Ex Parte Castillo et alDownload PDFPatent Trial and Appeal BoardFeb 12, 201512119212 (P.T.A.B. Feb. 12, 2015) 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. 12/119,212 05/12/2008 Gerardo Castillo P27C1 2590 74651 7590 02/12/2015 PROTEOTECH, INC. 12040 115TH AVE NE KIRKLAND, WA 98034-6931 EXAMINER COVINGTON, RAYMOND K ART UNIT PAPER NUMBER 1622 MAIL DATE DELIVERY MODE 02/12/2015 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 PATENT TRIAL AND APPEAL BOARD __________ Ex parte GERARDO CASTILLO, BETH NGUYEN, PAULA CHOI, LESLEY LARSEN, STEPHEN LORIMER, and ALAN SNOW1 __________ Appeal 2012-008619 Application 12/119,212 Technology Center 1600 __________ Before ERIC B. GRIMES, ULRIKE W. JENKS, and CHRISTOPHER J. PAULRAJ, Administrative Patent Judges. GRIMES, Administrative Patent Judge. DECISION ON APPEAL This is an appeal under 35 U.S.C. § 134 involving claims to a treatment method, which have been rejected as obvious. We have jurisdiction under 35 U.S.C. § 6(b). We reverse. 1 According to Appellants, the Real Party in Interest is ProteoTech Inc. (Br. 1). Appeal 2012-008619 Application 12/119,212 2 STATEMENT OF THE CASE The Specification discloses “[t]he use of procyanidin B2 and related procyanidins . . . for treatment and prevention of amyloid and α-synuclein diseases, such as Alzheimer’s disease” (Spec. 1 ¶ 3). Procyanidin B2 is also referred to as epicatechin-4β→8-epicatechin or epicatechin-epicatechin dimer (id.). Claims 1–9 are on appeal. Claim 1 is illustrative and reads as follows: 1. A method for improving cognitive performance and/or slowing cognitive decline in a patient suffering from an amyloid disease comprising administering a therapeutically effective amount of a procyanidin B2 to reduce formation, deposition, accumulation, or persistence of beta-amyloid protein fibrils in the patient wherein the amount of the procyanidin B2 administered is between about 0.1 mg/kg of body weight and about 1000 mg/kg of body weight of the patient per day. The claims stand rejected under 35 U.S.C. § 103(a) as follows: Claims 1–9 based on Kuznicki,2 Hashimoto,3 and Tuckmantel4 (Ans. 5); Claims 1–9 based on Hashimoto (Ans. 11); and Claims 1–9 based on JP 10-2453425 (Ans. 9). 2 Kuznicki et al., US 5,681,569, October 28, 1997. 3 Fumio Hashimoto et al., Tannins and Related Compounds. XC. 8-C- Ascorbyl (–)-Epigallocatechin 3-O-Gallate and Novel Dimeric Flavan-3-ols, Oolonghomobisflavans A and B, from Oolong Tea, 37 CHEM. PHARM. BULL. 3255–3263 (1989). 4 Werner Tuckmantel et al., Studies in Polyphenol Chemistry and Bioactivity. 1. Preparation of Building Blocks from (+)-Catechin. Procyanidin Formation. Synthesis of the Cancer Cell Growth Inhibitor, 3-O- Galloyl-(2R,3R)-epicatechin-4β,8-[3-O-galloyl-(2R,3R)-epicatechin], 121 J. AM. CHEM. SOC. 12073–12081 (1999). Appeal 2012-008619 Application 12/119,212 3 I. The Examiner has rejected all of the claims on appeal as obvious based on Kuznicki, Hashimoto, and Tuckmantel (Ans. 5) or based on Hashimoto alone (id. at 11). The same issue is dispositive with respect to both of these rejections. The Examiner finds that Kuznicki discloses a composition comprising green tea solids (id. at 5) and Hashimoto provides evidence that Kuznicki’s composition inherently contains procyanidins B2 (id. at 6). The Examiner also finds that Kuznicki discloses that its composition is useful in improving cognitive performance (id.) and that Tuckmantel teaches that an analogous procyanidin is known to have neuroprotective activity (id. at 9). The Examiner concludes that the claimed method would have been obvious based on these teachings. Appellants argue that the cited references would not have rendered the claimed method obvious because, among other things, “Kuznicki teaches a method of increasing cognitive performance or decreasing recovery time from dehydration after exercise” (Br. 11). Appellants argue that the skilled person, in view of Kuznicki, would not have a reasonable expectation of success that a sport beverage designed to be consumed after exercise to allegedly hasten the cognitive recovery and cellular rehydration would be useful for alleviating the medically and histologically confirmed cognitive deficits accumulated over time and associated with an amyloid disease such as Alzheimers. 