12202774 (B.P.A.I. Nov. 10, 2011)

Ex Parte Demuth et al

Board of Patent Appeals and InterferencesNov 10, 2011

12202774 (B.P.A.I. Nov. 10, 2011)

UNITED STATES PATENT AND TRADEMARK OFFICE UNITED STATES DEPARTMENT OF COMMERCE United States Patent and Trademark Office Address: COMMISSIONER FOR PATENTS P.O. Box 1450 Alexandria, Virginia 22313-1450 www.uspto.gov APPLICATION NO. FILING DATE FIRST NAMED INVENTOR ATTORNEY DOCKET NO. CONFIRMATION NO. 12/202,774 09/02/2008 Hans-Ulrich Demuth 20075610-0078 1994 26263 7590 11/10/2011 SNR DENTON US LLP P.O. BOX 061080 CHICAGO, IL 60606-1080 EXAMINER CHERNYSHEV, OLGA N ART UNIT PAPER NUMBER 1649 MAIL DATE DELIVERY MODE 11/10/2011 PAPER Please find below and/or attached an Office communication concerning this application or proceeding. The time period for reply, if any, is set in the attached communication. PTOL-90A (Rev. 04/07) UNITED STATES PATENT AND TRADEMARK OFFICE __________ BEFORE THE BOARD OF PATENT APPEALS AND INTERFERENCES __________ Ex parte HANS-ULRICH DEMUTH, ANTS KASK, HUU PHUC NGUYEN, STEPHAN VON HOERSTEN, SUSANNE KRUBER, and MATTHIAS HOFFMANN __________ Appeal 2011-005030 Application 12/202,774 Technology Center 1600 __________ Before DONALD E. ADAMS, MELANIE L. McCOLLUM, and STEPHEN WALSH, Administrative Patent Judges. McCOLLUM, Administrative Patent Judge. DECISION ON APPEAL This is an appeal under 35 U.S.C. § 134 involving claims to a method of treating schizophrenia or depression. The Examiner has rejected the claims as nonenabled. We have jurisdiction under 35 U.S.C. § 6(b). We reverse. STATEMENT OF THE CASE Claims 1-19 are on appeal (App. Br. 2). Claim 1 is representative and reads as follows: Appeal 2011-005030 Application 12/202,774 2 1. A method of treating schizophrenia or depression, the method comprising administering to a subject in need thereof, a therapeutically effective amount of a composition comprising an inhibitor of dipeptidyl peptidase IV (DPIV), or a pharmaceutically acceptable salt thereof. Claims 1-19 stand rejected under 35 U.S.C. § 112, first paragraph, “as failing to comply with the enablement requirement” (Ans. 3). In particular, the Examiner finds that “[t]here are no teachings within the specification to substantiate the only statement at p. 1 [of the specification] of the proposed and currently claimed method to treat schizophrenia and/or depression by administration of DP IV inhibitors” (id. at 4). ISSUE Has the Examiner set forth a prima facie case that the Specification fails to enable the treatment of schizophrenia and/or depression? ANALYSIS As noted by Appellants (Reply Br. 2), the Examiner does not dispute that the Specification “establishes that DP IV inhibitors can increase endogenous NPY” (Ans. 9). In addition, we agree with Appellants that the Examiner “does not challenge the assertion that the scope of compounds in the genus of DP IV inhibitors is known in the art and well characterized” (Reply Br. 2 (referencing Ans. 13-14)). We also agree with Appellants that the Examiner “does not dispute the validity of proof-of-principle evidence that DP IV inhibitors are shown to be effective in the treatment of depression or schizophrenia submitted in the Declaration of Prof. Stephan von Hoersten” (Reply Br. 2-3) and we note the Examiner instead argues that this evidence cannot support the enablement because “it is limited to additional data collected after the filing date of the instant specification” (Ans. 17). Appeal 2011-005030 Application 12/202,774 3 The Examiner does question whether Appellants have adequately shown that increasing NPY “is beneficial to treat depression and/or schizophrenia” (Ans. 10). However, with regard to both depression and schizophrenia, we conclude that Appellants have the better position. According to the above-mentioned Declaration, 1 Appellants “have performed further in vivo experiments, conducted after filing of the above referenced application and performed consistent with the approach as outlined in the present application, demonstrating proof of concept for the efficacy of DP IV inhibitors in the treatment of schizophrenia and depression” (Dec. 