Trials@uspto.gov
`571-272-7822
`
`
`
`
`
`Paper No. 11
`
` Entered: July 28, 2016
`
`UNITED STATES PATENT AND TRADEMARK OFFICE
`____________
`
`BEFORE THE PATENT TRIAL AND APPEAL BOARD
`____________
`
`AMNEAL PHARMACEUTICALS LLC,
`Petitioner,
`
`v.
`
`JAZZ PHARMACEUTICALS IRELAND LTD. and
`JAZZ PHARMACEUTICALS, INC.,
`Patent Owner.
`____________
`
`Case IPR2016-00546
`Patent 8,772,306 B1
`____________
`
`
`
`Before ERICA A. FRANKLIN, SUSAN L. C. MITCHELL, and
`CHRISTOPHER G. PAULRAJ, Administrative Patent Judges.
`
`PAULRAJ, Administrative Patent Judge.
`
`DECISION
`Denying Institution of Inter Partes Review
`37 C.F.R. § 42.108
`
`
`
`
`
`
`
`571-272-7822
`
`
`
`
`
`Paper No. 11
`
` Entered: July 28, 2016
`
`UNITED STATES PATENT AND TRADEMARK OFFICE
`____________
`
`BEFORE THE PATENT TRIAL AND APPEAL BOARD
`____________
`
`AMNEAL PHARMACEUTICALS LLC,
`Petitioner,
`
`v.
`
`JAZZ PHARMACEUTICALS IRELAND LTD. and
`JAZZ PHARMACEUTICALS, INC.,
`Patent Owner.
`____________
`
`Case IPR2016-00546
`Patent 8,772,306 B1
`____________
`
`
`
`Before ERICA A. FRANKLIN, SUSAN L. C. MITCHELL, and
`CHRISTOPHER G. PAULRAJ, Administrative Patent Judges.
`
`PAULRAJ, Administrative Patent Judge.
`
`DECISION
`Denying Institution of Inter Partes Review
`37 C.F.R. § 42.108
`
`
`
`
`
`
`
`
`IPR2016-00546
`Patent 8,772,306 B1
`
`I.
`
`INTRODUCTION
`Amneal Pharmaceuticals LLC (“Petitioner”) filed a Petition (Paper 1,
`“Pet.”), requesting institution of an inter partes review of claims 1–34 of
`U.S. Patent No 8,772,306 B1 (Ex. 1001, “the ’306 patent”). Jazz
`Pharmaceuticals Ireland Ltd. and Jazz Pharmaceuticals, Inc. (collectively,
`“Patent Owner”) timely filed a Preliminary Response (Paper 10,
`“Prelim. Resp.”). We have jurisdiction under 35 U.S.C. § 314, which
`provides that an inter partes review may not be instituted “unless . . . there is
`a reasonable likelihood that the petitioner would prevail with respect to at
`least 1 of the claims challenged in the petition.”
`Upon consideration of the Petition and the Preliminary Response, and
`for the reasons explained below, we determine Petitioner has not shown a
`reasonable likelihood that it would prevail with respect to any of the
`challenged claims. We, therefore, decline to institute an inter partes review
`of claims 1–34 of the ’306 patent.
`
`A. Related Proceedings
`The parties have identified the following related litigation proceedings
`involving the ’306 patent: Jazz Pharmaceuticals, Inc. v. Amneal
`Pharmaceuticals, LLC, No. 2:13-cv-391 (D.N.J.); Jazz Pharmaceuticals,
`Inc. v. Roxane Laboratories, Inc., No. 2:15-cv-1360 (D.N.J.); Jazz
`Pharmaceuticals, Inc. v. Wockhardt Bio AG, No. 2:15-cv-5619 (D.N.J.); and
`Jazz Pharmaceuticals, Inc. v. Lupin Ltd., No. 2:15-cv-6548 (D.N.J.). Pet.
`58–59; Paper 8. The parties have also identified other cases, including Jazz
`Pharmaceuticals, Inc. v. Amneal Pharmaceuticals, LLC, No. 2:15-cv-6562
`(D.N.J.) and Jazz Pharmaceuticals, Inc. v. Par Pharmaceutical, Inc., No.
`
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`2
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`2:15-cv-7580 (D.N.J.), concerning a patent related to the ’306 patent. Pet.
`59; Paper 8.
