Ex Parte Brod

Patent Trial and Appeal Board

Nov 8, 2013

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

UNITED STATES PATENT AND TRADEMARK OFFICE
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BEFORE THE PATENT TRIAL AND APPEAL BOARD
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Ex parte STALEY A. BROD
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Appeal 2012-005010
Application 12/897,591
Technology Center 1600
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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

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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

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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).