Ex Parte Oron et alDownload PDFPatent Trial and Appeal BoardMay 11, 201612231601 (P.T.A.B. May. 11, 2016) 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. 12/231,601 09/03/2008 Laurence Oron 2609/77675-A/JPW/GJG/CSS 3996 23432 7590 05/11/2016 COOPER & DUNHAM, LLP 30 Rockefeller Plaza 20th Floor NEW YORK, NY 10112 EXAMINER FAY, ZOHREH A ART UNIT PAPER NUMBER 1621 MAIL DATE DELIVERY MODE 05/11/2016 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 LAURENCE ORON, CHERYL FITZER-ATTAS, and RON NEUMANN1 __________ Appeal 2014-004933 Application 12/231,601 Technology Center 1600 __________ Before ERIC B. GRIMES, JOHN G. NEW, and JOHN E. SCHNEIDER, Administrative Patent Judges. SCHNEIDER, Administrative Patent Judge. DECISION ON APPEAL This is an appeal under 35 U.S.C. § 134(a) involving claims to the treatment of retinal ganglion damage or death, which have been rejected as obvious. We have jurisdiction under 35 U.S.C. § 6(b). We affirm. STATEMENT OF THE CASE The invention relates to the use of R(+)-N-propargyl-1-aminoindan or a pharmaceutically acceptable salt thereof to reduce retinal ganglion cell death or damage. Appeal Br. 6. 1 Appellants identify the Real Party in Interest as Teva Pharmaceuticals, Ltd. Appeal Br. 1. Appeal 2014-004933 Application 12/231,601 2 Claims 2–18, 20, and 21 are on appeal. Claim 2 is illustrative and reads as follows: 2. A method of treating a subject suffering from retinal ganglion cell death or retinal ganglion cell damage, or of reducing retinal ganglion cell death or damage in a subject, consisting of administering to the subject an amount of R(+)-N-propargyl-1- aminoindan or a pharmaceutically acceptable salt thereof effective to reduce retinal ganglion cell death or retinal ganglion cell damage. The claims stand rejected as follows: Claims 2–18, 20, and 21 stand rejected under 35 U.S.C. § 103(a) as unpatentable over Kocsis, et al., WO 2007/060491 A2 (Published May 31, 2007)(“Kocsis”) in view of Tatton US 5,981,598 (issued Nov. 9, 1999)(“Tatton”); Stjernschantz, et al. WO 96/05840 (published Feb. 29, 1996)(“Stjernschantz”) and Garcia-Valenzuela, et al., Programmed Cell Death of Retinal Ganglion Cells During Experimental Glaucoma, 61 EXP. EYE RES., 33–44 (1995)(“Garcia”) DISCUSSION Issue The Examiner has rejected claims 2–18, 20, and 21 under 35 U.S.C. § 103(a) as obvious in view of Kocsis combined with Tatton, Stjernschantz and Garcia. The Examiner finds that Kocsis teaches treating a subject having retinopathy caused by glaucoma with R(+)-N-propargyl-1- aminoindan (rasagiline). Final Act. 3. Tatton teaches the use of the racemic form of the claimed compound to treat glaucoma. Id. Stjernschantz teaches the use of prostaglandins combined with monoamine oxidase B (“MAO B”) Appeal 2014-004933 Application 12/231,601 3 inhibitors to treat glaucoma. Id. The Examiner finds that Garcia teaches that retinal ganglion cell death is caused by glaucoma. Id. The Examiner finds that it is expected that rasagiline can be used to treat retinopathy caused by glaucoma and that it would have been obvious to one skilled in the art to use rasagiline to treat retinal ganglion cell death. Final Act. 3–4. Appellants contend that glaucoma is not synonymous with retinal ganglion cell death and that the references do not teach the use of rasagiline to treat retinal cell death or damage. Appeal Br. 9–10. Appellants contend that Kocsis is directed to the use of sodium channel blockers to treat retinopathy caused by glaucoma. Appeal Br. 11. Appellants argue that retinopathy caused by glaucoma is not the same as retinal ganglion cell death. Id. Appellants argue that Tatton is only directed to treating glaucoma and not retinal ganglion cell death. Appeal Br. 12. Appellants also argue that the racemic N-propargyl-1-aminoindan (PAI) is not rasagiline and that the (-) enantiomer of PAI does not have the same properties of rasagiline. Appeal Br. 12–14. Appellants further argue that Stjernschantz is silent about using MAO B inhibitors to treat retinal ganglion cell death or damage and that Garcia only suggests that some cases of glaucoma will result in retinal ganglion cell death. Appeal Br. 14–15. Appellants conclude by arguing that one skilled in the art would not have a reasonable expectation that using rasagiline would work in that Tatton teaches away from using MAO B inhibitors to treat glaucoma. Appeal Br. 15–16. The issue with respect to this rejection is whether the Examiner has proven by a preponderance of the evidence that the claims are unpatentable Appeal 2014-004933 Application 12/231,601 4 as obvious over Kocsis combined with Tatton, Stjernschantz, and Garcia as defined by 35 U.S.C. § 103(a). Findings of Fact FF1. Kocsis teaches the use of a sodium channel inhibitor combined with a MAO B inhibitor to