`In addition, the ’306 patent was also the subject of petitions for inter
`partes review filed by Ranbaxy Inc. (IPR2016-00024) and Par
`Pharmaceutical, Inc. (IPR2016-00002). We denied institution in IPR2016-
`00002. See Par Pharm., Inc. v. Jazz Pharm. Ireland Ltd., Case IPR2016-
`00002, Decision, Denying Institution of Inter Partes Review (Paper 12)
`(PTAB Apr. 12, 2016). We instituted an inter partes review in IPR2016-
`00024 on limited grounds, but that proceeding was terminated due to
`settlement before we reached a final decision on the merits. See Ranbaxy
`Inc. v. Jazz Pharm., Inc., Case IPR2016-00024, Decision, Institution of Inter
`Partes Review (Paper 10) (PTAB Apr. 12, 2016); Order, Termination of the
`Proceeding (Paper 15) (PTAB May 23, 2016).
`B.
`The ’306 Patent (Ex. 1001)
`The ’306 patent issued on July 8, 2014, and claims a priority date as
`early as March 1, 2013. See Ex. 1001, Title Page. It names Mark Eller as
`the sole inventor. Id.
`The ’306 patent relates generally to methods for improving the safety
`and efficacy of the administration of gamma-hydroxybutyrate (“GHB”) or a
`salt thereof to a patient. Id., Abstract. More specifically, the ’306 patent is
`concerned with treating patients suffering from certain disorders such as
`cataplexy or narcolepsy, who are concomitantly receiving treatment with
`valproate, with a reduced dose of GHB. Id. at 1:15–36. The specification
`states that valproate can increase or prolong the effects of GHB, resulting in
`unsafe conditions such as excessive daytime sleepiness. Id. at 17:49–62. In
`
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`Patent 8,772,306 B1
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`certain embodiments, the reduced amount of GHB ranges from 1% to 50%
`of the effective dose normally given to the patient. Id. at 1:32–36.
`C. Illustrative Claims
`Petitioner challenges claims 1–34 of the ’306 patent. All of the
`challenged claims are directed to methods of treating certain sleep disorders
`by orally administering a reduced dosage of GHB to patients who are
`concomitantly receiving valproate.
`Claims 1, 11, 19, 30, and 33 are independent. Independent claim 1 is
`illustrative, and reproduced below:
`
`1. A method for treating a patient who is suffering from
`excessive daytime sleepiness, cataplexy, sleep paralysis, apnea,
`narcolepsy, sleep time disturbances, hypnagogic hallucinations,
`sleep arousal, insomnia, or nocturnal myoclonus with gamma-
`hydroxybutyrate (GHB) or a salt thereof, said method
`comprising:
`orally administering to the patient in need of treatment at
`least 5% decrease in an effective dosage amount of the
`GHB or salt thereof when the patient is receiving a
`concomitant administration of valproate, an acid, salt, or
`mixture thereof.
`Independent claims 11, 19, 30, and 33 also require either administering or
`recommending a reduced dose of GHB to a patient who is taking valproate.
`Petitioner treats all independent claims similarly under each ground asserted
`in the Petition.
`
`D. The Asserted Grounds of Unpatentability
`Petitioner challenges the patentability of the claims of the ’306 patent
`on the following grounds:
`
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`
`References
`Xyrem Label,1 Hechler,2
`Shinka,3 and Depakote Label,4
`Xyrem Label, Hechler, Shinka,
`Cagnin,5 and Depakote Label
`Xyrem Label, Hechler, Shinka,
`Depakote Label, and Kaufman6
`Xyrem Label, Hechler, Shinka,
`Depakote Label, Cagnin, and
`Kaufman
`
`
`
`
`Basis
`§ 103(a)
`
`Claims challenged
`1–34
`
`§ 103(a)
`
`1–34
`
`§ 103(a)
`
`6, 17, 27
`
`§ 103(a)
`
`6, 17, 27
`
`
`1 Jazz Pharm., Inc., NDA 21-196/S-005, FDA Approved Labeling Text Dated
`11/18/05 (2005) (Ex. 1005).
`2 Viviane Hechler et al., γ-Hydroxybutyrate Conversion into GABA Induces
`Displacement of GABAB Binding That Is Blocked by Valproate and
`Ethosuximide, 281 J. Pharmacology & Experimental Therapeutics 753
`(1997) (Ex. 1006).
`3 Toshihiro Shinka et al., Effect of Valproic Acid on the Urinary Metabolic
`Profile of a Patient with Succinic Semialdehyde Dehydrogenase Deficiency,
`792 J. Chromatography 99 (2003) (Ex. 1007).
