IN THE UNITED STATES PATENT AND TRADEMARK OFFICE
`_____________________
`
`BEFORE THE PATENT TRIAL AND APPEAL BOARD
`_____________________
`
`
`PAR PHARMACEUTICAL, INC.,
`Petitioner,
`
`v.
`
`HORIZON THERAPEUTICS, LLC,
`Patent Owner.
`
`_____________________
`
`Case IPR2017-01767
`Patent 9,254,278
`_____________________
`
`REPLY DECLARATION OF NEAL SONDHEIMER, M.D., Ph.D.
`
`
`
`
`
`
`
`
`
`
`
`
`
`
`EXHIBIT 1028
`
`
`_____________________
`
`BEFORE THE PATENT TRIAL AND APPEAL BOARD
`_____________________
`
`
`PAR PHARMACEUTICAL, INC.,
`Petitioner,
`
`v.
`
`HORIZON THERAPEUTICS, LLC,
`Patent Owner.
`
`_____________________
`
`Case IPR2017-01767
`Patent 9,254,278
`_____________________
`
`REPLY DECLARATION OF NEAL SONDHEIMER, M.D., Ph.D.
`
`
`
`
`
`
`
`
`
`
`
`
`
`
`EXHIBIT 1028
`
`
`
`IPR2017-01767
`Patent No. 9,254,278
`Reply Declaration of Neal Sondheimer, M.D., Ph.D. (Exhibit 1028)
`TABLE OF CONTENTS
`Introduction ...................................................................................................... 1
` Qualifications ........................................................................................ 1
`
`Scope of Work ....................................................................................... 1
`The ’859 Publication Discloses All the Elements of Claims 1-3. ................... 2
` Ground 3 of Par’s Petition Renders the Challenged Claims
`Obvious. ........................................................................................................... 4
` A POSA Would Have Increased Drug Doses for
`Patients Having “Normal” Ammonia Levels. ....................................... 4
` A POSA Would Have Used Fasting Plasma Ammonia
`Levels to Determine Dosing .................................................................. 6
` Dr. Enns Exaggerates the Risk of Overdosing ...................................... 7
` Grounds 2 and 4 of Par’s Petition Renders the Challenged
`Claims Obvious. .............................................................................................. 9
`The Prior Art Does Not Teach Away from the Challenged
`Claims ............................................................................................................ 10
` Conclusion ..................................................................................................... 13
`
`
`
`
`
`
`
`i
`
`
`
`IPR2017-01767
`Patent No. 9,254,278
`Reply Declaration of Neal Sondheimer, M.D., Ph.D. (Exhibit 1028)
`I, Neal Sondheimer, do hereby declare as follows:
`
`
`
`INTRODUCTION
` Qualifications
`1. My background and qualifications are described in Section II of my
`
`initial declaration submitted in the proceeding on July 13, 2017 (“Initial
`
`Declaration”) (EX1002, ¶¶7-13). I incorporate those qualifications by reference
`
`here. I am being compensated as set forth in my Initial Declaration (EX1002, ¶2),
`
`and I continue to have no personal or financial interest in Par or in the outcome of
`
`this proceeding.
`
`
`2.
`
`Scope of Work
`For this declaration, I was asked to review and discuss the declaration
`
`of Dr. Gregory M. Enns (“the Enns Declaration”). (EX2006.) I have also
`
`reviewed Horizon’s Patent Owner Response (Paper 22) (“Horizon’s POR”).
`
`Nothing in the Enns Declaration or Horizon’s POR alters or changes my opinions
`
`set forth in my previous Declaration.
`
`3.
`
`This declaration is a statement of my additional opinions in this matter
`
`and the basis and reasons for those opinions. In forming the opinions expressed in
`
`this declaration, I have relied upon my education, experience, and knowledge of
`
`the subject matter discussed. In addition to my Initial Declaration and the
`
`materials identified therein, I have also reviewed, considered, or relied upon
`
`documents and other materials, which are cited in the table below:
`
`1
`
`
`
`IPR2017-01767
`Patent No. 9,254,278
`Reply Declaration of Neal Sondheimer, M.D., Ph.D. (Exhibit 1028)
`
`Exhibit
`No.