treat retinopathy caused by glaucoma. Kocsis 3. FF2. Kocsis discloses and claims rasagiline as a MAO B inhibitor that can be used in practice of the disclosed method. Kocsis 2, 4, and claim 7. Rasagiline is R(+)-N-propargyl-1-aminoindan. Spec. 3. FF3. Kocsis discloses that deprenyl is a MAO B inhibitor. Kocsis 2. FF4. Kocsis teaches that “[t]he compositions may be used in oral form, parenteral form, including intravenous, subcutaneous, intradermal, intramuscular, intrathecal, rectal, topical, buccal, dermal or sublingual forms, as well as in forms suitable for inhalation.” Kocsis 5. FF5. Tatton teaches the use of deprenyl compounds to treat glaucoma. Tatton col. 2, ll. 23–27. FF6. Tatton discloses the use of N-propargyl-1-aminoindan2as one of the deprenyl compounds that can be used in the practice of the invention. Tatton, col. 5, ll. 40–45. FF7. Tatton discloses the deprenyl compounds increase the survival of retinal ganglion cells. Tatton, Fig. 3 and col. 19, ll. 33–46. FF8. Stjernschantz teaches that “there are clear indications that in glaucoma the intraocular pressure is the most important factor causing 2 Appellants acknowledge that the compound that Tatton refers to as “AGN- 1135” is N-propargyl-1-aminoindan. Appeal Br. 12, n.1. Appeal 2014-004933 Application 12/231,601 5 degenerative changes in the retina and the optic nerve head.” Stjernschantz 1. FF9. Stjernschantz teaches the use of compositions to treat glaucoma and to treat “the ganglion cells of the retina directly . . . to prevent further loss of nerve cells.” Stjernschantz 2. FF10. The compositions used in Stjernschantz include prostaglandin and prostaglandin derivatives combined with MAO B inhibitors. Stjernschantz 6–8. FF11. Garcia teaches that “[t]he characteristic pathological change in the glaucomatous retina is the loss of retinal ganglion cells.” Garcia 33. Principles of Law A proper § 103 analysis requires “a searching comparison of the claimed invention—including all its limitations—with the teaching of the prior art.” In re Ochiai, 71 F.3d 1565, 1572 (Fed. Cir. 1995). “Under the proper legal standard, a reference will teach away when it suggests that the developments flowing from its disclosures are unlikely to produce the objective of the applicant’s invention. A statement that a particular combination is not a preferred embodiment does not teach away absent clear discouragement of that combination.” Syntex (U.S.A.) LLC v. Apotex, Inc., 407 F.3d 1371, 1380 (Fed. Cir. 2005) (citations omitted). Analysis Claim 2 is representative of the rejected claims and recites a method for treating retinal ganglion death or damage by administering R(+)-N- propargyl-1-aminoindan (rasagiline) or a salt thereof. We agree with the Appeal 2014-004933 Application 12/231,601 6 Examiner that the method of claim 2 would have been obvious to one of ordinary skill in the art at the time the invention was made. Kocsis teaches the use of rasagiline with a sodium channel blocker to treat retinopathy caused by glaucoma. FF1 and 2. Tatton discloses the use of deprenyl compounds such as N-propargyl-1-aminoindan to treat glaucoma. FF5 and 6. Garcia teaches that glaucoma causes retinal ganglion cell death. FF11. Thus, it would have also been obvious to a person skilled in the art to use the claimed compound for the treatment of glaucoma with an expectation of reducing retinal ganglion nerve cell damage or death, motivated by Garcia, which teaches retinal ganglion cell damage or death as a result of glaucoma. Appellants argue that Kocsis is limited to the use of sodium channel blockers and does not teach the use of rasagiline by itself to treat retinopathy caused by glaucoma. Appeal Br. 11. While claim 2 specifically refers to the use of rasagiline, it does not exclude the presence of other compounds. That is, claim 2 is directed to a method consisting of a single step of administering, but does not limit the composition that is administered to one “consisting of” rasagiline or a salt thereof. Appellants’ Specification discloses that rasagiline compositions can contain other ingredients. Spec. 12–18. In addition, Tatton teaches the use of deprenyl compounds (FF5), which are MAO B inhibitors (FF3), by themselves to treat glaucoma and specifically references N-propargyl-1-aminoindan. FF5 and 6. Given the teachings of Garcia that the effect of glaucoma on the retina is retinal ganglion cell death, FF11, one skilled in the art would have been motivated Appeal 2014-004933 Application 12/231,601 7 to administer rasagiline alone to reduce retinal ganglion cell death resulting from glaucoma. Appellants argue that retinopathy caused by glaucoma is not the same as retinal ganglion cell death. Appeal Br. 11. Regardless of whether the two terms are synonymous, however, the references