Ex Parte ShichiriDownload PDFPatent Trial and Appeal BoardMay 11, 201613060753 (P.T.A.B. May. 11, 2016) Copy Citation UNITED STA TES p A TENT AND TRADEMARK OFFICE APPLICATION NO. FILING DATE 13/060,753 02/25/2011 23413 7590 05/13/2016 CANTOR COLBURN LLP 20 Church Street 22nd Floor Hartford, CT 06103 FIRST NAMED INVENTOR Masayoshi Shichiri 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 ATTORNEY DOCKET NO. CONFIRMATION NO. SOB0029US 1682 EXAMINER LI, RUIXIANG ART UNIT PAPER NUMBER 1646 NOTIFICATION DATE DELIVERY MODE 05/13/2016 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): usptopatentmail@cantorcolbum.com PTOL-90A (Rev. 04/07) UNITED STATES PATENT AND TRADEMARK OFFICE BEFORE THE PATENT TRIAL AND APPEAL BOARD Ex parte MASA YOSHI SHICHIRI 1 Appeal2013-009282 Application 13/060,753 Technology Center 1600 Before DONALD E. ADAMS, MELANIE L. McCOLLUM, and RICHARD J. SMITH, Administrative Patent Judges. McCOLLUM, Administrative Patent Judge. DECISION ON APPEAL This is an appeal under 35 U.S.C. § 134 involving claims to an antiangiogenic agent screening method. The Examiner has rejected the claims as not enabled. We have jurisdiction under 35 U.S.C. § 6(b). We reverse. 1 Appellant identifies the real party in interest as National University Corporation Tokyo Medical and Dental University (App. Br. 2). Appeal2013-009282 Application 13/060,753 STATEMENT OF THE CASE Claims 3---6 are on appeal (App. Br. 3). 2 Claim 3 is representative and reads as follows: 3. A method for screening for an antiangiogenic agent, comprising: a candidate compound administration step of administering a candidate compound for the antiangiogenic agent to a vascular endothelial cell or a cultured cell derived from the vascular endothelial cell; a cell-maintaining step of maintaining the vascular endothelial cell or the cultured cell derived from the vascular endothelial cell to which the candidate compound has been administered; a signal detection step of detecting phosphorylation of a protein, wherein the protein whose phosphorylation is detected in the signal detection step is at least one of a double stranded RNA-dependent protein kinase PKR and a eukaryotic translation initiation factor eIF2.alpha; and an antiangiogenic agent selection step of selecting the candidate compound as the antiangiogenic agent based on the signal detected in the signal detection step; wherein the candidate compound that increases the phosphorylation is selected as the antiangiogenic agent. Claims 3---6 stand rejected under 35 U.S.C. § 112, first paragraph, as failing to comply with the enablement requirement (Ans. 2). The Examiner finds: [T]he specification merely discloses methods of detecting phosphorylation of a protein, such as PKR or eIF2a induced by known antiangiogenic agents, endostatin and rifampicin in vascular endothelial cells (Examples 1-4), but fails to provide sufficient evidence establishing a correlation between an increase in phosphorylation of PKR or eIF2a and an antiangiogenic agent and the selection criteria. 2 Claims 7-13 are also pending but have been withdrawn from consideration (App. Br. 2). 2 Appeal2013-009282 Application 13/060,753 (Id. at 3--4.) In support of this position, the Examiner relies on several references (id. at 4--5). Based on these references, the Examiner concludes: In view of the complex signalling mechanism and the broad range of diversified targets of endostatin, and many factors leading to the phosphorylation of PKR and eIF-2a, it is unpredictable whether a candidate compound that causes an increase in phosphorylation of PKR or eIF2a is an antiangiogenic agent. In other words, an antiangiogenic agent, such as endostatin or rifampicin, causes an increase in phosphorylation of PKR or eIF2a, but an agent that causes an increase in phosphorylation of PKR or eIF2a is not necessarily an antiangiogenic agent. It would take undue experimentation for one skilled in the art to use the claimed method to screen an antiangiogenic agent. (Id. at 5.) PRINCIPLES OF LAW When rejecting a claim under the enablement requirement of section 112, the PTO bears an initial burden of setting forth a reasonable explanation as to why it believes that the scope of protection provided by that claim is not adequately enabled by the description of the invention provided in the specification of the application; this includes, of course, providing sufficient reasons for doubting any assertions in the specification as to the scope of enablement. In re Wright, 999 F.2d 1557, 1561-62 (Fed. Cir. 1993). "It is not a function of the claims to specifically exclude ... possible inoperative substances." In re Dinh-Nguyen, 492 F.2d 856, 858-59 (CCPA 197 4 ). "Even if some of the claimed combinations were inoperative, the claims are not necessarily invalid." Atlas Powder Co. v. E.I. Du Pont De Nemours & Co., 750 F.2d 1569, 1576 (Fed. Cir. 1984). "Of course, ifthe number of inoperative combinations becomes significant, and in effect 3 Appeal2013-009282 Application 13/060,753 forces one of ordinary skill in the art to experiment unduly in order to practice the claimed invention, the claims might indeed be invalid." Id. at 1576-77. ANALYSIS The Specification discloses that "the inventors of the present invention discovered that the phosphorylation of double stranded RNA- dependent protein kinase PKR and/or eukaryotic translation initiation factor eIF2a, correlated tightly with the inhibition of expression of the genes involved in angiogenesis in human vascular endothelial cells" (Spec. 23). In particular, the Specification discloses that the "antiangiogenic agents that induce phosphorylation of double stranded RNA-dependent protein kinase PKR and/or eukaryotic translation initiation factor eIF2a, include rifampicin, endostatin and angiostatin" (id. at 23-24). We conclude that the Examiner has not provided sufficient evidence to doubt this assertion and to demonstrate that an antiangiogenic agent could not have been selected without undue experimentation. The Examiner finds that "the double-stranded RNA-dependent protein kinase PKR and eIF-2a can be activated by many agents, such as interleukins, interferons, heparin, tumor necrosis factor-a, [and] bacterial lipopolysac-charides" (Ans. 8). However, the Examiner has not provided sufficient evidence indicating that many if not all of these agents are not antiangiogenic or that it would have required undue experimentation to distinguish between those that are antiangiogenic and those that are not. The Examiner also finds that "an antiangiogenic agent, such as endostatin has a broad spectrum of antiangiogenic mechanisms of action and 4 Appeal2013-009282 Application 13/060,753 down-regulates or up-regulates many different genes" (Ans. 8). However, the Examiner has not adequately explained why it is not possible to "screen[] candidates for an antiangiogenic agent ... regardless of endostatin interacting with a variety of proteins, provided that the candidates at least activate PKR and/or eIF2alpha" (App. Br. 7). In particular, even if "all compounds that are antiangiogenic agents [do] not bring about an increase in phosphorylation of PKR or eIF2a," it is not clear to us why the evidence fails to support the conclusion that "an antiangiogenic agent includes compounds that bring about an increase in phosphorylation of PKR or eIF2a[,] ... which permits screening of candidate compounds for an antiangiogenic agent as defined by [claim 3]" (Reply Br. 4). CONCLUSION The Examiner has not set forth a prima facie case that the claims are not enabled. We therefore reverse the enablement rejection. REVERSED 5 Copy with citationCopy as parenthetical citation