Ex Parte Bush et alDownload PDFPatent Trial and Appeal BoardDec 21, 201713673327 (P.T.A.B. Dec. 21, 2017) Copy Citation 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. 13/673,327 11/09/2012 Ashley I. BUSH 141-011D 2320 36844 7590 12/26/2017 Pp.rmak Nalcaiima Rr Mofrnwan T T P EXAMINER 127 S. Peyton Street, Suite 200 ALEXANDRIA, VA 22314 HEARD, THOMAS SWEENEY ART UNIT PAPER NUMBER 1675 NOTIFICATION DATE DELIVERY MODE 12/26/2017 ELECTRONIC 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. Notice of the Office communication was sent electronically on above-indicated "Notification Date" to the following e-mail address(es): CGOODE@cnmiplaw.COM IP@cnmiplaw.com ACERM AK @ cnmiplaw. com PTOL-90A (Rev. 04/07) UNITED STATES PATENT AND TRADEMARK OFFICE BEFORE THE PATENT TRIAL AND APPEAL BOARD Ex parte ASHLEY I. BUSH, DAVID L. COPOLOV, and MICHAEL BERK1 Appeal 2017-001752 Application 13/673,327 Technology Center 1600 Before ERIC B. GRIMES, RICHARD J. SMITH, and DAVID COTTA, Administrative Patent Judges. SMITH, Administrative Patent Judge. DECISION ON APPEAL This is an appeal under 35 U.S.C. § 134 involving claims to a method for the treatment of a neuropsychiatric disorder in a mammal. We have jurisdiction under 35 U.S.C. § 6(b). We affirm. 1 According to Appellants, the real parties in interest are the Florey Institute of Neuroscience and Mental Health, formerly known as the Mental Health Research Institute, of Victoria, Australia, and the exclusive licensee Collaborative Medical Development, LLC of Sydney, NSW, Australia. (Appeal Br. 2.) Appeal 2017-001752 Application 13/673,327 STATEMENT OF THE CASE Background The Specification states that “[rjecently, reports have emerged that glutathione is [] depleted in schizophrenia, and that the antioxidant enzymic activities related to glutathione metabolism are markedly perturbed.” (Spec. 2.) Claims on Appeal Claims 27—36 are on appeal. (Claims Appendix, Appeal Br. 11—12.) Claim 27 is illustrative and reads as follows: 27. A method for the treatment of a neuropsychiatric disorder in a mammal, said method comprising administering to said mammal cysteine or derivative thereof or a glutathione precursor in an amount effective to treat the disorder. (Id. at 11.) Examiner’s Rejections 1. Claims 27—36 stand rejected under pre-AIA 35 U.S.C. § 102(b) as anticipated by Hebert.2 (Ans. 6—7.) 2. Claims 27—36 stand rejected under pre-AIA 35 U.S.C. § 103(a) as unpatentable over Halevie-Goldman3 and Hebert. (Id. at 3—5.) 2 Hebert, US 2002/0002136 Al, pub. Jan. 3, 2002. 3 Halevie-Goldman, US 2002/0002146 Al, pub. Jan. 3, 2002. 2 Appeal 2017-001752 Application 13/673,327 FINDINGS OF FACT The following findings are provided for emphasis and reference purposes. Additional finding may also be found in this Decision and the Examiner’s Answer. FF 1. The Specification states that “reference to a ‘glutathione precursor’ should be understood as a reference to any molecule from which glutathione can be directly or indirectly derived. The subject molecule may be naturally or non-naturally occurring.” (Spec. 14.) FF 2. The Specification identifies N-acetyl cysteine as a glutathione precursor. (Id. at 4.) FF 3. Hebert discloses new salts of glutathione, n-nitroso-glutathione and monoesthers [sic, monoesters?] of glutathione, methods for the use thereof and synthetic methods for their preparation. These new salts of glutathione . . . have utility in increasing blood and other tissue or fluid levels of glutathione, as well as treating or preventing a wide variety of conditions related to the aforementioned mechanisms of action of glutathione. (Hebert 123; see also Ans. 9.) FF 4. Hebert discloses that “[a] composition containing . . . nitroso glutathione or glutathione monoalkyl ester with a polycation to obtain a water soluble salt” may be administered to treat schizophrenia. (Hebert claims 1, 7, and 16; see also Ans. 6—7.) FF 5. Hebert discloses that “[djiabetic neuropathy is