`2012
`
`2013
`
`2015
`
`2018
`
`2019
`
`2025
`
`2031
`
`2032
`
`2046
`
`Description
`
`U.S. Patent Publication No. 2012/0022157, filed August 27, 2009,
`published January 26, 2012
`Tuchman & Batshaw, Management of Inherited Disorders of
`Ureagenesis, 12 The Endocrinologist 99–109 (2002). (“Tuchman”).
`Broomfield & Grunewald, How to Use Serum Ammonia, 97 Arch.
`Dis. Child Educ. Pract. Ed. 72-77 (2011)
`Kasumov et al., New Secondary Metabolites of Phenylbutyrate in
`Humans and Rats, 32 Drug Metabolism and Disposition 10-19
`(2004)
`Häberle et al., Suggested Guidelines for the Diagnosis and
`Management of Urea Cycle Disorders, 7 Orphanet J. Rare Diseases
`1-30 (2012)
`Colloquium, Consensus Statement from a Conference for the
`Management of Patients with Urea Cycle Disorders, 138 J.
`Pediatrics S1-S5 (2001)
`Cheson et al., Novel Therapeutic Agents for the Treatment of
`Myelodysplastic Syndromes, 27 Seminars in Oncology 560-77 (John
`W. Yarbro, et al. eds., 2000)
`Scaglia et al., Effect of Alternative Pathway Therapy on Branched
`Chain Amino Acid Metabolism in Urea Cycle Disorder Patients, 81
`Molecular Genetics and Metabolism, Supplement 1 S79-S85 (2004)
`Transcript of the Deposition of Dr. Neal Sondheimer, taken April
`19, 2018
`
`
`
`THE ’859 PUBLICATION DISCLOSES
`ALL THE ELEMENTS OF CLAIMS 1-3.
`4.
`Horizon claims that “a [person of ordinary skill in the art (“POSA”)]
`
`would not understand Example 3 to disclose that patient 1006 received an amount
`
`of GPB sufficient to produce a fasting plasma ammonia level that is necessarily
`
`less than half the ULN.” (Paper 22 at 60.) Horizon states this is because “a POSA
`
`2
`
`
`
`IPR2017-01767
`Patent No. 9,254,278
`Reply Declaration of Neal Sondheimer, M.D., Ph.D. (Exhibit 1028)
`would not assume [the fasting plasma ammonia level] was necessarily the lowest,”
`
`and therefore, lower than 8.30µmol/L. (Id. at 62.) I disagree.
`
`5.
`
`Example 3 of the ’859 Publication discloses that Subject 1006 had a
`
`maximum plasma concentration, i.e., Cmax, for the plasma ammonia level of
`
`13µmol/L. (EX1004, [0201].) The ’859 Publication reports that the ULN for the
`
`study sites in Example 3 was 26-35µmol/L. (Id.) One-half ULN would be in the
`
`range of 13-17.5µmol/L. The maximum plasma ammonia level of Subject 1006,
`
`therefore, was the same as the lowest end of the one-half ULN range, i.e.,
`
`13µmol/L. As a result of Subject 1006’s maximum plasma ammonia level being
`
`13µmol/L, at every other time point, Subject 1006 had to have had a plasma
`
`ammonia level lower than one-half ULN.
`
`6.
`
`Further, the time-normalized area under the curve (“TN-AUC”)
`
`provides an AUC value that is normalized based on values obtained from
`
`measurements taken at various points in a 24-hour period. A POSA, therefore,
`
`would have easily understood that the only way Subject 1006’s TN-AUC can be
`
`8.30µmol/L with a Cmax of 13µmol/L, is if there were plasma ammonia levels that
`
`were measured to be lower than 8.30µmol/L.
`
`7.
`
`Given that the fasting plasma ammonia level would have been one of
`
`the lowest measurements in the day and Subject 1006 had a maximum plasma
`
`ammonia level at one-half the lowest end of the ULN range, i.e., 13µmol/L, the
`
`3
`
`
`
`IPR2017-01767
`Patent No. 9,254,278
`Reply Declaration of Neal Sondheimer, M.D., Ph.D. (Exhibit 1028)
`’859 Publication discloses administering glycerol phenylbutyrate (“GPB”) to a
`
`UCD patient in an amount sufficient to produce a fasting plasma ammonia level
`
`that is less than half the ULN.
