Ex Parte Bush et al

Patent Trial and Appeal Board

Dec 21, 2017

13673327 (P.T.A.B. Dec. 21, 2017)

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
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APPLICATION NO. FILING DATE FIRST NAMED INVENTOR ATTORNEY DOCKET NO. CONFIRMATION NO.
13/673,327 11/09/2012 Ashley I. BUSH 141-011D 2320
36844 7590 12/26/2017
Pp.rmak Nalcaiima Rr Mofrnwan T T P
EXAMINER
127 S. Peyton Street, Suite 200
ALEXANDRIA, VA 22314
HEARD, THOMAS SWEENEY
ART UNIT PAPER NUMBER
1675
NOTIFICATION DATE DELIVERY MODE
12/26/2017 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
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PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte ASHLEY I. BUSH, DAVID L. COPOLOV,
and MICHAEL BERK1
Appeal 2017-001752
Application 13/673,327
Technology Center 1600
Before ERIC B. GRIMES, RICHARD J. SMITH, and
DAVID COTTA, Administrative Patent Judges.
SMITH, Administrative Patent Judge.
DECISION ON APPEAL
This is an appeal under 35 U.S.C. § 134 involving claims to a method
for the treatment of a neuropsychiatric disorder in a mammal.
We have jurisdiction under 35 U.S.C. § 6(b).
We affirm.
1 According to Appellants, the real parties in interest are the Florey Institute
of Neuroscience and Mental Health, formerly known as the Mental Health
Research Institute, of Victoria, Australia, and the exclusive licensee
Collaborative Medical Development, LLC of Sydney, NSW, Australia.
(Appeal Br. 2.)
Appeal 2017-001752
Application 13/673,327
STATEMENT OF THE CASE
Background
The Specification states that “[rjecently, reports have emerged that
glutathione is [] depleted in schizophrenia, and that the antioxidant enzymic
activities related to glutathione metabolism are markedly perturbed.” (Spec.
2.)
Claims on Appeal
Claims 27—36 are on appeal. (Claims Appendix, Appeal Br. 11—12.)
Claim 27 is illustrative and reads as follows:
27. A method for the treatment of a neuropsychiatric disorder in a
mammal, said method comprising
administering to said mammal cysteine or derivative thereof or a glutathione
precursor in an amount effective to treat the disorder.
(Id. at 11.)
Examiner’s Rejections
1. Claims 27—36 stand rejected under pre-AIA 35 U.S.C. § 102(b) as
anticipated by Hebert.2 (Ans. 6—7.)
2. Claims 27—36 stand rejected under pre-AIA 35 U.S.C. § 103(a) as
unpatentable over Halevie-Goldman3 and Hebert. (Id. at 3—5.)
2 Hebert, US 2002/0002136 Al, pub. Jan. 3, 2002.
3 Halevie-Goldman, US 2002/0002146 Al, pub. Jan. 3, 2002.
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Application 13/673,327
FINDINGS OF FACT
The following findings are provided for emphasis and reference
purposes. Additional finding may also be found in this Decision and the
Examiner’s Answer.
FF 1. The Specification states that “reference to a ‘glutathione precursor’
should be understood as a reference to any molecule from which glutathione
can be directly or indirectly derived. The subject molecule may be naturally
or non-naturally occurring.” (Spec. 14.)
FF 2. The Specification identifies N-acetyl cysteine as a glutathione
precursor. (Id. at 4.)
FF 3. Hebert discloses
new salts of glutathione, n-nitroso-glutathione and monoesthers
[sic, monoesters?] of glutathione, methods for the use thereof and
synthetic methods for their preparation. These new salts of
glutathione . . . have utility in increasing blood and other tissue
or fluid levels of glutathione, as well as treating or preventing a
wide variety of conditions related to the aforementioned
mechanisms of action of glutathione.
(Hebert 123; see also Ans. 9.)
FF 4. Hebert discloses that “[a] composition containing . . . nitroso
glutathione or glutathione monoalkyl ester with a polycation to obtain a
water soluble salt” may be administered to treat schizophrenia. (Hebert
claims 1, 7, and 16; see also Ans. 6—7.)
FF 5. Hebert discloses that “[djiabetic neuropathy is associated with
decrease[d] levels of GSH [glutathione]. Supplementation with a GSH
precursor, N-acetyl-cysteine resulted in the reversal of some of the
neuropathy symptoms in an experimental diabetes animal model.” (Hebert