associated with decrease[d] levels of GSH [glutathione]. Supplementation with a GSH precursor, N-acetyl-cysteine resulted in the reversal of some of the neuropathy symptoms in an experimental diabetes animal model.” (Hebert 3 Appeal 2017-001752 Application 13/673,327 115, citing Sagara.4) FF 6. Halevie-Goldman teaches that N-acetylcysteine “aids in converting L- methionine into SAMe [S-adenosylmethionine]” and that “[t]he method of the present invention may be used to treat any condition for which SAMe is indicated,” including “schizophrenia and disorders related to it.” (Halevie- Goldman 1131, 32; see also Ans. 3.) FF 7. Halevie-Goldman teaches a method of treating schizophrenia and other neuropsychiatric disorders “by administering to a subject a formulation comprising L-methionine . . . wherein the formulation further comprises N- acetylcysteine.” (Halevie-Goldman 132 and claims 1, 2.) DISCUSSION We adopt the Examiner’s findings, analysis, and conclusions as our own, including with regard to the scope and content of, and motivation to combine, the prior art, as set forth in the Answer (Ans. 2—14). We discern no error in the rejection of the claims as anticipated and obvious. We limit our consideration of both rejections to claim 27 because the claims were not argued separately. Rejection No. 1 Issue Whether a preponderance of evidence of record supports the Examiner’s rejection under pre-AIA 35 U.S.C. § 102(b). 4 M. Sagara et al., Inhibition of development ofperipheral neuropathy in streptozotocin-induced diabetic rats with N-acetylcysteine, Diabetologia 39, 263-69 (1996) (“Sagara”). 4 Appeal 2017-001752 Application 13/673,327 Analysis The Examiner finds that Hebert anticipates claim 27. (Ans. 6—7.) We agree with the Examiner that Hebert discloses every limitation of, and thus anticipates, claim 27. (FF 1—5.) Appellants contest the Examiner’s anticipation finding with several arguments. Appellants argue that claims 1,7, and 16 of Hebert do not teach cysteine, a cysteine derivative, or a glutathione precursor. (Appeal Br. 5—7.) We are not persuaded. Appellants’ Specification makes clear that the term “glutathione precursor” as used in claim 27 includes “any molecule from which glutathione can be directly or indirectly derived.” (FF 1.) As the Examiner points out, the salts described and claimed by Hebert are glutathione precursors, as that term is defined by Appellants. (Ans. 9; FF 3, 4.) We agree, and likewise note Hebert’s disclosure that glutathione is derived from the disclosed salts of glutathione. (FF 3.) Appellants contest the Examiner’s finding by arguing that, based on the Specification’s definitions of “glutathione” and “glutathione precursor,” the salts disclosed by Hebert are “glutathiones” and not “glutathione precursors.” (Reply Br. 2—3.) Appellants further contend that the Specification “clearly defines ‘precursors’ as compounds in the metabolic pathway of glutathione.” {Id. at 3.) We remain unpersuaded. As an initial matter, we agree with the Examiner that the salts of Hebert fall within the Specification’s definition of “glutathione precursor” (see Spec. 14—15; Hebert 123),5 and we are not 5 To be clear, the salts of Hebert may also fall within the definition of “glutathione,” as that term is defined in the Specification (Spec. 14). 5 Appeal 2017-001752 Application 13/673,327 persuaded that a glutathione precursor as defined in the Specification is limited to a compound in the metabolic pathway of glutathione (see id.). Furthermore, even if Hebert’s glutathione salts were not deemed to be glutathione precursors as defined in the Specification, Hebert also expressly discloses the administration of a glutathione precursor to address depletion of glutathione. (FF 5.) Appellants further argue that the Examiner’s reliance on the disclosure of a glutathione precursor in paragraph 15 of Hebert (FF 5) is improper because “diabetic neuropathy is a disorder that affects the peripheral nervous system, while neuropsychiatric disorders are diseases of the central nervous system” (Appeal Br. 6), and because the cited portion of Hebert appears in the “Background of the Invention” section and is not connected with the Hebert invention (Reply Br. 3).