
` higher proportion in multiple sclerosis patients
` than in normal patients?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: Where? Maybe you should
` clarify, again, your question. Do you mean is there
` a -- is there a -- have people shown that patients
` with MS have some higher circulating levels of Th1
` cytokines? The answer is, yes.
` Have people looked at cell populations in
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` patients with MS and shown a shift over to Th1 in
` general? Yes.
` I think it's difficult to say at an
` individual level whether or not it's true that
` patients have a higher proportion of Th1 cells than
` Th2 cells or how the proportion is changed in
` patients who have MS.
` BY MR. JAMES:
` Q. But it would be true that MS patients
` demonstrate a higher level of Th1 cytokines;
` correct?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: Again, with the challenge
` being that experiments with cytokines are
` challenging. There is evidence to suggest that that
` is the case.
` BY MR. JAMES:
` Q. And is there evidence that Th1 cells -- let
` me strike that.
` Is there evidence that there's a higher
` proportion of Th1 cells in the central nervous
` system of MS patients than in normal patients?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: Yes.
` ///
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` BY MR. JAMES:
` Q. And is it thought that these higher levels
` of Th1 cells in the central nervous system are part
` of the cause of the inflammation seen with multiple
` sclerosis?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: Yes.
` BY MR. JAMES:
` Q. And does anybody know why MS patients have
` this higher proportion of inflammatory Th1 cells in
` their central nervous system?
` MR. ANSTAETT: Objection to form and
` foundation.
` THE WITNESS: There's a -- it's not really
` a "yes" or "no" question. The answer would be no
` one knows the principal cause of why there is an
` aberrant immune response in patients with MS.
` But the second part of your question would
` be why are they found in a higher proportion, I
` think was the word you used --
` BY MR. JAMES:
` Q. Yes.
` A. -- in the central nervous system. Well,
` that would be because, as I think we discussed a few
` moments ago, activated lymphocytes cross the
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` blood-brain barrier more readily than those that are
` not activated.
` Q. So in MS patients, their Th1 cells are
` activated and they cross in the central nervous
` system; is that right?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: It should be clarified that
` that's one of the predominant theories of
` pathogenesis of the disease.
` BY MR. JAMES:
` Q. Okay. Thank you.
` And do we know whether or not this
` increased level, I'll say, of Th1 cells that's found
` in the central nervous system of MS patients,
` whether that is a constant process? In other words,
` that there are these inflammatory Th1 cells that are
` created in the MS patients on a constant basis?
` MR. ANSTAETT: Objection to the form of the
` question.
` THE WITNESS: No.
` BY MR. JAMES:
` Q. "No" meaning we don't know?
` A. We don't know.
` Q. Okay. We just know that there is some
` evidence that there is a higher amount, proportion,
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` of Th1 cells in the central nervous system of MS
` patients than in normal people; right?
` MR. ANSTAETT: Objection to form.
` THE WITNESS: The principal challenge here
` is that making assessments in patients from within
` the brain is extraordinarily challenging. There's
` not pathology tissue at every stage of the disease
` to assess. And so most of our pathology is based on
` end-of-life samples that may look different
` immunologically than what the disease looks like in
` realtime, while the patient is suffering with the
` condition.
` BY MR. JAMES:
` Q. And what we know from animal studies;
` correct?
` A. Correct. With the caveats being that the
` animal studies often inform us about some features
` of the disease, but they are different in that
` they're not spontaneous, and they don't recapitulate
` all the features of the disease.
` Q. And in this theory of the mechanism of
` action of Copaxone that we've been talking about,
` with the proportion of Th1 cells versus the
` proportion of Th2 cells, there's thought to be this
` balance between inflammation, pro-inflammation and
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` anti-inflammatory effect, if you will; is that
` correct?
` MR. ANSTAETT: Objection to the form of the
` question.
` THE WITNESS: In what context?
` BY MR. JAMES:
` Q. In the mechanism of action in the
` glatiramer acetate.
` MR. ANSTAETT: Objection to form.
` THE WITNESS: I'm confused, because I
` thought we were talking about multiple sclerosis,
` and now you mentioned just GA. So maybe we can walk
` back and you can clarify which one you're talking
` about.
` BY MR. JAMES:
` Q. Right. We've been talking about -- let me
` strike that.
` One of the theories of the mechanism of
` action of glatiramer acetate is that glatiramer
` acetate will increase the number of
` anti-inflammatory Th2 cells; correct?
` A. Yes.
` Q. It will increase -- let me strike that.
` One of the theories is that it will
` increase the number of anti-inflammatory Th2 cells
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` that cross into the central nervous system and act
` on the inflammation of MS; correct?
` A. I'm sorry. Say that one more time for me.
` MR. JAMES: Can you read that back for me.
` (Record read as follows:
` "Q One of the theories is that it
` will increase the number of
` anti-inflammatory Th2 cells that cross into
` the central nervous system and act on the
` inflammation of MS; correct?")
` THE WITNESS: Yes. That's correct.
` BY MR. JAMES:
` Q. Under this theory, the mechanism by which
` glatiramer acetate would work would be that the
` inflammation of MS is counteracted by the Th2 cells
` that are present in the brain; right?
` MR. ANSTAETT: Object to the form.
` THE WITNESS: Yes.
` BY MR. JAMES:
` Q. 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?
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` MR. ANSTAETT: Objection to form.
` THE WITNE