`4 Abbott Labs., NDA 018723/S-037/S-040/S-043/S-045/S-046, Depakote
`(Divalproex Sodium) Tablets for Oral Use, FDA Approved Labeling Text
`Dated October 7, 2011 (2011) (Ex. 1009).
`5 Annachiara Cagnin et al., γ-Hydroxybutyric Acid-Induced Psychosis and
`Seizures, 21 Epilepsy & Behav. 203 (2011) (Ex. 1008).
`6 Elaine E. Kaufman & Thomas Nelson, An Overview of γ-Hydroxybutyrate
`Catabolism: The Role of the Cytosolic NADP+-Dependent Oxidoreductase
`EC 1.1.1.19 and of a Mitochondrial Hydroxyacid-Oxoacid
`Transhydrogenase in the Initial, Rate-Limiting Step in This Pathway, 16
`Neurochemical Res. 965 (1991) (Ex. 1015).
`
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`IPR2016-00546
`Patent 8,772,306 B1
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`II. DISCUSSION
`A. Claim Construction
`We interpret claims using the “broadest reasonable construction in
`light of the specification of the patent in which [they] appear[].” 37 C.F.R.
`§ 42.100(b); see also Cuozzo Speed Techs., LLC v. Lee, 136 S. Ct. 2131,
`2142 (2016) (affirming applicability of broadest reasonable construction
`standard to inter partes review proceedings).
`We determine that no explicit construction of any claim term is
`necessary to determine whether to institute a trial in this case. See, e.g.,
`Wellman, Inc. v. Eastman Chem. Co., 642 F.3d 1355, 1361 (Fed. Cir. 2011)
`(“[C]laim terms need only be construed ‘to the extent necessary to resolve
`the controversy.’” (quoting Vivid Techs., Inc. v. Am. Sci. & Eng’g, Inc.,
`200 F.3d 795, 803 (Fed. Cir. 1999))).
`
`B. Prior Art Relied Upon
`Petitioner relies upon the following prior art in its challenges.
`1. Xyrem Label (Ex. 1005)
`The Xyrem Label discloses the prescribing information for an oral
`administration of sodium oxybate (i.e., a GHB salt), a central nervous
`system depressant for treating excessive daytime sleepiness and cataplexy.
`Ex. 1005, 1, 7. According to the Xyrem Label, the “dose of Xyrem should
`be titrated to effect.” Id. at 22. The Xyrem Label recommends a starting
`dose of sodium oxybate of 4.5 g/night, divided into two equal doses of 2.25
`g. Id. at 22–23. The Xyrem Label also recommends increasing the dosage
`to a maximum of 9 g/night in increments of 1.5 g/night (0.75 g per dose),
`and further discloses that the effective dose range is 6 to 9 g/night. Id. at 23.
`
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`
`The Xyrem Label includes a black box warning on the first page that
`the drug “[s]hould not be used with alcohol or other CNS depressants.” Id.
`at 1. Additionally, the Xyrem Label indicates that “[s]odium oxybate is
`contraindicated in patients with succinic semialdehyde dehydrogenase
`[SSADH] deficiency.” Id. at 8.
`2. Depakote Label (Ex. 1009)
`The Depakote Label discloses the prescribing information for an oral
`administration of divalproex sodium (valproate), an anti-epileptic drug for
`treating seizures, migraine headaches, and bipolar disorder. Ex. 1009, 1.
`The Depakote Label warns that “[s]ince valproate products may produce
`CNS depression, especially when combined with another CNS depressant
`(e.g., alcohol), patients should be advised not to engage in hazardous
`activities.” Id. at 48.
`3. Cagnin (Ex. 1008)
`Cagnin is a case report describing a patient affected with bipolar
`disorder and alcohol dependence who experienced seizures after co-
`administration of valproate and GHB. Ex. 1008, 203. The patient had been
`receiving a 500 mg dose of valproate, twice daily, as mood-stabilizing
`treatment. Id. The patient also began receiving a dose of 3500 mg/day of
`GHB for treatment of alcohol dependence. Id. Subsequently, the patient
`developed psychotic behavior and experienced seizures. Id. at 203–04.
`Cagnin states that “[o]nly GHB discontinuation restored the neurotransmitter
`balance and caused seizures to cease.” Id. at 205.
