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

Ex Parte Dobrzanski et al

Patent Trial and Appeal BoardDec 22, 2014

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

UNITED STATES PATENT AND TRADEMARK OFFICE __________ BEFORE THE PATENT TRIAL AND APPEAL BOARD __________ Ex parte PAWEL DOBRZANSKI and BRUCE A. RUGGERI1 __________ Appeal 2012-006311 Application 11/880,063 Technology Center 1600 __________ 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). Appeal 2012-006311 Application 11/880,063 2 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). Appeal 2012-006311 Application 11/880,063 3 . . . 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 Appeal 2012-006311 Application 11/880,063 4 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. Appeal 2012-006311 Application 11/880,063 5 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). Appeal 2012-006311 Application 11/880,063 6 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 lp