* * 6 However, Hebert states that “[t]he nervous system is [] vulnerable to GSH depletion,” and “[cjertain regions of the brain are particularly susceptible to GSH depletion.” (Hebert 115, emphasis added.) Hebert states that “[o]ne such region is the substantia nigra responsible for dopamine production,” that “Parkinson’s disease is caused by the decreased production of dopamine in the substantia nigra of the brain,” and “[n]ew salts of glutathione are needed ... for prevention and treatment of conditions However, Hebert distinguishes its glutathione salts from glutathione. (See Hebert H 18, 23, and claim 1.) 6 Although Appellants advance certain contentions regarding Sagara (cited at Hebert 115) and include a copy of Sagara in the Evidence Appendix (see, e.g., Appeal Br. 6 and n.2), the Examiner relies on Hebert (and not Sagara) for the Section 102 and 103 rejections. Appellants do not point to anything in Sagara that contradicts the statement in Hebert (FF 5) for which Sagara is cited. We rely on Hebert and not Sagara for purposes of this Decision. 6 Appeal 2017-001752 Application 13/673,327 previously described.” (Id. Tflf 15, 18.) Furthermore, the fact that the cited portion of paragraph 15 of Hebert (see FF 5) appears in the “Background of the Invention” section is of no moment since it is within the “four comers” of Hebert. See Advanced Display Sys., Inc. v. Kent State Univ., 212 F.3d 1272, 1282 (Fed. Cir. 2000). Appellants also argue that claim 1 of Hebert is a composition claim and claims 7 and 16 are method claims. (Appeal Br. 5.) Thus, according to Appellants, claims 7 and 16 are indefinite under Section 112. (Id.) Appellants further argue that the wording of claim 16 of Hebert (relating to the use of the method of claim 1 to treat neurological conditions such as schizophrenia) is “non-statutory” and “nonsensical.” (Id. at 6.) Appellants thus contend that “[rjeliance on these ‘claims’ requires a more than generous interpretation of what they would convey to the person of ordinary skill in the art.” (Id.) We are not persuaded. In considering the disclosure of a reference for anticipation, it is proper to take into account not only specific teachings of the reference but also the inferences that one skilled in the art would reasonably be expected to draw from it. In re Preda, 401 F.2d 825, 826 (CCPA 1968). We thus agree with the Examiner that “one skilled in the art can discern that while Claim 1 is a product,” the method claims in Hebert encompass “administering the compounds of Claim 1 for the purpose of treating” disorders including schizophrenia. (Ans. 8.) Appellants state in the Reply Brief that the Examiner “argues that Hebert teaches treating schizophrenia,” but argue that “Hebert does not provide an enabling disclosure of treatment of schizophrenia.” (Reply Br. 3.) However, that enablement argument is waived because it was not 7 Appeal 2017-001752 Application 13/673,327 presented in the Appeal Brief in response to the Examiner’s position that Hebert teaches treating schizophrenia, as set forth in the Final Action dated September 17, 2015, at 9—10. See 37 C.F.R. § 41.37(c)(l)(iv); see also MPEP § 1205.02. Accordingly, for the reasons of record and as set forth above, we affirm the rejection of claim 27 as anticipated by Hebert. Claims 28—36 were not argued separately and fall with claim 27. Rejection No. 2 Issue Whether a preponderance of evidence of record supports the Examiner’s rejection under pre-AIA 35 U.S.C. § 103(a). Analysis The Examiner concluded, based on findings regarding the teachings and suggestions of Halevie-Goldman and Hebert, that: It would have been obvious to one of ordinary skill in the art