Ex Parte Dobrzanski et al

Patent Trial and Appeal Board

Dec 22, 2014

11880063 (P.T.A.B. Dec. 22, 2014)

UNITED STATES PATENT AND TRADEMARK OFFICE
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BEFORE THE PATENT TRIAL AND APPEAL BOARD
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Ex parte PAWEL DOBRZANSKI and BRUCE A. RUGGERI1
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Appeal 2012-006311
Application 11/880,063
Technology Center 1600
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Before MELANIE L. McCOLLUM, JEFFREY N. FREDMAN, and
CHRISTOPHER G. PAULRAJ, Administrative Patent Judges.

McCOLLUM, Administrative Patent Judge.

DECISION ON APPEAL
This is an appeal under 35 U.S.C. § 134 involving claims to a
treatment method. The Examiner has rejected the claims as obvious. We
have jurisdiction under 35 U.S.C. § 6(b). We affirm.

STATEMENT OF THE CASE
Claims 8 and 13–17 are pending and on appeal (App. Br. 5). Claim 8
is representative and reads as follows:
8. A method of palliatively treating a myeloproliferative disorder
associated with activation of JAK2 comprising administering to a patient a

1 Appellants identify the real party in interest as Cephalon, Inc. (App. Br. 3).
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therapeutically effective amount of a compound that is a JAK2 inhibitor
wherein the compound has the structure:

Claims 8 and 13–17 stand rejected under 35 U.S.C. § 103(a) as
obvious over Miknyoczki2 in view of Kralovics3 (Ans. 4).
The Examiner relies on Miknyoczki for teaching “a method of
inhibiting protein kinase C . . . with administration of CEP-701” (id. at 5).
However, the Examiner finds that Miknyoczki “is silent on the use of
CEP-701 for the treatment of polycythemia vera” (id.).
The Examiner relies on Kralovics for teaching “that protein kinase C
is implicated as a mechanism underlying factor-independent erythropoiesis
in polycythemia vera” (id.). The Examiner concludes that it would have
been obvious “to administer CEP-701 for the treatment of polycythemia vera

2 Sheila J. Miknyoczki et al., The Trk Tyrosine Kinase Inhibitor CEP-701
(KT-5555) Exhibits Significant Antitumor Efficacy in Preclinical Xenograft
Models of Human Pancreatic Ductal Adenocarcinoma, 5 Clinical Cancer
Research 2205–2212 (1999).
3 Robert Kralovics & Radek C. Skoda, Molecular Pathogenesis of
Philadelphia Chromosome Negative Myeloproliferative Disorders, 19 Blood
Reviews 1–13 (2005).
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. . . because CEP-701 is known to inhibit protein kinase C which in turn is
known as the mechanism underlying pathogenesis of polycythemia vera”
(id.).

ANALYSIS
Miknyoczki discloses that “CEP-701 possess inhibitory effects against
. . . protein kinase C (IC50 of 226 nM . . . )” (Miknyoczki 2211). Kralovics
discloses that “[a]lterations in protein kinase C activity were . . . implicated
as a mechanism underlying factor-independent erythropoiesis in PV
[polycythemia vera]” (Kralovics 3). In view of these disclosures, we
conclude that the Examiner has set forth a prima facie case that it would
have been obvious to administer CEP-701 to a patient to palliatively treat
polycythemia vera (Ans. 5).
Appellants argue, however, that “Miknyoczki and Kralovics fail to
teach or suggest that myeloproliferative disorders are associated with
activated JAK2, that CEP-701 is a JAK2 inhibitor and that CEP-701 may be
used for the palliative treatment of myeloproliferative disorders such as
polycythemia vera” (App. Br. 14). We are not persuaded.
The Examiner does not base the rejection on a finding that
Miknyoczki and/or Kralovics teach or suggest that myeloproliferative
disorders are associated with activated JAK2 or that CEP-701 is a JAK2
inhibitor (Ans. 5). Instead, the Examiner concludes that it would have been
obvious “to administer CEP-701 for the treatment of polycythemia vera”
(id.), which, as noted in the Specification, is a myeloproliferative disorder
[MPD] associated with activation of JAK2 (Spec. 2: 20–22; see also current
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claim 17, which recites that the MPD is polycythemia vera (App. Br. 22)).
We conclude that Appellants have not adequately explained why the
combination of Miknyoczki and Kralovics fails to suggest “that CEP-701
may be used for the palliative treatment of . . . polycythemia vera” (App.
Br. 14).
In particular, Appellants argue that “altered protein kinase C activity
was not known as the mechanism underlying the pathogenesis of
polycythemia vera; nor was protein kinase C inhibition known as a
therapeutic approach for the treatment of polycythemia vera” (id. at 16). We
are not persuaded.
As noted above, Kralovics discloses that “[a]lterations in protein
kinase C activity were . . . implicated as a mechanism underlying factor-
independent erythropoiesis in PV” (Kralovics 3). We conclude that
Appellants have not adequately explained why this statement is “purely
speculative” (App. Br. 16).4
We acknowledge that Kralovics states that the cause of polycythemia
vera “remains unknown” (Kralovics 1). However, it is not clear why the
cause of the disease needs to be identified in order to identify a palliative
treatment therefor. We also acknowledge that Kralovics states that “[o]ne of
the expected mechanisms for the increased cytokine sensitivity in MPD

4 It seems like the reference cited in Kralovics to support this statement –
Etsuo Kawada et al., Possible Involvement of Protein Kinase C in the
Aberrant Regulation of Erythropoiesis in Polycythemia Vera, 21 Leukemia
Research 101–105 (1997) – may indicate whether this statement is “purely
speculative.” However, given that neither the Examiner nor Appellants
chose to rely on this reference, we are taking Kralovics’ statement at face
value.
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might include an alteration in protein kinase or phosphatase activity in
hematopoietic progenitors” (id. at 2 (emphasis added)). However, we do not
find it surprising that Kralovics, in providing a summary of the art, would
not definitively state that alteration in protein kinase C is one of the
mechanisms for the increased cytokine sensitivity in MPD. Thus, we
conclude that Appellants have not adequately explained why the claimed
invention only would have been “obvious to try” (App. Br. 16).
In addition, Appellants argue that “one of ordinary skill in the art
would not have a reasonable expectation of success in palliatively treating
polycythemia vera via an agent that inhibited protein kinase C because
science has shown that activated JAK2 is the molecular basis for the
pathogenesis of polycythemia vera and other MPDs” (id. at 17). We are not
persuaded.
We acknowledge the references Appellants presented to support their
position “that activated JAK2 is the molecular basis for the pathogenesis of
polycythemia vera (PV) and other MPDs” (id. at 17–18). However, we
agree with the Examiner that Appellants have not adequately explained how
these references “guide one of ordinary skill in the art away from targeting
protein kinase C for the treatment of polycythemia vera” (Ans. 9).

CONCLUSION
The evidence supports the Examiner’s conclusion that Miknyoczki
and Kralovics suggest the method of claim 8. Claims 13–17 have not been
separately argued and therefore fall with claim 8. 37 C.F.R.
§ 41.37(c)(1)(vii).
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TIME PERIOD FOR RESPONSE
No time period for taking any subsequent action in connection with
this appeal may be extended under 37 C.F.R. § 1.136(a).

AFFIRMED

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