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`Paper No. ___
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`Date Filed: February 16, 2018
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`UNITED STATES PATENT AND TRADEMARK OFFICE
`________________
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`BEFORE THE PATENT TRIAL AND APPEAL BOARD
`________________
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`AMERIGEN PHARMACEUTICALS LIMITED,
`ARGENTUM PHARMACEUTICALS LLC,
`
`Petitioners
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`v.
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`JANSSEN ONCOLOGY, INC.,
`Patent Owner
`________________
`
`Case IPR2016-002861
`________________
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`Patent No. 8,822,438 B2
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`
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`PATENT OWNER’S REQUEST FOR REHEARING
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`1 Case IPR2016-01317 has been joined with this proceeding.
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`IPR2016-00286
`Patent 8,822,438
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`I.
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`INTRODUCTION
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`Janssen Oncology, Inc. (“Patent Owner”) respectfully requests rehearing of
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`the Board’s Final Written Decision (Paper 86) regarding U.S. Patent 8,822,438
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`pursuant to 37 C.F.R. §42.71(d). The Board misapprehended or overlooked
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`evidence, and improperly relied on theories and evidence presented only in
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`Petitioners’ Reply, to find claims 1-20 unpatentable as obvious.
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`First, the Board misapprehended evidence contradicting the sole reason
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`advanced in the Petition (which the Board adopted in its Institution Decision) as to
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`why a skilled person would have found it obvious to administer prednisone with
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`abiraterone acetate (“AA”) – that there supposedly was a need to treat the side
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`effects of mineralocorticoid excess caused by “CYP17 inhibitors.” As Petitioners’
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`expert admitted, ketoconazole – which the Board inaccurately portrayed as being
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`equivalent to AA because both were alleged “CYP17 inhibitors”– does not cause
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`mineralocorticoid excess. As he stated in his opening declaration, Petitioners’
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`expert also confirmed that cortisol reductions alone are not enough to justify
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`glucocorticoid replacement therapy and opined that such treatment is warranted
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`only if cortisol reduction results in mineralocorticoid excess. Consequently,
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`Petitioners failed to show by a preponderance of the evidence that a skilled person
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`would have been motivated to co-administer prednisone with an alleged “CYP17
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`inhibitor” like ketoconazole or AA to treat (non-existent) symptoms of
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`mineralocorticoid excess.
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`The Board compounded its error by relying on a supposed new theory on
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`motivation to combine prednisone with AA that Petitioners raised for the first time
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`in Reply – that “CYP17 inhibitors” reduce cortisol production that results in
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`adrenal insufficiency. But the rationale advanced in the Petition was not based on
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`adrenal insufficiency. Further, other evidence in the record contradicted that new
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`theory.
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`The Board also overlooked or misapprehended the evidence demonstrating
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`that Petitioners’ “congenital CYP17 deficiency” arguments were also new
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`arguments and could not support the obviousness rationale set forth in the Petition.
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`The Board’s decision cannot be sustained when Petitioners’ admissions are
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`accepted, and when the new theories advanced for the first time in Reply are
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`properly excluded from the analysis. The decision improperly disregards the
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`presumption of validity that all patents – including those undergoing inter partes
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`review – are entitled to under 35 U.S.C. § 282. The statutory presumption of
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`validity means that, in the absence of proof under the applicable evidentiary
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`standard, the court must find the claims valid. In these proceedings, the Petitioners
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`are required to establish the claims are unpatentable for the reasons set forth in
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`their Petition by a preponderance of the evidence. Where the evidence before the
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`Board on the Petitioners’ theory of unpatentability falls short of that threshold –
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`IPR2016-00286
`Patent 8,822,438
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`such as when a key fact underpinning the Petitioners’ theory has been disproven –
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`the presumption of validity compels the Board to affirm the patentability of the
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`claims.
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`Finally, the Board misapprehended the logical consequence of its dual
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`findings that (i) O’Donnell taught that 500mg of AA effectively “treats” prostate
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`cancer but (ii) results in “unquestionably abnormal” cortisol side effects. Under
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`the Board’s own reasoning, a skilled artisan would have had no reason to increase
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`the dose of AA from 500mg to 1000mg/day, as dependent claims 4, 11, 19 and 20
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`require, because doing so was unnecessary and would cause more severe adverse
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`effects. Patent Owner also could not have responded to the inconsistencies in the
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`Board’s reasoning with respect to these dependent claims because these two
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`arguments were not articulated in any paper prior to the Final Decision. There is
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`thus no rational basis for finding claims 4, 11, 19 and 20 obvious on this record.