`
` GROUND 3 OF PAR’S PETITION
`RENDERS THE CHALLENGED CLAIMS OBVIOUS.
`8.
`From my review of the Enns Declaration and Horizon’s POR, I
`
`understand Horizon to only argue that the prior art does not teach (1) adjusting
`
`doses in patients who have plasma ammonia levels between one-half the ULN and
`
`the ULN; and (2) using “fasting” plasma ammonia levels in making decisions
`
`about drug dosing, with respect to Horizon’s challenge to Ground 3 of Par’s
`
`Petition. I disagree.
`
` A POSA Would Have Increased Drug Doses
`for Patients Having “Normal” Ammonia Levels.
`Dr. Enns states “Fernandes only suggests that plasma ammonia levels
`
`9.
`
`at emergency levels (i.e., >120 μmol/L) warrant dosage increases.” (EX2006,
`
`¶68.) And he states that “Fernandes defines the normal range for plasma ammonia
`
`as <50 μmol/L,” not the <80µmol/L presented in Fernandes’s Figure 17.2. (Id. at
`
`¶66.) But as I stated in my Initial Declaration, Fernandes clearly advises
`
`increasing the dosage of medication in patients with plasma ammonia levels
`
`<80µmol/L. (EX1002, ¶73.) And while Fernandes discloses 50μmol/L as one
`
`ULN, Fernandes also expressly discloses that “[h]ealthy neonates have slightly
`
`4
`
`
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`IPR2017-01767
`Patent No. 9,254,278
`Reply Declaration of Neal Sondheimer, M.D., Ph.D. (Exhibit 1028)
`higher values.” (EX1015, 217-18.) To that end, Blau describes hyperammonemia
`
`as being “plasma ammonia >80 in newborns or >50 µmol/L after 28 days
`
`postnatally.” (EX1006, 5.) A POSA would understand that 80µmol/L in Figure
`
`17.2, therefore, is a reasonable ULN for some UCD patients, for example,
`
`newborns.
`
`10. Fernandes’s Figure 17.2 is reproduced below with a red box
`
`highlighting the branch of the treatment protocol for patients having a “normal”
`
`plasma ammonia:
`
`
`
`(EX1015, Fig. 17.2 (annotated).) Fernandes teaches in Figure 17.2 that in patients
`
`with plasma ammonia levels <80µmol/L, and in consideration of biomarkers such
`
`as plasma glutamine and essential amino acids (“EAAs”), medicine doses should
`
`5
`
`
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`IPR2017-01767
`Patent No. 9,254,278
`Reply Declaration of Neal Sondheimer, M.D., Ph.D. (Exhibit 1028)
`be increased. Fernandes expressly shows, therefore, that patients with plasma
`
`ammonia levels below the ULN may require an increased dosage of nitrogen
`
`scavenging drug.
`
` A POSA Would Have Used Fasting
`Plasma Ammonia Levels to Determine Dosing.
`11. As I noted in my Initial Declaration, Fernandes teaches that protein
`
`intake affects plasma ammonia levels. (EX1002, ¶68.) Likewise, the
`
`’859 Publication teaches that dietary protein affects plasma ammonia levels.
`
`(EX1004, [0003].) Also as I noted in my Initial Declaration, Blau, Simell, and Lee
`
`each describes measuring fasting plasma ammonia levels. (EX1002, ¶¶76-77, 79.)
`
`12.
`
`In view of these disclosures, I stated in my Initial Declaration that a
`
`POSA would have known that fasting plasma ammonia levels should be used to
`
`avoid the variability in ammonia levels that were caused by food and other daily
`
`activities. (EX1002, ¶¶106, 109-110, 112.) Dr. Enns’s and Horizon’s arguments
`
`that the prior art does not teach using fasting plasma ammonia levels do not change
`
`my opinion.