to administer N-acetyl cysteine (NAC) as taught by both Halevie- Goldman and Herbert [sic] for the benefit of increasing glutathione levels for the treatment of mental health diseases such as schizophrenia. One would have been motivated to administer NAC and would have had a reasonable expectation of success in treating schizophrenia given that low levels of SAM and/or glutathione are implicated in the disease. (Ans. 3-A\ see also FF 1—7.) We agree with the Examiner’s findings and conclusions, and address Appellants’ arguments below. We note at the outset, however, that Appellants advance arguments regarding Hebert (including its reference to Sagara) in connection with the obviousness rejection (see Appeal Br. 8—9), but those arguments are deemed to be fully addressed by the anticipation 8 Appeal 2017-001752 Application 13/673,327 finding discussed above. See In re McDaniel, 293 F.3d 1379, 1385 (Fed. Cir. 2002) (“anticipation is the epitome of obviousness”) (citations omitted). We thus limit our discussion to Appellants’ arguments regarding Halevie- Goldman. Appellants argue that none of the compounds disclosed for use by Halevie-Goldman, such as L-methionine, are required by the rejected claims. (Appeal Br. 7.) Furthermore, according to Appellants, in order to arrive at claim 27, “the skilled person would have to discard the principal components of the main claims of Halevie-Goldman, while retaining N- acetylcysteine, despite the clear teachings of Halevie-Goldman that the only purpose of including N-acetylcysteine in the composition is to aid conversion of L-methionine to SAMe.” (Id. at 7—8.) Appellants also argue that Halevie-Goldman “does not teach or suggest that administration of any amount of N-acetylcysteine alone is effective in treating a neuropsychiatric disorder.” (Id. at 8 (emphasis added).) We are not persuaded. Claim 27 uses the transition term “comprising.” (Appeal Br. 11; Ans. 14.) “The transition ‘comprising’ in a method claim indicates that the claim is open-ended and allows for additional steps.” Invitrogen Corp. v. Biocrest Mfg., L.P., 327 F.3d 1364, 1368 (Fed. Cir. 2003). The allowance of additional steps in a method claim (such as claim 27) is also consistent with Appellants’ use of “comprising,” as reflected in the Specification. (Spec. 5.) As properly construed, claim 27 includes the step of administering a glutathione precursor, but does not exclude the step(s) of administering additional components or compounds, such as the compounds recited in claim 1 of Halevie-Goldman (e.g., L-methionine). That is, claim 27 is not 9 Appeal 2017-001752 Application 13/673,327 limited to administration of a glutathione precursor alone as Appellants contend. Claim 27, as properly construed, thus reads on Halevie-Goldman.7 (FF 6, 7.) Moreover, at least because the Examiner is not proposing to modify Halevie-Goldman by “discarding] the two main ingredients of the composition of Halevie-Goldman,” we are not persuaded by Appellants’ argument that such alleged modification “would render [Halevie-Goldman] unsatisfactory for its intended purpose.” (Reply Br. 5.) We discern no error in the Examiner’s rejection of claim 27 for obviousness. Accordingly, we affirm the rejection of claim 27, and claims 28—36 fall with claim 27 because they were not argued separately. Conclusions A preponderance of evidence of record supports the Examiner’s rejections of claim 27 for anticipation and obviousness. Claims 28—36 were not argued separately and fall with claim 27. SUMMARY We affirm the rejections of all claims on appeal. 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 7 We also note that Halevie-Goldman teaches administering up to 200 mg of N-acetyl-cysteine to treat neuropsychiatric disorders such as schizophrenia. (Halevie-Goldman 120.) Cf. Spec. 33 (“[A]n oral dosage unit form contains between about 0.1 pg and 3000 mg of active compound.”). 10 Copy with citationCopy as parenthetical citation