Nolan Zebulon. FrantzDownload PDFPatent Trials and Appeals BoardSep 4, 201913642576 - (D) (P.T.A.B. Sep. 4, 2019) 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. 13/642,576 10/22/2012 Nolan Zebulon Frantz 8968-00-US-01-HL 1036 23909 7590 09/04/2019 COLGATE-PALMOLIVE COMPANY 909 RIVER ROAD PISCATAWAY, NJ 08855 EXAMINER RODRIGUEZ, RAYNA B ART UNIT PAPER NUMBER 1628 NOTIFICATION DATE DELIVERY MODE 09/04/2019 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): Patent_Mail@colpal.com PTOL-90A (Rev. 04/07) UNITED STATES PATENT AND TRADEMARK OFFICE ____________ BEFORE THE PATENT TRIAL AND APPEAL BOARD ____________ Ex parte NOLAN ZEBULON FRANTZ Appeal 2019-002120 Application 13/642,576 Technology Center 1600 ____________ Before ULRIKE W. JENKS, JOHN G. NEW, and JOHN E. SCHNEIDER, Administrative Patent Judges. JENKS, Administrative Patent Judge. DECISION ON APPEAL Pursuant to 35 U.S.C. § 134(a), Appellant1 appeals from the Examiner’s decision to reject the claims as obvious. We have jurisdiction under 35 U.S.C. § 6(b). We REVERSE. STATEMENT OF THE CASE Claims 1, 2, 6, 7, 9–12, and 14 are on appeal, and can be found in the Claims Appendix of the Appeal Brief. 1 Appellant identifies the real party in interest as Hill’s Pet Nutrition, Inc. Appeal Br. 2. Appeal 2019-002120 Application 13/642,576 2 Claim 1, is representative of the claims on appeal, and reads as follows: 1. A method of treating or controlling osteoarthritis in a canine, the method comprising: detecting the osteoarthritis in the canine, wherein detecting the osteoarthritis in the canine comprises measuring decreased levels of one or more osteoarthritis biomarkers and increased levels of ANXA1 (Annexin A1) in blood of the canine as compared to healthy canines, and wherein the decreased levels of the one or more osteoarthritis biomarkers and the increased levels of ANXA1 (Annexin A1) in the blood indicate the presence of the osteoarthritis in tissue of the canine; and administering to the canine in need thereof a diet comprising, on a dry weight basis: protein: 18-22%; fat: 14.4-17.6%; carbohydrates: 45.9-56.1 %; crude fiber: 8.1-9.9%; DHA: 0.27-0.33%; EPA: 0.45-0.55%; Vitamin C: 202.5-247.5 ppm; Vitamin E: 526.5-643.5 ppm; and L-carnitine: 315.9-386.1 mg/kg, wherein the one or more osteoarthritis biomarkers to be measured are one or more of: interleukin 6 (IL-6), a disintegrin and metallopeptidase with thrombospondin type 1 motif 4 (ADAMTS-4), interferon gamma (IFNG), hyaluronic acid synthase 2 (HAS2), biglycan (BGN), sex determining region Y- box 9 (SOX-9), a disintegrin and metallopeptidase with thrombospondin type 1 motif 5 (ADAMTS-5), matrix metalloproteinase 3 (MMP3), acid phosphastase 5 (ACP5), interleukin 1A (ILIA), tenasin C (TNC), hyaluronic acid synthase 3 (HAS3), cartilage oligomeric matrix protein (COMP), insulin-like growth factor 1 (IGF-1), ghrelin (GHR), X-prolyl dipeptidyl aminopeptidase (Xaa-Pro Peptidase), receptor activator of NF-Kappa B ligand (RANKL), mothers against decapentaplegic, drosophila, homolog of SMAD family member 7 (SMAD7), prostaglandin E2 (PGE2), toll-like Appeal 2019-002120 Application 13/642,576 3 receptor 9 (TLR9), plasminogen (PLOD I), and SCL2A9 glucose transporter (SCL2A9). Appeal Br. 15–16 (Claims Appendix) (emphasis added). The only other independent claim, claim 12, is directed to a “method for treating an inflammatory condition in a canine.” Id. at. 18. The claims stand rejected as follows: Claims Rejected Basis 1, 2, 6, 7, 9–12, and 14 pre-AIA 35 U.S.C. § 103(a) over Yamka,2 Toll,3 Waldron,4 Shields,5 Tagoe,6 and Kevorkian7 Examiner finds that Yamka teaches the claimed nutritional composition for administration to canines, specifically, for the purpose of treating animals suffering from an inflammatory condition. Ans. 5. Examiner acknowledges that Yamka does not teach that the inflammatory condition is osteoarthritis. Id. at 6. Examiner acknowledges that Yamka does not teach the claimed carbohydrate, fiber, DHA, and EPA concentrations, but relies on the teachings of Toll, Waldron, and Shields for these limitations. See id. at 5–10. Examiner also relies on Toll and Waldron 2 Yamka et al., US 2009/0111877 A1, published Apr. 30, 2009 (“Yamka”). 3 Toll, Nutritional Management: Optimal Osteoarthritis Diet, SUPPLEMENT TO NAVC CLINICIAN’S BRIEF 6 (2005) (“Toll”). 