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`Accordingly, the Board should vacate its Final Decision and confirm the
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`patentability of claims 1-20 of the ’438 patent.
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`II.
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`STANDARD OF REVIEW
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`A request for rehearing may be filed that “specifically identif[ies] all matters
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`the party believes the Board misapprehended or overlooked.” 37 C.F.R. §42.71(d).
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`III. ARGUMENT
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`A. The Board Misapprehended the Significance of Petitioners’
`Admission that Ketoconazole Does Not Cause Mineralocorticoid
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`Excess.
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`Amerigen’s Petition articulated a single rationale why the challenged claims
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`were unpatentable:
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`… it was known in the art that administering ketoconazole, also a
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`CYP17 inhibitor like abiraterone acetate, to treat a prostate cancer may
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`result in significant side effects, such as hypertension, hypokalemia and
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`fluid retention as a result of a decrease in cortisol levels and consequent
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`ACTH drive.
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`Paper 1 (Petition) at 55-56, citing Ex. 1002 at ¶¶ 34, 68-70.
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`To support this assertion, Petitioners relied on their expert, Dr. Serels who testified:
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`The administration of ketoconazole to treat prostate cancer was known
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`to reduce cortisol levels and potentially result in mineralocorticoid
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`excess, giving rise to side effects commonly associated with
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`mineralocorticoid excess, including hypertension, hypokalemia, and
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`fluid retention…These side effects reduced the safety and tolerability of
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`administering ketoconazole…To address these side effects, it was
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`standard practice in the art to co-administer a glucocorticoid such
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`as…prednisone with ketoconazole to improve the safety and tolerability
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`of ketoconazole to treat prostate cancer.
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`Ex. 1002 at ¶34 (emphasis added).
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`The Board relied on these representations to find a reasonable likelihood that
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`Petitioners would prevail in challenging the claims as obvious, stating:
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`Our review of Dr. Serels’s declaration and supporting evidence leads us
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`to credit his testimony that “one of skill in the art would have expected
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`that the co-administration of prednisone with abiraterone would
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`improve the safety and tolerability of administering abiraterone by
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`reducing the potential for side effects associated with the administration
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`of a CYP17 inhibitor.”
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`See Paper 14 (ID) at 10, citing Petition at 27-28, Ex. 1002 ¶ 34.
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`In response, Patent Owner explained that the prior art relied upon by
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`Petitioners (and the Board) did not show that ketoconazole caused
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`mineralocorticoid excess and, in fact, other prior art showed that ketoconazole
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`suppressed production of mineralocorticoids. (Paper 33 (PO Response) at 23-26).
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`Petitioners’ expert, Dr. Serels, agreed with Patent Owner: “I have reviewed the
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`steroid synthesis pathways…and now more fully appreciate…that
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`mineralocorticoid excess would not occur with ketoconazole.” (Ex. 1095 ¶10
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`(Paper 69 at 17-18)) (emphasis added). This concession entirely refutes
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`Petitioners’ theory of obviousness – a skilled artisan thus would have had no
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`reason to administer a glucocorticoid with AA, given that AA (as a supposed
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`“CYP17 inhibitor” like ketoconazole) would not cause mineralocorticoid excess.
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`In its Final Decision, the Board acknowledged Dr. Serels’s admission, but
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`stated “we do not understand Petitioners’ argument for motivation to combine to be
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`premised on this assertion alone. See Pet. 6, 26, 37–39.” (Final Decision at 21-22).
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`The Board then, drawing upon Petitioners’ Reply, adopted a supposedly different
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`rationale as to why a skilled person would co-administer prednisone with AA to
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`address two effects of administration of AA, namely: “cortisol deficiency
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`…hav[ing] significant negative clinical impact” and “predicted ACTH drive.”
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`(Final Decision at 22). But in so doing, the Board misapprehended or overlooked
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`that the Petition did not portray these supposed problems of “cortisol deficiency”
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`and “ACTH drive” as “independent” reasons to administer prednisone with AA
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`(i.e., other than to treat side effects supposedly caused by mineralocorticoid
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`excess). Instead, as Petitioners’ expert explained:
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`…the administration of ketoconazole to treat prostate cancer was
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`known to reduce cortisol levels and potentially result in
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`mineralocorticoid excess, giving rise to side effects commonly
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`associated with mineralocorticoid excess, including hypertension,
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`hypokalemia, and fluid retention.