`
`13. For instance, as I noted in my Initial Declaration, Lee teaches that
`
`only 27.0% of ammonia values exceeded ULN while patients were taking GPB, in
`
`contrast to 39.6% while on PBA. (EX1002, ¶¶115-116; EX1010, 224.) Lee states
`
`that “[t]hese differences were attributable to lower ‘overnight’ ammonia levels
`
`(12-24 h)....” (EX1002, ¶116; EX1010, 224 (emphasis added).)
`
`6
`
`
`
`IPR2017-01767
`Patent No. 9,254,278
`Reply Declaration of Neal Sondheimer, M.D., Ph.D. (Exhibit 1028)
`I also disagree with Dr. Enns’s and Horizon’s argument that fasting
`
`14.
`
`ammonia levels are not the lowest during the day, because, in Lee’s Figure 2, the
`
`plasma ammonia value at t=30 minutes is lower than at t=0 minutes. (EX2006,
`
`¶122; Paper 22 at 41-42.) Dr. Enns and Horizon ignore that protein is not
`
`instantaneously absorbed and metabolized such that there is a lag before dietary
`
`protein is reflected in the body as plasma ammonia. I explained as much during
`
`my deposition by explaining that there is a bioavailability issue that explains the
`
`lag after eating before plasma ammonia levels begin to rise. (EX2046, 49:18-
`
`50:8.) Furthermore, the lowest plasma ammonia level occurs at t=24 hours, which
`
`is a fasting plasma ammonia level. (Id.)
`
`15.
`
`In sum, Dr. Enns’s testimony about the prior art does not change my
`
`conclusions regarding the ’278 patent claims. Therefore, it remains my opinion
`
`that a POSA would have successfully arrived at a method of treating a UCD using
`
`the claimed methods.
`
` Dr. Enns Exaggerates the Risk of Overdosing.
`16. Dr. Enns claims that a POSA “would have been reluctant to
`
`[administer an initial dose or] increase the dosage of nitrogen scavengers when a
`
`patient already had a normal fasting plasma ammonia level due to concerns about
`
`the potentially harmful effects of over-treatment.” (EX2006, ¶104; Paper 22 at 32-
`
`33.) I disagree.
`
`7
`
`
`
`IPR2017-01767
`Patent No. 9,254,278
`Reply Declaration of Neal Sondheimer, M.D., Ph.D. (Exhibit 1028)
`17. First, Dr. Enns relies on adverse events that occurred with drugs other
`
`than GPB. (See EX1006, 262 (phenylbutyrate); EX2013, 105 (phenylacetate,
`
`phenylbutyrate); EX2018, 10 (phenylbutyrate); EX2019, Table 4 (phenylacetate,
`
`phenylbutyrate); EX2031, 564 (phenylbutyrate); EX2032, S79 (phenylacetate and
`
`phenylbutyrate).) GPB (also known as HPN-100) was well-known to be better
`
`tolerated than the drugs on which Dr. Enns relies. (EX1004, [0086].)
`
`18. Second, I understand the challenged claims to encompass
`
`administering any amount of initial dosage or adjusted dosage. Consequently, Dr.
`
`Enns ignores that an increase in dose may not cause the concerns he espouses.
`
`Additionally, if a patient’s treatment is initiated with a dose of GPB below the
`
`maximum recommended dose, an increased dose would remain within the range of
`
`FDA-approved dosing for safety and efficacy.
`
`19. For example, in Lee, “8 of 10 patients were being prescribed lower
`
`NaPBA doses than currently recommended in the approved product labeling.”
`
`(EX1010, 226.) These patients could receive an increase in dosing – indeed, Lee
`
`recommended doing so (id.) – and still remain within the approved dosing range.
`
`None of these are relevant to or would constitute a “massive over-dosage,” as
`
`described by Dr. Enns (EX.2006, ¶104).
`
`8
`
`
`
`IPR2017-01767
`Patent No. 9,254,278
`Reply Declaration of Neal Sondheimer, M.D., Ph.D. (Exhibit 1028)
` GROUNDS 2 AND 4 OF PAR’S PETITION
`RENDERS THE CHALLENGED CLAIMS OBVIOUS.