teach that both are caused by glaucoma. Kocsis describes using a sodium channel inhibitor and MAO B inhibitor to treat retinopathy caused by glaucoma (FF1), and Garcia clearly states that “[t]he characteristic pathological change in the glaucomatous retina is the loss of retinal ganglion cells.” FF11. This conclusion is further supported by Stjernschantz where it teaches that intraocular pressure from glaucoma is the most important factor in causing degenerative changes to the retina. FF8. The references teach that both retinopathy and retinal ganglion cell death are caused by glaucoma, and a skilled artisan would reasonably expect that treating glaucoma would reduce damage caused by the glaucoma. Appellants also argue that Tatton does not teach the treatment of retinal ganglion cell death but only the treatment of glaucoma. Appeal Br. 12. While Tatton does not use the term retinal cell death, it does teach the treatment of glaucoma and, as taught by Garcia, retinal ganglion cell death is one of the pathological changes that glaucoma cause to the retina. FF5 and 11. Moreover, Tatton discloses the deprenyl compounds increase the survival of retinal ganglion cells. FF7. A person of ordinary skill in the art would understand that part of treating glaucoma as taught in Tatton involved protecting retinal ganglion cells from death or damage. Appeal 2014-004933 Application 12/231,601 8 Appellants further argue that Stjernschantz does not teach the treatment of retinal ganglion cell death. Appeal Br. 14–15. While it is true that Stjernschantz does not use the term retinal ganglion cell death and does not specifically mention rasagiline, Stjernschantz does teach the use of prostaglandins and MAO B inhibitors to treat glaucoma and to treat the retina with neuroprotective agents to “prevent further loss of nerve cells.” FF9 and 10. Thus, Stjernschantz teaches the use of MAO B inhibitors to prevent nerve cell death or damage. Appellants next argue that one skilled in the art would not expect stereoisomers of N-propargyl-1-aminoindan to have the same activity. While Appellant is correct that the different isomers exhibit different activities, Appellants’ argument is unpersuasive. Kocsis specifically discloses rasagiline, the + stereoisomer, and teaches that it is a MAO B inhibitor, like the deprenyl compounds used in Tatton. FF2 and 3. It would be obvious to one skilled in the art to substitute one MAO B inhibitor for another. Appellants next argue that Tatton teaches away from the use of rasagiline to treat glaucoma. Appeal Br. 16. While Tatton states that MAO B inhibitory activity is not required to treat glaucoma and the absence of a MAO B inhibitor results in fewer side effects, we do not find this to be a teaching away from using the claimed compound. Moreover, the deprenyl compounds disclosed in Tatton are classified as MAO B inhibitors. FF3. Thus one skilled in the art would read Tatton as teaching the use of MAO B inhibitors to treat glaucoma rather that teaching away from using them to treat glaucoma. Appeal 2014-004933 Application 12/231,601 9 With respect to the Garcia article, Appellants note that its teaching is limited to showing that retinal cell death occurs in some, but not all glaucoma patients. Appeal Br. 15. The fact remains that Garcia demonstrates that glaucoma characteristically results in retinal ganglion cell death, the disorder recited in the claims. FF11. Moreover, both Tatton and Stjernschantz teach that MAO B inhibitors exhibit a neuroprotective effect preventing retinal cell damage. FF7 and 9. Finally, Appellants argue that one skilled in the art would not have a reasonable expectation of success because Tatton only discloses a racemic mixture of N-propargyl-1-aminoindan and stereoisomers do not always have the same activity. Appeal Br. 16–17. Appellants also argue that Tatton’s teaching away would also negate any reasonable expectation of success. Id. We disagree. As discussed above, Tatton discloses the MAO B inhibitors such as deprenyl are effective in treating glaucoma and one skilled in the art would expect similar MAO B inhibitors to yield similar results. Further, as discussed previously, Tatton does not teach away from using MAO B inhibitors such as rasagiline. Conclusion of Law We find that the Examiner has proved by a preponderance of the evidence that claim 2 is obvious in view of Kocsis combined with Tatton, Stjernschnatz and Garcia as defined by 35 U.S.C. § 103(a). Claims 3–18, 20, and 21 have not been argued separately and therefore fall with claim 2. 37 C.F.R. § 41.37(c)(1)(iv). Appeal 2014-004933 Application 12/231,601 10 SUMMARY We affirm the rejection of claims 2–18, 20, and 21. 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 Copy with citationCopy as parenthetical citation