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`Ex. 1002, ¶ 34, cited at Final Decision at 12.
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`In other words, while cortisol deficiency and potential ACTH drive can (but
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`do not necessarily) lead to mineralocorticoid excess, it is only mineralocorticoid
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`excess that causes side effects like hypertension, hypokalemia and fluid retention.2
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`2
`Petition at 6 (“it was known that …the CYP17 inhibitor also…caused
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`adverse effects, including hypertension, hypokalemia (decrease in circulating
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`potassium levels), and fluid retention.”) (citing Ex. 1002 at ¶¶ 32, 34, 48); Petition
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`at 26 (“When a CYP17 inhibitor is administered…as an undesired side effect
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`cortisol production is compromised…. It was known that CYP17 inhibition of
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`In fact, a cortisol deficiency without mineralocorticoid excess causes the opposite
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`clinical outcome – hypotension. (Paper 60 (Reply at 9); Ex. 1093 at 20-24, 64-65).
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`Consequently, Petitioners’ assertion in their Reply that “[c]ortisol is
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`‘necessary for other biochemical cycles in the body and its reduced production
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`caused adverse effects, including hypertension, hypokalemia …, and fluid
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`retention,’” which the Board relied on in its Final Decision (Decision at 12, citing
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`Ex. 1002¶¶ 32, 34, 48) is not only scientifically inaccurate, it employs a materially
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`different rationale for obviousness than what was set forth in the Petition.
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`The Board thus overlooked or misapprehended the consequences of the now
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`undisputed fact that ketoconazole does not cause mineralocorticoid excess. (Ex.
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`1095 ¶10 (Paper 69 at 17-18)). First, that fact refutes the proposition in the
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`Petition that a skilled artisan would have been motivated to administer prednisone
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`to an individual being treated with ketoconazole (and by extension, AA) to treat
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`side effects of mineralocorticoid excess. Second, it confirms that Petitioners
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`advanced new and different obviousness grounds in their Reply, which the Board
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`cortisol increased ACTH drive…which resulted in a corresponding increase in
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`mineralocorticoids. An increase in mineralocorticoids beyond normal levels,
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`known as “mineralocorticoid excess,” was known to have adverse effects,
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`including hypertension, hypokalemia…and fluid retention.”) (citing Ex. 1002 at ¶¶
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`30, 31, 32) (emphasis added).
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`improperly relied upon to hold the claims obvious. (Petition at 55-56, ID at 10;
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`Final Decision at 21-22); see Intelligent Bio-Systems, Inc. v. Illumina Cambridge
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`Ltd., 821 F.3d 1359, 1369-70 (Fed. Cir. 2016).
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`The Board compounded its error by overlooking or misapprehending
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`evidence showing that AA was not known to cause side effects characteristic of
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`mineralocorticoid excess. That evidence included observations in O’Donnell that
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`patients treated with AA retained normal cortisol levels, as well as evidence
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`showing that the body naturally offsets modest decreases in cortisol production by
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`increased production of corticosterone. (PO Response at 17-19, 21, citing Ex.
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`1003 at 2320-23; Ex. 2038 ¶¶ 107-114; Ex. 2040 ¶¶ 13, 14, 15, 30-35, 46, 54).
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`The Board likewise misapprehended O’Donnell’s Synacthen test results,
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`stating that the skilled artisan would know from them that “something was amiss
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`with the O’Donnell Study C patients’ cortisol levels following administration of
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`abiraterone acetate.” (Final Decision at 19). But, critically, the Board identified no
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`evidence suggesting that AA was known to cause the side effects associated with
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`mineralocorticoid excess at the time of the invention – the only rationale advanced
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`in the Petition for why a skilled person would have been motivated to administer
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`prednisone with AA.
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`The Board also improperly credited a reply declaration from Petitioners’
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`expert that, according to the Board, “implied that [AA] could result in chronic
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`cortisol deficiency ‘for which glucocorticoid replacement could be required.’”
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`(Final Decision at 19). That hindsight-driven speculation is not evidence
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`demonstrating a skilled person at the time of the invention would have believed
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`there was a need for co-administration of a glucocorticoid with AA.