4 Waldron et al., WO 2006/002976 A2, published Jan. 12, 2006 (“Waldron”). 5 Shields, Jr. et al., US 6,156,355, issued Dec. 5, 2000 (“Shields”). 6 Clement E. Tagoe et al., Annexin-1 Mediates TNF -a-Stimulated Matrix Metalloproteinase Secretion from Rheumatoid Arthritis Synovial Fibroblasts, 181 J. IMMUNOL. 2813–20 (2008) (“Tagoe”). 7 Kevorkian et al., Expression Profiling of Metalloproteinases and Their Inhibitors in Cartilage, 50 ARTHRITIS & RHEUMATISM 131–41 (2004) (“Kevorkian”). Appeal 2019-002120 Application 13/642,576 4 for teaching using dietary supplements to treat canines with osteoarthritis. Id. at 5–8. Examiner’s position is that the combination of Yamka, Toll, Waldron, and Shields renders obvious a conclusion that osteoarthritis can be treated using diet. See Ans. 5–10. The present claims require two steps. Step one detects the inflammatory condition, such as osteoarthritis. Step two instructs the administration of a dietary supplement to a canine identified as suffering from an inflammatory condition in step one. 8 Examiner acknowledges that Yamka does not teach that the inflammatory condition is osteoarthritis. Ans. 6. “Yamka [also] does not explicitly teach the biomarker is ANXA1 or that levels [of] ANXA1 are increased and one or more of the listed biomarkers are decreased.” Id. at 10. Examiner relies on the teachings of Tagoe and Kevorkian for the differential biomarker expression limitation as recited in step one of the claims. Specifically Examiner finds that Tagoe “teach[es] that annexin-1 is secreted by rheumatoid arthritis synovial fibroblasts in response to TNFa and stimulates MMP-1 secretion (abstract). Moreover, Kevorkian teaches ADAMTS5 (a disintegrin and metalloproteinase domain with thrombospondin motif-5) expression is decreased in osteoarthritis (abstract).” Id. at 11. Examiner concludes that it would have of been obvious to treat osteoarthritis in an animal based on a decreased expression of an osteoarthritis biomarker and an increased expression of ANXA1 (Annexin A1). Id. 8 In a prior decision we affirmed claims directed at treating or controlling inflammatory conditions by administering a dietary supplement to a canine. See Board Decision mailed March 30, 2017 (“Decision”). Appeal 2019-002120 Application 13/642,576 5 Examiner finds that “Tagoe teaches annexin-1 mediates TNFa stimulated matrix metalloproteinase secretion from rheumatoid arthritis synovial fibroblasts.” Ans. 10. Examiner finds that Kevorkian “Kevorkian teaches ADAMTS5 (a disintegrin and metalloproteinase domain with thrombospondin motif-5) expression is decreased in osteoarthritis.” Id. at 13. Examiner finds that “[t]he motivation [for the combination] would have been the establishment by Tagoe that RA SF secrete ANXA1 and the establishment by Kevorkian that ADAMTS5 expression is decreased in osteoarthritis.” Id. at 11. The Examiner acknowledges that the cited references do not explicitly teach the inverse correlation between the specific inflammatory biomarkers in blood cited in the claims and ANXA1. As set forth above, Yamka teaches cartilage protection can be measured by various means, including an analysis of arthritis biomarkers and potential arthritis biomarkers such as TI collagen synthesis, matrix metalloproteinase (MPP), osteocalcin, alkaline phosphatase activity, COMP, and fragments of cartilage damage [0037]. . . . The motivation would have been the establishment by Tagoe that RA SF secrete ANXA1 and the establishment by Kevorkian that ADAMTSS expression is decreased in osteoarthritis. Id. at 17–18. The issue is whether the preponderance of evidence of record supports Examiner’s conclusion that the method of controlling or treating osteoarthritis (or an inflammatory condition) by administering a nutritional supplement after identifying the animal in need of treatment by measuring differential expression of biomarkers is obvious? Appeal 2019-002120 Application 13/642,576 6 A. Findings of Fact (FF) FF1. Tagoe teaches that “[a]nnexins are highly conserved calcium- and phospholipidbinding proteins that share common structures but exert diverse functions.” Tagoe 2813. “Annexin-1 (previously lipocortin- 1) is a potent inhibitor of inflammation both in vitro and in vivo.” Id. Annexin-1 has also been shown to be