`20. Horizon argues that the prior art is “completely silent” regarding “any
`
`particular ammonia level within the normal range let alone the claimed target.”
`
`(Paper 22 at 51.) I disagree.
`
`21. The ’859 Publication reports that “a plasma ammonia level of less
`
`than about 40 µmol/L, or of not greater than 35 µmol/L would indicate the
`
`treatment was effective.” (EX1004, [0074].) Likewise, Fernandes discloses that
`
`“[t]he aim [of treatment] is to keep plasma ammonia levels below 80 µmol/l....”
`
`(EX1015, 219.) The prior art, therefore, repeatedly teaches that maintaining
`
`plasma ammonia levels below the ULN is desirable.
`
`22. Further, a POSA would have understood from the teachings of the
`
`’859 Publication and Lichter-Konecki that further improvements in plasma
`
`ammonia control were still possible for patients having “normal” fasted plasma
`
`ammonia levels. For instance, Lichter-Konecki notes GPB’s non-inferiority
`
`compared to NaPBA because it decreased the frequency of excursions above ULN.
`
`(EX1017, 326.) Lichter-Konecki, then, states that “further studies, including
`
`longer-term studies of safety and ammonia control, are warranted.” (Id. at 329.)
`
`And the ’859 Publication states that “the mean percentage of normal ammonia
`
`values increased from 58% after sodium PBA treatment to 83% after HPN-100
`
`treatment.... Based on preliminary results, HPN-100 also provides more stable
`
`9
`
`
`
`IPR2017-01767
`Patent No. 9,254,278
`Reply Declaration of Neal Sondheimer, M.D., Ph.D. (Exhibit 1028)
`ammonia levels, and reduces risk of hyperammonemia.” (EX1004, [0201-0202].)
`
`Consequently, a POSA would have understood that getting fasted plasma ammonia
`
`levels in the normal range would have been significant, as well as decreasing the
`
`frequency at which patients’ plasma ammonia levels exceeded ULN.
`
`
`
`THE PRIOR ART DOES NOT TEACH
`AWAY FROM THE CHALLENGED CLAIMS.
`23.
`I understand that the prior art is considered to teach away from the
`
`claimed invention when a POSA, upon reading the reference, would be
`
`discouraged from following the path set out in the reference, or would be led in a
`
`direction divergent from the path that was taken by the patentee.
`
`24. Horizon and Dr. Enns allege that a POSA would be discouraged from
`
`relying on normal plasma ammonia levels to make dosage adjustments because of
`
`the known variability in ammonia levels. (Paper 22 at 35-40; EX2006, ¶¶106-
`
`117.) I have reviewed the references cited by Horizon and Dr. Enns and do not
`
`find them to discourage using normal plasma ammonia levels to make dose
`
`adjustments.
`
`25. Specifically, Fernandes expressly asserts that “[a]ll treatment must be
`
`monitored with regular quantitative estimation of plasma ammonia....” (EX1015,
`
`219.) Fernandes further states that “[t]he most important diagnostic test in urea
`
`cycle disorders is measurement of the plasma ammonia concentration.” (Id., 217.)
`
`10
`
`
`
`IPR2017-01767
`Patent No. 9,254,278
`Reply Declaration of Neal Sondheimer, M.D., Ph.D. (Exhibit 1028)
`26. Lee reports that “[c]ontrol of blood ammonia levels is the main
`
`objective of both acute and chronic management of UCD patients.” (EX1010,
`
`222.)
`
`27. Similarly, the ’859 Publication discloses a method having the step of
`
`“measuring blood ammonia to determine if the initial dosage is sufficient to control
`
`blood ammonia levels, or to establish a suitable average ammonia level,” and then
`
`“adjusting the initial dosage of the new drug as needed.” (EX1004, [0095-0099];
`
`see also id., [0088-0091].)
`
`28. Häberle teaches that “[l]aboratory monitoring must include plasma
`
`ammonia determination in venous samples....” (EX2019, 18.)