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`The evidence before the Board thus conclusively refutes Petitioners’
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`supposed motivation for administering prednisone with AA – namely, to treat the
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`side effects caused by mineralocorticoid excess that result from use of
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`ketoconazole (and by extension AA).
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`The Board’s decision to credit an expert’s speculation and to disregard
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`admissions by Petitioners’ expert that refute the premise of Petitioners’
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`obviousness ground improperly shifted the burden of proof to Patent Owner. That
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`cannot be reconciled with the presumption of validity under 35 U.S.C. § 282. It
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`also cannot be reconciled by the standards the Board must follow before instituting
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`trial and in its final written decision, both requiring the Board to find by a
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`preponderance of the evidence that Petitioners have established that the claimed
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`invention would have been unpatentable. See, e.g., 35 U.S.C. § 316(e).
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`B.
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`The Board Considered New Arguments Regarding Congenital
`CYP17 Deficiency Improperly Presented on Reply.
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`The Board overlooked or misapprehended that Petitioners’ arguments
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`concerning patients with congenital CYP17 deficiency were presented for the first
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`time in their Reply and in an entirely different context. Patent Owner advised the
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`Board that these were new arguments. (Paper 74, citing Reply p. 4, l. 13 – p. 5, l. 3;
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`p. 10, l. 20 – p. 11, l. 5.). The Board nonetheless relied on these new arguments
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`and evidence to support its finding of obviousness. (See Final Decision at 21).
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`“Congenital CYP17 deficiency” was not used to support any ground in the
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`Petition. Indeed, the only citations the Board provided to support its findings on
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`this issue are to Petitioners’ Reply, which in turn cites to Dr. Serels’s declaration.
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`(Ex. 1002 at ¶¶ 31-32). Those paragraphs, however, nowhere mention “congenital
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`CYP17 deficiency,” but instead reiterate the incorrect claim by Petitioners that
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`CYP17 inhibitors were known to cause mineralocorticoid excess. (See e.g., Ex.
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`1002 at ¶ 31 (“CYP17 inhibition of cortisol increased ACTH drive … which
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`resulted in a corresponding increase in mineralocorticoids”); ¶ 32 (when ACTH
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`drive is suppressed “fewer mineralocorticoids are produced and the adverse side
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`effects of hypertension, hypokalemia, and fluid retention [from mineralocorticoid
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`excess] are reduced...”)). In other words, none of the evidence cited by Petitioners
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`and relied on by the Board actually supports the proposition that a skilled artisan
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`would look to congenital CYP17 deficiency “for guidance with respect to the
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`anticipated clinical symptoms and appropriate options for managing such
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`symptoms in patients.” (Final Decision at 20-21, citing Reply at 4).
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`The Board further overlooked that Petitioners’ new Reply arguments
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`concerning “congenital CYP17 deficiency” relied upon: (1) non-prior art
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`references included for the first time on Reply (see Ex. 1085, Ex. 1188); (2)
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`deposition testimony taken well after submission of Amerigen’s Petition (Ex.
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`1188); and (3) prior art references not cited in the Petition (Ex. 1023). None of the
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`evidence provided with the Petition supports the obviousness ground advanced in
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`the Reply and adopted by the Board.
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` “[N]ew evidence that could have been presented earlier to support the
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`movant’s motion” is not permitted on reply under 37 C.F.R. §§ 42.22 (a)(2) and
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`42.23(b). See Baxter Healthcare Corp. v. Millenium Biologix, LLC, IPR2013-
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`00582, Paper 39, at 3-4 (Oct. 30, 2014). When a petitioner raises an entirely new
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`rationale to explain why one of skill in the art would have been motivated to
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`combine prior art references, it is appropriate to refuse the entire reply brief as
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`improper. Intelligent Bio-Systems, 821 F.3d at 1369-70. (“[i]t is of the utmost
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`importance that petitioners in the IPR proceedings adhere to the requirement that
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`the initial petition identify ‘with particularity’ the ‘evidence that supports the
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`grounds for the challenge to each claim.’”) (citing 35 U.S.C. §312(a)(3)). The
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`Board’s obviousness conclusion cannot stand without consideration of this
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`improper evidence.
