Ex Parte Brod

Patent Trial and Appeal BoardNov 8, 2013

12897591 (P.T.A.B. Nov. 8, 2013)

UNITED STATES PATENT AND TRADEMARK OFFICE __________ BEFORE THE PATENT TRIAL AND APPEAL BOARD __________ Ex parte STALEY A. BROD __________ Appeal 2012-005010 Application 12/897,591 Technology Center 1600 __________ Before FRANCISCO C. PRATS, ERICA A. FRANKLIN, and JOHN G. NEW, Administrative Patent Judges. FRANKLIN, Administrative Patent Judge. DECISION ON APPEAL This is an appeal under 35 U.S.C. § 134(a) involving claims to a method of treating or delaying the onset of a T cell mediated inflammatory autoimmune disease. The Patent Examiner rejected the claims as lacking enablement. We have jurisdiction under 35 U.S.C. § 6(b). We reverse. STATEMENT OF THE CASE Claims 1, 5, 6, and 11-14 are on appeal. Claim 1 is representative and reads as follows: Appeal 2012-005010 Application 12/897,591 2 1. A method for treating or delaying the onset of a T cell mediated inflammatory autoimmune disease in a human subject comprising orally administering to the subject an effective dose of ACTH (adrenocorticotropic hormone). The Examiner rejected claims 1, 5, 6, and 11-14 under 35 U.S.C. § 112, first paragraph, as lacking enablement. According to the Examiner, the Specification “does not reasonably provide enablement for a method of treating or delaying the onset of all autoimmune diseases, comprising orally administering to the subject an effective amount of … ACTH.” (Ans. 4.) The Examiner acknowledged that the Specification enables a method of treating or delaying the onset of multiple sclerosis by teaching that oral administration of ACTH significantly improved recovery from EAE, experimental allergic encephalomyelitis, which is a model for multiple sclerosis. (Id. at 5.) However, the Examiner found that “it is not predictable that all of the encompassed ‘T cell mediated inflammatory autoimmune diseases’… are treatable or able to be delayed” similarly. (Id.) Appellant asserts that the Specification enables treating or delaying the onset of any T cell mediated inflammatory autoimmune disease, and not just multiple sclerosis, because the Specification describes not only that “EAE is a T cell mediated inflammatory autoimmune process of the central nervous system (CNS) that resembles the human demyelinating disease multiple sclerosis (MS),” but also that EAE “provides a useful animal system for the evaluation of potential therapies for human autoimmune [] disease.” (App. Br. 3)(quoting Spec. [0003].) In support of this disclosure, Appeal 2012-005010 Application 12/897,591 3 Appellant submits Lehmann,1 a scientific journal article, which also considers “EAE as a model for T-cell mediated autoimmune disease, in general, and multiple sclerosis in particular ….” (Id.) It might be true, as the Examiner argues, that the claims encompass different variants of ACTH. The Examiner has not, however, advanced any clear or specific evidence controverting Lehmann’s disclosure that EAE is a suitable model for T-cell mediated autoimmune disease, nor has the Examiner adequately explained why it would constitute undue experimentation to test any potential variants in that model. Therefore, after considering the evidence and arguments, we agree with Appellant (see Reply Br. 5) that the Examiner has not established a reasonable basis to question the enablement of the claimed method. See In re Wright, 999 F.2d 1557, 1562 (Fed. Cir. 1993). Accordingly, we reverse the enablement rejection of claims 1, 5, 6, and 11-14. REVERSED lp 1 Paul V. Lehmann et al., Spreading of T-cell autoimmunity to cryptic determinants of an autoantigen, 358 NATURE 155-156 (1992).