`
`29. Barsotti emphasizes a need for better methods of measuring ammonia
`
`levels, stating that
`
`[a]lternative methods are still sought that are noninvasive
`or require a small catheter in a peripheral vein but provide
`a continuous monitor of blood ammonia levels. Such
`methods could alert medical staff to an impending
`hyperammonemic condition and would more easily permit
`earlier
`selection
`and
`regulation
`of
`therapeutic
`interventions.
` Two promising methods…are under
`development....
`(EX1022, S15.) Barsotti’s “Consensus Statement” proposes that “[b]oth the
`
`plasma ammonia level and the clinical picture should be considered when choosing
`
`therapy” and “[a]n elevated ammonia level during a clinic visit in a patient without
`
`symptoms, however, does require adjustment of therapy or better compliance with
`
`11
`
`
`
`IPR2017-01767
`Patent No. 9,254,278
`Reply Declaration of Neal Sondheimer, M.D., Ph.D. (Exhibit 1028)
`the recommended treatment regimen.” (EX2025, S3.) Barsotti notes only that
`
`“certain centers” are moving away from using plasma ammonia (EX1022, S19),
`
`but still describes the continuing importance of plasma ammonia levels.
`
`30. While Blau and Broomfield do not specifically discuss drug dosing,
`
`they also note the importance of plasma ammonia levels. Broomfield discloses
`
`that “[p]lasma ammonia can be used both as part of diagnostic investigations and
`
`for monitoring of efficacy of treatment….” (EX2015, 73-75.) Blau provides
`
`information on the proper condition for obtaining plasma ammonia levels
`
`(EX1006, 268.) and notes the need for “frequent monitoring during treatment.”
`
`(Id., 262.)
`
`31.
`
`I also disagree that the ’157 Publication discourages reliance on
`
`plasma ammonia levels. Indeed, the ’157 Publication discloses an embodiment
`
`which includes the step of “adjusting dietary protein and/or drug dosage as
`
`appropriate based upon measurement of blood ammonia….” (EX2012, [0134-
`
`0137]; see also id., [0127-0131].) The ’157 Publication also has claims directed to
`
`improved plasma ammonia control (e.g., claims 19 and 29). (EX2012, 47-48.)
`
`32. While Lichter-Konecki states “that random values for blood ammonia
`
`are of limited utility,” it goes on to immediately state that “ammonia values should
`
`be drawn at a constant time in relation to meals and medication for monitoring of
`
`treatment.” (EX1017, 328.)
`
`12
`
`
`
`IPR2017-01767
`Patent No. 9,254,278
`Reply Declaration of Neal Sondheimer, M.D., Ph.D. (Exhibit 1028)
`33. Likewise, Lee notes that variability in plasma ammonia levels over
`
`the course of a day but also recognizes the “clinical importance” of plasma
`
`ammonia levels. (EX1010, 226.) Further, while Lee states using urinary PAGN is
`
`still “preliminary” and “deserves further exploration,” it does not disclose that it is
`
`a replacement for plasma ammonia levels. (Id., 226-27.)
`
`34.
`
`In sum, I do not consider the prior art to teach away from using
`
`plasma ammonia for making decisions about dosing nitrogen scavenging drugs,
`
`like GPB.
`
` CONCLUSION
`35.
`In sum, Dr. Enns’s testimony about the prior art does not change my
`
`conclusions regarding the ’278 patent claims based on the discussion above and in
`
`my Initial Declaration. Therefore, it remains my conclusion that a POSA would
`
`have successfully arrived at a method of treating a UCD using the claimed methods
`
`and that claims 1-3 are anticipated by the ’859 Publication.
`
`13
`
`
`
`IPR2017-01767
`Patent No. 9,254,278
`Reply Declaration of Neal Sondheimer, M.D., Ph.D. (Exhibit 1028)
`I hereby declare that all statements made herein of my own knowledge are
`
`true and that all statements made on information and belief are believed to be true;
`
`and further that these statements were made with the knowledge that willful false
`
`statements and the like so made are punishable by fine or imprisonment, or both,
`
`under Section 1001 of the Title 18 of the United States Code.
`
`
`
`Dated: August 15, 2018
`
`
`
`
`
`
`
`
`
`
`By: __________________________
`
` Dr. Neal Sondheimer, M.D., Ph.D.
`
`
`
`
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