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`The Board also overlooked evidence contradicting Petitioners’ “congenital
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`CYP17 deficiency” theory, including the Attard 2005 publication and testimony
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`from Patent Owner’s expert Dr. Auchus showing that if a skilled person would
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`have analogized AA’s impact to any congenital disorder, it would have considered
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`isolated C17,20-lyase deficiency a more appropriate comparison, which would not
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`suggest glucocorticoid treatment. See Ex. 1023 at 1242-43; Ex. 2040 ¶¶ 58. That
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`evidence, when properly considered in light of the presumption of validity,
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`confirms the patentability of claims 1-20 of the ’438 patent.
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`C. The Board Overlooked the Evidence that AA Does Not Cause
`Adrenal Insufficiency.
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`The Board overlooked or misapprehended evidence refuting Petitioners’ new
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`theory, presented for the first time in their Reply, that a skilled person would have
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`been motivated to combine AA with prednisone because AA might cause “adrenal
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`insufficiency” and/or a “diminish[ed] adrenal reserve.”3 (Final Decision at 16).
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`“Adrenal insufficiency” and “diminished adrenal reserve” are phenomena
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`distinct from “mineralocorticoid excess” and present different clinical
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`manifestations. For example, one side effect caused by mineralocorticoid excess is
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`hypertension (Petition at 26), while, as Petitioners state in their Reply, the “clinical
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`manifestations of adrenal insufficiency [i.e., cortisol deficiency]” include
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`“hypotension, orthostatic hypotension, and tachycardia” (Reply at 9) (emphasis
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`added). Obviously, different therapeutic interventions are needed to address these
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`3
`Patent Owner identified these as new arguments in Paper 74 at p. 3, l. 20 – p.
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`4, l. 3; p. 7 ll. 12-16, p. 8, l. 7 – p. 9, l. 9, and p. 12, ll. 4-8.
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`contrary symptoms.
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`The Board overlooked or misapprehended that the phenomena of “adrenal
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`insufficiency” and “diminish[ed] adrenal reserve” do not provide a motivation to
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`combine AA with prednisone, based on O’Donnell or any other prior art, and thus
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`cannot support the rationale for obviousness in the Petition.
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`The Board compounded its error by overlooking or misapprehending
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`evidence demonstrating that skilled artisans did not interpret the Synacthen test
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`results in O’Donnell as Petitioners contended. Just one year after the O’Donnell
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`publication, skilled artisans reviewing its Synacthen test results concluded that
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`while “[a]ll six patients had a reduced cortisol response to ACTH stimulation on
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`the 11th day after dosing…there were no clinical manifestations of adrenocortical
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`insufficiency.” (Ex. 1023 at 1245 (emphasis added), cited in PO Response at 41).
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`The Board overlooked that contemporaneous observations such as these are
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`entitled to more weight than the testimony of a paid expert. See, e.g., Union
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`Carbide Corp. v. Am. Can Co., 724 F.2d 1567, 1571-72 (Fed. Cir. 1984).
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`The Board also overlooked or misapprehended the evidence showing that
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`skilled artisans, after considering the data reported in O’Donnell, proceeded to
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`undertake studies based on AA monotherapy. For example, Attard 2005 indicated
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`that its next planned study of AA would not include co-administration of
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`prednisone: “[a] safety and efficacy evaluation of abiraterone acetate administered
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`daily and continuously to castrate men with advanced prostate cancer progressing
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`despite hormone treatment is planned.” Id. That evidence also refutes Petitioners’
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`assertion that a skilled artisan would have been motivated by the alleged “adrenal
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`insufficiency” data in O’Donnell to administer AA with prednisone.
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`The prior art, including Attard 2005, when properly considered with the
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`presumption of validity, confirms that claims 1-20 are not obvious.
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`D. The Board Misapprehended that the Prior Art Does Not Teach or
`Suggest a 1000 mg Abiraterone Acetate Dose.
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`The Petition contended a skilled person would have been motivated to
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`increase the dose of AA disclosed in O’Donnell and/or Barrie to 1000 mg because
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`“O’Donnell reports that a dose of 800 mg of abiraterone acetate can successfully
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`suppress testosterone levels to the castrate range, but this level of suppression may
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`not be sustained in all patients due to compensatory hypersecretion of luteinizing
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`hormone (‘LH’).” (Petition at 41-42, citing Ex. 1003, Abstract; see also id. at 44-
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`45, 47-48).4 Without any analysis, the Board adopted Petitioners’ assertion. (Final
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`Decision at 10). But elsewhere in its Final Decision, the Board held that “[w]e are
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`persuaded that one of ordinary skill in the art would understand the results of [the
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`4
`Patent Owner showed that the doses of AA tested in the O’Donnell study did
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`not establish clinical efficacy of AA (see, e.g., Paper 12 (Prelim. Response) at 8,
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`19-20, citing Ex. 2005 at ¶ 8; Ex. 2006 at 2, Ex. 1023 at 1245)).