`Cagnin suggests that an interaction between valproate and GHB may
`have triggered the seizures. Id. In particular, Cagnin states that valproate is
`a potent in vitro inhibitor of SSADH, which “catalyzes the production of
`
`
`
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`IPR2016-00546
`Patent 8,772,306 B1
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`succinate from succinic semialdehyde [SSA], an intermediate product in the
`metabolic pathway transforming GHB into GABA and vice versa.” Id.
`Cagnin also discloses that “[a]n inherited deficiency of SSADH activity
`leads to accumulation of [SSA] and, consequently, a 30-fold increase in
`GHB level and a 2- to 4-fold increase in GABA in the brains of affected
`rats,” resulting in tonic-clonic seizures and convulsive status epilepticus. Id.
`4. Hechler (Ex. 1006)
`Hechler teaches that “GHB is a naturally occurring substance that is
`located in almost all brain regions, together with succinic semialdehyde
`reductase, the enzyme responsible for its synthesis.” Ex. 1006, 753 (citation
`omitted). Hechler discloses that valproate inhibits the metabolism of GHB
`to SSA by inhibition of GHB dehydrogenase in vivo, which results in an
`accumulation of GHB in the brain. Id. at 754, 757.
`5. Shinka (Ex. 1007)
`Shinka teaches that “[t]he effects of [valproate (“VPA”)] on GHB
`metabolism have been discussed and it is suspected that the inhibition of
`SSADH by therapeutic levels of VPA results in enhanced GHB production.”
`Ex. 1007, 99–100. Shinka further teaches that “GHB is converted to
`succinic semialdehyde by the reverse reaction with non-specific reductase,
`and inhibition of this enzyme by VPA is believed to be another reason for
`accumulation of GHB.” Id. at 103–04.
`6. Kaufman (Ex. 1015)
`Kaufman teaches that anticonvulsants, such as valproate, are good
`inhibitors of GHB dehydrogenase and that, “[i]n addition, GHB
`dehydrogenase is inhibited by salicylates.” Ex. 1015, 967.
`
`
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`
`C. Analysis of Petitioner’s Patentability Challenges
`1. Obviousness of Claims 1–34 Based on the Xyrem Label, the
`Depakote 2011 Label, Hechler, and Shinka
`Petitioner contends that claims 1–34 are obvious based on the
`combination of the Xyrem Label, the Depakote Label, Hechler, and Shinka.
`Pet. 22–43. In addition to the teachings of the references, Petitioner relies
`upon the Declaration of John Horn, Pharm.D., F.C.C.P. Ex. 1003. 7
`With respect to each of the challenged claims 1–34, Petitioner asserts
`that, a) “[t]he Xyrem Label disclosed a FDA approved GHB formulation for
`the treatment of narcolepsy and cataplexy” and “that the primary metabolic
`pathway for GHB involves the enzymes GHB dehydrogenase and
`SSADH”; b) a skilled artisan “considering drug-drug interactions for GHB
`would have found Hechler and Shinka relevant as each reference disclosed
`increases in GHB levels due to inhibited GHB metabolism by valproate”;
`and c) the skilled artisan “would have considered the Depakote Label for
`guidance about valproate in assessing drug-drug interactions between GHB
`and valproate.” Pet. 22–23.
`
`
`7 Petitioner defines the person of ordinary skill in the art (POSA) as someone
`“hav[ing] at least a bachelor’s degree, master’s degree, Ph.D., Doctor of
`Pharmacy degree, or medical degree, and at least five years of experience in
`the field of drug interactions,” with “an understanding of the
`pharmacokinetics and pharmacodynamics of drugs, and the risks associated
`with concomitant administration of certain drug combinations.” Pet. 4; Ex.
`1003 ¶ 31. Petitioner further asserts that a “POSA could have worked as a
`part of a multidisciplinary team and utilize his or her own skills, and also
`take advantage of certain specialized skills of others in the team to solve a
`given problem.” Pet. 4; Ex. 1003 ¶ 30. We apply that description in our
`analysis.
`
`
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`
`Petitioner further asserts that the skilled artisan “would have been
`motivated to decrease the dose of GHB with concomitant administration of
`valproate based on the Xyrem Label and Depakote Label” and the
`understanding “that concomitant administration of valproate and GHB may
`produce pharmacodynamic and pharmacokinetic drug-drug interactions that
`could potentially result in enhanced CNS depression and adverse events.”