5 JP 10-245342 A (1998). Our citations are to the machine-generated English-language translation of record. Appeal 2012-008619 Application 12/119,212 4 (Id. at 12.) Appellants argue that neither Hashimoto (id. at 13) nor Tuckmantel remedies this deficiency (id. at 14–15). We agree with Appellants that the Examiner has not shown that the cited references would have made obvious the claimed method of treating a patient suffering from an amyloid disease. As Appellants point out, Kuznicki discloses that its composition provides “increased cognitive performance after heat dehydration” (Kuznicki 1:63, emphasis added). Kuznicki also states that its compositions “have been shown to improve cognitive performance after, and decrease recovery time from, dehydration relative to water” (id. at 3:32–34). The Examiner has not pointed to any disclosure in Kuznicki of treating the effects of Alzheimer’s disease or other amyloid disease. Nor has the Examiner pointed to any teaching related to Alzheimer’s disease or other amyloid disease in either Hashimoto or Tuckmantel. Thus, the Examiner has not provided adequate evidence to support a conclusion that the cited references would have made obvious a method of treating the effects of Alzheimer’s disease or any other amyloid disease with a reasonable expectation of success. We reverse the rejection of claims 1–9 based on Kuznicki, Hashimoto, and Tuckmantel. For the same reason, we reverse the rejection of claims 1–9 based on Hashimoto alone. II. The Examiner has rejected claims 1–9 as obvious based on JP 10- 245342 (Ans. 9). The Examiner finds that the reference “discloses a pharmaceutical composition for diminishing the toxicity in nerve cells caused by [β]-amyloid protein comprising a catechin or two or more of Appeal 2012-008619 Application 12/119,212 5 catechin such as epigallocatechin gallate and epicatechin gallate” (id.). The Examiner also finds that “the green tea composition in JP 10245342 inherently comprises proanthocyanidins oligomers” including procyanidins (id. at 9–10), and concludes that the claimed method would have been obvious based on these teachings. Appellants argue that “JP 10245342 does not teach a ‘green tea composition’ as alleged by the Examiner, it teaches that isolated catechin and theaflavin components of tea are useful for reducing nerve cell toxicity” (Br. 19). Appellants also argue that “Formulas I and II of JP10245342 illustrate respectively catechin and theaflavin and not proanthocyanidin oligomers” (id.). We agree with Appellants that the Examiner has not shown that JP 10- 245342 would have made obvious a method of administering procyanidin B2 to treat an amyloid disease. JP 10-245342 discloses a “nerve cell toxicity reduction agent of beta-amyloid protein” and a “method . . . of reducing the nerve cell toxicity of beta-amyloid protein” (JP 10-245342, page 1 ¶ 1). The disclosed method involves administering “tea catechin and/or theaflavin” (id. at 2 ¶ 6). The structure of tea catechins is given in formula I (id. at 2 ¶ 7), which defines a monomeric catechin (id. at 2 ¶ 8). Examples of tea catechins include epicatechin (id. at 3, ¶ 16). JP 10-245342 describes manufacture of its active ingredients by a method that includes obtaining an extract from tea leaves (id. at 4 ¶ 27). JP 10-245342 states that “[t]he extraction component concentrate produced by doing in this way is separable into each above-mentioned substance in a high-speed liquid chromatograph” (id.) Appeal 2012-008619 Application 12/119,212 6 JP 10-245342 provides a working example in which the effect of different tea catechins or theaflavins on rat hippocampus cells was determined (id. at 5–6 ¶¶ 30–33). JP 10-245342 states that “[w]hen 50 microM addition of EC [epicatechin] or EGC [epigallocatechin] is done, in the case of tea catechin, 100% of hippocampus nerve cell survives” (id. at 6 ¶ 33). Thus, while JP 10-245342 suggests the use of epicatechin to reduce nerve cell toxicity due to beta-amyloid protein, it does not suggest the use of procyanidin B2 (epicatechin dimer) for this purpose. As Appellants have pointed out, JP 10-245342 does not disclose the use of green tea extract itself to reduce nerve cell toxicity due to beta-amyloid protein, but only uses specific compounds isolated from tea leaves for this purpose. The compounds disclosed to be useful for reducing nerve cell toxicity due to beta-amyloid protein do not include procyanidin B2, and the Examiner has not provided a sound reason for concluding that using procyanidin B2 to reduce nerve cell toxicity due to beta-amyloid protein would nonetheless have been obvious. We therefore reverse the rejection of claims 1–9 as obvious based on JP 10-245342. SUMMARY We reverse all of the rejections on appeal. REVERSED lp Copy with citationCopy as parenthetical citation