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`Synacthen test] to be an indicator that something was amiss with the O’Donnell
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`Study C patients’ cortisol levels following administration of [500mg or 800mg of]
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`abiraterone acetate” and that the results were “significant enough” to cause a
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`POSA concern that abiraterone acetate at these doses could result in “chronic
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`cortisol deficiency.” (Final Decision at 19).
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`The Board overlooked or misapprehended that these two findings cannot be
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`reconciled or support a conclusion that increasing the 500/800 mg dose of AA
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`specified in O’Donnell and in Barrie would have been obvious to a skilled artisan.
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`Under the former finding (that doses of AA reported in O’Donnell are sufficient for
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`“treating” prostate cancer), there would be no motivation for a skilled artisan to
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`increase the AA dose beyond 500mg or 800mg. Under the latter finding, a skilled
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`person would have been motivated to maintain or reduce, but not increase the AA
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`dose. The Board’s finding that claims 4, 11, 19, and 20 would have been obvious
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`is not supported by a rational articulation of obviousness, and is not consistent with
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`the evidence of record. Considered in light of the presumption of validity, claims
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`4, 11, 19 and 20 of the ’438 patent are not obvious, and are patentable.
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`IV. Conclusion and Relief Requested
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`For the reasons described above, Patent Owner respectfully requests that the
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`PTAB vacate its Final Decision with respect to claims 1-20 and/or claims 4, 11, 19
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`and 20 of the ’438 patent, and confirm the patentability of these claims.
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`Dated: February 16, 2018
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`Respectfully Submitted,
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`By: /Dianne B. Elderkin/
`Dianne B. Elderkin (Reg. No. 28,598)
`delderkin@akingump.com
`Barbara L. Mullin (Reg. No. 38,250)
`bmullin@akingump.com
`Ruben H. Munoz (Reg. No. 66,998)
`rmunoz@akingump.com
`AKIN GUMP STRAUSS HAUER &
`FELD LLP
`Two Commerce Square
`2001 Market Street, Suite 4100
`Philadelphia, PA 19103
`Tel: (215) 965-1200
`Fax: (215) 965-1210
`
`David T. Pritikin (pro hac vice)
`dpritikin@sidley.com
`Bindu Donovan (pro hac vice)
`bdonovan@sidley.com
`Paul Zegger (Reg. No. 33,821)
`pzegger@sidley.com
`Todd Krause (Reg. No. 48,860)
`tkrause@sidley.com
`Alyssa B. Monsen (pro hac vice)
`amonsen@sidleyaustin.com
`SIDLEY AUSTIN LLP
`787 Seventh Avenue
`New York, NY 10019
`Tel.: (212) 839-5300
`Fax: (212) 839-5599
`ZytigaIPRTeam@sidley.com
`Counsel for Patent Owner
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`CERTIFICATE OF SERVICE
`The undersigned hereby certifies that a copy of the foregoing Patent
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`Owner’s Request for Rehearing was served on counsel of record on February 16,
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`2018 by filing this document through the End-to-End System, as well as delivering
`
`a copy via electronic mail to counsel of record for the Petitioners and Patent Co-
`
`Owner at the following addresses:
`
`William Hare - bill@miplaw.com
`Gabriela Materassi - materassi@miplaw.com
`Christopher Casieri - chris@miplaw.com
`Renita Rathinam – rathinam@miplaw.com
`
`Teresa Stanek Rea - TRea@Crowell.com
`Shannon M. Lentz - SLentz@Crowell.com
`
`Anthony C. Tridico - anthony.tridico@finnegan.com
`Jennifer H. Roscetti - jennifer.roscetti@finnegan.com
`
`
`
`
`Date: Feb. 16, 2018
`
`Respectfully submitted,
`
`By: /Dianne B. Elderkin/
`Dianne B. Elderkin
`Registration No. 28,598
`
`Counsel for Patent Owner
`Janssen Oncology, Inc.
`
`
`
`
`
`- 17 -
`
`
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