`Id. at 24–25. Petitioner also asserts that the skilled artisan “would have been
`further motivated to decrease the administered dose of GHB based on the
`titration dosing instructions in the Xyrem Label,” which states that the dose
`of GHB should be “titrated to effect” and discloses a recommended starting
`dose of 4.5 grams per night that can be increased to a maximum of 9 grams
`per night in increments of 1.5 grams per night. Id. at 27. Petitioner also
`asserts that the skilled artisan “could have reasonably been motivated to
`reduce the GHB dose by 50%, as the Xyrem Label discloses that ‘it is
`prudent to reduce the starting dose of sodium oxybate by one-half in patients
`with liver dysfunction’ as liver dysfunction will result in increases in GHB
`in patients.” Id. at 28 (citing Ex. 1005, 4, 11). In addition, Petitioner
`contends that the skilled artisan “would have further understood that routine
`pharmacokinetic studies could be conducted to identify the specific dosage
`adjustment needed to safely co-administer GHB and valproate.” Id.
`Patent Owner argues that a) the prior art’s teachings were inconsistent
`and contradictory, such that the effects of valproate on GHB in humans
`would have been unpredictable (Prelim. Resp. 9–22), b) the prior art taught
`away from co-administration of GHB and valproate (id. at 23–28), c)
`Petitioner failed to show that the skilled artisan would have been motivated
`to administer reduced GHB doses if valproate caused GHB-related side
`
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`IPR2016-00546
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`effects (id. at 28–33), and d) Petitioner fails to show that the skilled artisan
`would have reasonably expected that the reduced GHB doses would treat the
`claimed sleep disorders, and do so without resulting side effects (id. at 33–
`39).
`
`We determine that Petitioner has not demonstrated a reasonable
`likelihood of prevailing with respect to any of the challenged claims.
`Although the language in each of the independent claims differs somewhat,
`Petitioner recognizes that each of those claims require the concomitant
`administration of GHB and valproate, and asserts that the claims would have
`been obvious for essentially the same reasons. See Pet. 29–34. Therefore,
`our analysis applies to all the challenged claims.
`As an initial matter, Petitioner does not sufficiently account for the
`prior art’s teaching away of the co-administration of GHB and valproate. A
`reference teaches away from a claimed invention if it “criticize[s],
`discredit[s], or otherwise discourage[s]” modifying the reference to arrive at
`the claimed invention. In re Fulton, 391 F.3d 1195, 1201 (Fed. Cir. 2004);
`see also KSR Int’l Co. v. Teleflex Inc., 550 U.S. 398, 416 (2007) (“[W]hen
`the prior art teaches away from combining certain known elements,
`discovery of a successful means of combining them is more likely to be
`nonobvious.”). Here, we find it particularly relevant that Petitioner
`acknowledges that both Xyrem (GHB) and Depakote (valprotate) are CNS
`depressants that can cause potential drug-drug interactions, but does not
`otherwise address the explicit black box warning in the Xyrem Label that
`GHB should not be taken with other CNS depressants. Ex. 1005, 1; Pet. 24–
`25. Nor does Petitioner address the Xyrem Label’s contraindication of GHB
`in patients with SSADH deficiency, despite Petitioner’s acknowledgement
`
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`IPR2016-00546
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`that valproate was known to inhibit SSADH activity. Ex. 1005, 8; Pet. 26.
`Petitioner does not provide any reason why the skilled artisan would have
`ignored the black box warning and contraindication in the Xyrem Label and
`co-administer GHB, even at a reduced dose, when valproate is being
`concomitantly administered to the patient.
`Moreover, even if the prior art did not teach away from reducing the
`effective dosage of GHB by at least 5% when valproate is co-administered,
`Petitioner has not demonstrated sufficiently that a skilled artisan would have
`had a reasonable expectation of success in treating the claimed sleep
`disorders with such a reduced dosage of GHB. Petitioner’s reliance upon the
`Xyrem Label’s teaching that GHB doses should be “titrated to effect,” which
`is based on the administration of GHB alone, does not necessarily suggest
`that a lower dose of GHB could effectively compensate for any increase in
`endogenous GHB levels caused by valproate administration as discussed in
`Hechler (Ex. 1006) or Shinka (Ex. 1007) when treating the claimed sleep
`disorders. Patent Owner points to evidence of record showing that GHB is
`eliminated from the body through alternate pathways that are not inhibited
`by valproate, and these alternate elimination pathways may actually decrease
`GHB levels. Prelim. Resp. 10–13. Petitioner does not account for these
`other pathways by which GHB may be eliminated. Petitioner, therefore, has
`not identified a sufficient basis on this record to conclude that any increased
`brain levels of endogenous GHB caused by valproate could have been
`predictably compensated for by a corresponding decrease of at least 5% in
`the amount of GHB orally administered to patients.