3). As noted by the Examiner, enablement “is determined as of the application filing date.” In re Brana, 51 F.3d 1560, 1567 n.19 (Fed. Cir. 1995). However, a post-filing declaration “can be used to substantiate any doubts as to the asserted utility.” Id. The Examiner has not adequately explained why Appellants’ Declaration is not relevant for this purpose. With regard to depression, Appellants argue that the “specification describes the correlation between NPY levels and depression” (App. Br. 7). For example, the Specification discloses: Olfactory bulbectomy in the rat has been developed as a model of depression (Leonard and Tuite, 1981). In this model, most of the changes resemble those found in depressed patients (Song et al., 1996). A 7-day i.c.v. administration of NPY in olfactory bulbectomized rats attenuated behavioral and neurotransmitters deficits in this model (Song et al., 1996). (Spec. ¶ [0035].) 1 Declaration of Prof. Stephan von Hoersten, M.D., dated August 13, 2009. Appeal 2011-005030 Application 12/202,774 4 In response, the Examiner argues that “[t]here appears to be no definitive data to correlate depression as a human psychiatric disorder and NPY” (Ans. 9). However, the enablement requirement does not require definitive data. Instead, a specification disclosure which contains a teaching of the manner and process of making and using the invention in terms which correspond in scope to those used in describing and defining the subject matter sought to be patented must be taken as in compliance with the enabling requirement of the first paragraph of § 112 unless there is reason to doubt the objective truth of the statements contained therein which must be relied on for enabling support. In re Marzocchi, 439 F.2d 220, 223 (CCPA 1971) (emphasis in original). We recognize the Examiner’s concern that Maes 2 “discloses that DP IV activity was decreased in patients with major depression . . . , suggesting to one of ordinary skill that the addition[al] inhibition of DP IV activity in an individual by the administration of an inhibitor of the instant invention would be expected to actually exacerbate depression in that individual” (Ans. 5). However, the Examiner does not dispute that DP IV inhibitors can increase endogenous NPY (Ans. 9), nor has the Examiner provided adequate basis to doubt the truth of Appellants’ teachings concerning the correlation between NPY and depression. Thus, we cannot agree that the Examiner has provided adequate reason to doubt that DP IV inhibitors can be used to treat depression. 2 Michael Maes et al., Effects of Psychological Stress on Serum Prolyl Endopeptidase and Dipeptidyl Peptidase IV Activity in Humans: Higher Serum Prolyl Endopeptidase Activity is Related to Stress-Induced Anxiety, 23 PSYCHONEUROENDOCRINOLOGY 485-495 (1998). Appeal 2011-005030 Application 12/202,774 5 With regard to schizophrenia, the Specification states that the invention relates to the treatment of “schizophrenia, via a potentiation of NPY Y1 receptor mediated effects resulting from an inhibition of DPIV-like activity within the CNS” (Spec. ¶ [0002]). As discussed above, the Examiner does not dispute that DP IV inhibitors can increase endogenous NPY (Ans. 9). In addition, the Examiner has not provided sufficient basis to doubt that increasing NPY (via DP IV inhibition) can be used to treat schizophrenia. In fact, Wettstein, 3 which is relied upon by the Examiner to demonstrate unpredictability (Ans. 5 & 9), discloses that the “levels of NPY . . . in the temporal cortex, a region whose dysfunction may be related to schizophrenia, were reduced significantly to 52 . . . % of control levels” (Wettstein 401 (emphasis added)). This disclosure appears to support Appellants’ position, not demonstrate that there would have been reason to doubt it. CONCLUSION The Examiner has not set forth a prima facie case that the Specification fails to enable the treatment of schizophrenia or depression. We therefore reverse the enablement rejection. REVERSED cdc 3 J.G. Wettstein et al., Central Nervous System Pharmacology of Neuropeptide Y, 65 PHARMAC. THER. 397-414 (1995).