secreted and thereby provides additional anti-inflammatory effects. Id. In contrast to the anti-inflammatory effects of annexin-1, we observed that annexin-1 mediates TNF-α-stimulated secretion of MMP-1 from RA SF [(rheumatoid arthritis (RA) synovial fibroblasts (SF))]. Specifically, annexin-1 is rapidly secreted from preformed intracellular pools in response to TNF-α stimulation, and autoengages FPRL-1 to stimulate Erk, Jnk, and NF-KB activation, resulting in MMP-1 secretion. Id. at 2814. FF2. Tagoe “also observed increases in MMP-3 but not MMP-13 secretion in response to Ac2-26 [(annexin-1 N-terminal peptide)], alone or in combination with TNF-α (data not shown), suggesting that secreted annexin-1 may specifically regulate the secretion of multiple proteolytic enzymes.” Id. at 2819. FF3. Kevorkian shows the expression of MMP genes in cartilage from osteoarthritis patients (OA) in comparison to normal cartilage. “The most significant increases in expression of MMPs in cartilage from OA patients compared with normal were for MMP13 and MMP28 (P < 0.001), while the most significant decreases were for MMP1 and MMP3 (P < 0.001).” Kevorkian 135. FF4. Kevorkian also teaches that “the expressed aggrecanases, ADAMTS1, ADAMTS5, ADAMTS9, and ADAMTS15 were all significantly Appeal 2019-002120 Application 13/642,576 7 decreased in cartilage from OA patients compared with normal cartilage.” Id. B. Principle of Law “[E]xaminer bears the initial burden, on review of the prior art or on any other ground, of presenting a prima facie case of unpatentability.” In re Oetiker, 977 F.2d 1443, 1445 (Fed. Cir. 1992). C. Analysis Appellant contends that Tagoe does not “teach or suggest that blood from canines suffering from osteoarthritis or inflammation exhibits increased expression of ANXA1 without the external stimulation of TNF-α.” Br. 9 (emphasis omitted). At best, Tagoe teaches a need for TNF-α stimulation for annexin-1 secretion. Id. Because “Tagoe explicitly discloses that both normal and rheumatoid arthritic patients exhibit expression of annexin-1; and thus, teaches that annexin-1 is not reliable as a biomarker to distinguish between normal and rheumatoid arthritic patients.” Id. at 11 (emphasis omitted). Appellant also contends that “Kevorkian does not even discuss biomarker ANXA1.” Id. at 10. “[A]t best, [Kevorkian] discloses measuring expression levels of biomarkers in human tissue. Nowhere, however, does Kevorkian teach or suggest measuring one or more osteoarthritic biomarkers in blood of canines, much less, measuring a decrease in the expression of ADAMTS5 in the blood of canines.” Id. (emphasis omitted). After considering the art and arguments presented, we find that the preponderance of the evidence does not support Examiner’s conclusion that the claims are rendered obvious. A prima facie case for obviousness “requires a suggestion of all limitations in a claim,” CFMT, Inc. v. Yieldup Appeal 2019-002120 Application 13/642,576 8 Int’l Corp., 349 F.3d 1333, 1342 (Fed. Cir. 2003) and “a reason that would have prompted a person of ordinary skill in the relevant field to combine the elements in the way the claimed new invention does.” KSR Int’l Co. v. Teleflex Inc., 550 U.S. 398, 418 (2007). To begin with we note that rheumatoid arthritis and osteoarthritis are distinct diseases with different etiologies. Although both describe inflammation of the joints – rheumatoid arthritis is an autoimmune disorder while osteoarthritis arthritis is a degenerative joint disorder, described as the wearing down of the cartilage that leads to bones rubbing against each other. See Spec. ¶¶ 2–3. Here, the claims require a differential expression of ANXA1 (Annexin A1) and an osteoarthritis biomarker, such as for example matrix metalloproteinase 3 (MMP3) or a disintegrin and metallopeptidase with thrombospondin type I motif 5 (ADAMTS-5) among others. We note that Tagoe teaches that TNF-α stimulation of rheumatoid arthritis synovial fibroblasts results in the secretion of not only ANXA1 but also an MMP-3. FF1–FF2. Increased expression level in MMP3 is the exact opposite of what is required by the claim. The claim requires detection of osteoarthritis based on showing an increased level in blood of ANXA1 (Annexin A1) while the concentration of the biomarker, such as an MMP-3, is