`Petitioner asserts that “routine pharmacokinetic studies” could be
`conducted to identify the dosage adjustment needed to safely co-administer
`
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`GHB and valproate. Pet. 28. Petitioner, however, does not provide any
`further explanation or evidence concerning what type of pharmokinetic
`studies could be conducted, and why any such studies would have been
`considered either “routine” or have provided a reasonable expectation of
`success with a lower dose of GHB concomitantly administered with
`valproate. Cf. In re Cyclobenzaprine Hydrochloride Extended-Release
`Capsule Patent Litig., 676 F.3d 1063, 1070 (Fed. Cir. 2012) (“While it may
`have been obvious to experiment with the use of the same PK profile when
`contemplating an extended-release formulation, there is nothing to indicate
`that a skilled artisan would have had a reasonable expectation that such an
`experiment would succeed in being therapeutically effective.”).
`We, therefore, decline to institute an inter partes review based on
`Petitioner’s first obviousness challenge for any of claims 1–34.
`
`2. Obviousness of Claims 1–34 Based on the Xyrem Label, the
`Depakote Label, Hechler, Shinka, and Cagnin
`
`As a second obviousness challenge, Petitioner contends that claims 1–
`34 are obvious based on the combination of the Xyrem Label, the Depakote
`Label, Hechler, Shinka, and the further teachings of Cagnin. Pet. 44–56.
`As discussed above, Petitioner has not shown that the combined
`teachings of the Xyrem Label, the Depakote Label, Hechler, and Shinka
`render any of the challenged claims obvious. Cagnin does not make up for
`this deficiency. Petitioner notes that “Cagnin disclosed a case report of a
`patient who developed psychotic behaviors and tonic-clonic seizures after
`being administered 3.5 grams of GHB per day concomitantly with
`valproate” and “suggests that a drug-drug interaction between valproate and
`GHB may have triggered the seizures.” Id. at 46. Petitioner, however, fails
`
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`to address the ultimate conclusion in Cagnin that “[o]nly GHB
`discontinuation restored the neurotransmitter balance and caused seizures to
`cease.” Ex. 1008, 205. Thus, as with the Xyrem Label, Cagnin appears to
`teach away from the co-administration of any amount of GHB with
`valproate.
`We, therefore, decline to institute an inter partes review based on this
`obviousness challenge.
`
`3. Obviousness of Claims 6, 17, and 27 Based on the Further
`Teachings of Kaufman
`
`Petitioner additionally relies upon Kaufman (Ex. 1015) to separately
`assert that dependent claims 6, 17, and 27 would have been obvious. These
`claims recite a step of further administering aspirin to the patient. Pet. 56–
`57. In particular, Petitioner asserts that Kaufman discloses that GHB
`dehydrogenase is inhibited by salicylates, e.g., aspirin, which could result in
`increases in GHB levels in vivo, and thus the skilled “would have been
`further motivated based on Kaufman to decrease the dose of GHB when a
`patient is concomitantly administered valproate and aspirin.” Id. at 57.
`Kaufman does not make up for the deficiencies with respect to
`Petitioner’s reliance on the Xyrem Label, the Depakote Label, Hechler,
`Shinka, and Cagnin, as discussed above. Accordingly, we decline to
`institute an inter partes review based on the additional obviousness
`challenges relying upon Kaufman in the combination.
`III. CONCLUSION
`
`For the foregoing reasons, we determine that Petitioner has not
`demonstrated that the information presented shows that there is a reasonable
`
`
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`likelihood that it would prevail in proving the unpatentability of claims 1–34
`of the ’306 patent.
`IV. ORDER
`In consideration of the foregoing, it is hereby:
`ORDERED that, pursuant to 35 U.S.C. § 314(a), the Petition for inter
`partes review is denied as to all challenged claims of the ’306 patent.
`
`
`
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`PETITIONER:
`Matthew C. Ruedy
`mruedy@meiplaw.com
`
`PATENT OWNER:
`F. Dominic Cerrito
`nickcerrito@quinnemanuel.com
`Evangeline L. Shih
`evangelineshih@quinnemanuel.com
`Frank C. Calvosa
`frankcalvosa@quinnemanuel.com
`
`
`
`16
`
`
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