decreased. Examiner has not explained why one of skill in the art would look to rheumatoid arthritis synovial fibroblasts for teaching a correlation with osteoarthritis in the first place. In addition, Examiner has not explained why one would only consider the ANXA1 teaching from Tagoe but then ignore the increased levels of MMP3 secretion taught in that reference. In other words, why is Appeal 2019-002120 Application 13/642,576 9 the secretion of ANXA1 in a rheumatoid arthritis model system indicative of osteoarthritis but the secretion of MMP3 is not indicative of osteoarthritis? We agree with Appellant that Kevorkian does not make up for the deficiency in Tagoe. Kevorkian looks at cartilage from human patients with osteoarthritis and compares it normal cartilage. Kevorkian teaches that MMP3 and ADAMTS5 gene expression is decreased in osteoarthritis cartilage as compared to normal cartilage. FF3–FF4. We agree with Appellant, however, that Kevorkian does not teach ANXA1 gene expression or secretion into the blood in the osteoarthritis model. Thus, we know nothing about the normal concentrations of ANXA1 in the blood in this patient population. Additionally, Kevorkian’s experimental results are derived from cartilage and not from blood samples as required by the claims. We understand that a decrease in gene expression implies a reduction in the protein encoded by the gene. However, a decrease in gene expression does not tell one of ordinary skill in the art whether the gene product is normally secreted and detectable in the blood. In order for the method to be able to measure a decrease in a particular product would require a showing that the product is ordinarily expressed and secreted in sufficient quantities to be detectable by assay in the blood. Examiner has not explained why based on the contradictory evidence, disclosed from different disease models, one of ordinary skill in the art would have reasonably selected parts from one reference while ignoring those part of the references that that do not support Examiner’s conclusion. Specifically, Tagoe’s observation of secretion MMP3 in conjunction with ANXA1 (Annexin A1). FF1–FF2. Prior art should be read in its entirety, and considered for all that it teaches and suggests to the skilled artisan. Appeal 2019-002120 Application 13/642,576 10 W.L. Gore & Assoc., Inc. v. Garlock, Inc., 721 F.2d 1540, 1547, 1554 (Fed. Cir. 1983). Focusing on one biomarker ANXA1 (Annexin A1) while ignoring the rest of the teaching in Tagoe violates the prohibition against picking and choosing only those parts that are favorable while ignoring the rest. In re Hedges, 783 F.2d 1038, 1041 (Fed. Cir. 1986)(“It is impermissible within the framework of section 103 to pick and choose from any one reference only so much of it as will support a given position, to the exclusion of other parts necessary to the full appreciation of what such reference fairly suggests to one of ordinary skill in the art.” (citation and internal quotes omitted)). Here, Tagoe teaches that both ANXA1 (Annexin A1) and MMP-3 are secreted from rheumatoid arthritis synovial fibroblasts. Examiner bears the burden of explaining why the particular Tagoe teaching of ANXA1 secretion from the rheumatoid arthritis synovial fibroblast are particularly relevant for a diagnosis of osteoarthritis but Tagoe’s teaching of secretion of MMP3 are not applicable for the diagnosis of osteoarthritis. Because Examiner has not explained the contradictory evidence presented in Tagoe and Kevorkian, we find that that Examiner has not established that the cited art meets all the claim limitations. Thus, considering the references as a whole, we cannot conclude that the Examiner has shown obviousness by a preponderance of the evidence. We therefore reverse the rejection of claims 1, 2, 6, 7, 9–12, and 14 as obvious based on the combination of Yamka, Toll, Waldron, Shields, Tagoe, and Kevorkian. Appeal 2019-002120 Application 13/642,576 11 SUMMARY Claims Rejected Basis Affirmed Reversed 1, 2, 6, 7, 9–12, and 14 35 U.S.C. § 103(a) 1, 2, 6, 7, 9– 12, and 14 Outcome 1, 2, 6, 7, 9– 12, and 14 No time period for taking any subsequent action in connection with this appeal may be extended under 37 C.F.R. § 1.136(a). REVERSED Copy with citationCopy as parenthetical citation