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115, citing Sagara.4)
FF 6. Halevie-Goldman teaches that N-acetylcysteine “aids in converting L-
methionine into SAMe [S-adenosylmethionine]” and that “[t]he method of
the present invention may be used to treat any condition for which SAMe is
indicated,” including “schizophrenia and disorders related to it.” (Halevie-
Goldman 1131, 32; see also Ans. 3.)
FF 7. Halevie-Goldman teaches a method of treating schizophrenia and
other neuropsychiatric disorders “by administering to a subject a formulation
comprising L-methionine . . . wherein the formulation further comprises N-
acetylcysteine.” (Halevie-Goldman 132 and claims 1, 2.)
DISCUSSION
We adopt the Examiner’s findings, analysis, and conclusions as our
own, including with regard to the scope and content of, and motivation to
combine, the prior art, as set forth in the Answer (Ans. 2—14). We discern
no error in the rejection of the claims as anticipated and obvious.
We limit our consideration of both rejections to claim 27 because the
claims were not argued separately.
Rejection No. 1
Issue
Whether a preponderance of evidence of record supports the
Examiner’s rejection under pre-AIA 35 U.S.C. § 102(b).
4 M. Sagara et al., Inhibition of development ofperipheral neuropathy in
streptozotocin-induced diabetic rats with N-acetylcysteine, Diabetologia 39,
263-69 (1996) (“Sagara”).
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Application 13/673,327
Analysis
The Examiner finds that Hebert anticipates claim 27. (Ans. 6—7.) We
agree with the Examiner that Hebert discloses every limitation of, and thus
anticipates, claim 27. (FF 1—5.) Appellants contest the Examiner’s
anticipation finding with several arguments.
Appellants argue that claims 1,7, and 16 of Hebert do not teach
cysteine, a cysteine derivative, or a glutathione precursor. (Appeal Br. 5—7.)
We are not persuaded. Appellants’ Specification makes clear that the term
“glutathione precursor” as used in claim 27 includes “any molecule from
which glutathione can be directly or indirectly derived.” (FF 1.) As the
Examiner points out, the salts described and claimed by Hebert are
glutathione precursors, as that term is defined by Appellants. (Ans. 9; FF 3,
4.) We agree, and likewise note Hebert’s disclosure that glutathione is
derived from the disclosed salts of glutathione. (FF 3.)
Appellants contest the Examiner’s finding by arguing that, based on
the Specification’s definitions of “glutathione” and “glutathione precursor,”
the salts disclosed by Hebert are “glutathiones” and not “glutathione
precursors.” (Reply Br. 2—3.) Appellants further contend that the
Specification “clearly defines ‘precursors’ as compounds in the metabolic
pathway of glutathione.” {Id. at 3.)
We remain unpersuaded. As an initial matter, we agree with the
Examiner that the salts of Hebert fall within the Specification’s definition of
“glutathione precursor” (see Spec. 14—15; Hebert 123),5 and we are not
5 To be clear, the salts of Hebert may also fall within the definition of
“glutathione,” as that term is defined in the Specification (Spec. 14).
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persuaded that a glutathione precursor as defined in the Specification is
limited to a compound in the metabolic pathway of glutathione (see id.).
Furthermore, even if Hebert’s glutathione salts were not deemed to be
glutathione precursors as defined in the Specification, Hebert also expressly
discloses the administration of a glutathione precursor to address depletion
of glutathione. (FF 5.)
Appellants further argue that the Examiner’s reliance on the
disclosure of a glutathione precursor in paragraph 15 of Hebert (FF 5) is
improper because “diabetic neuropathy is a disorder that affects the
peripheral nervous system, while neuropsychiatric disorders are diseases of
the central nervous system” (Appeal Br. 6), and because the cited portion of
Hebert appears in the “Background of the Invention” section and is not
connected with the Hebert invention (Reply Br. 3).* * 6
However, Hebert states that “[t]he nervous system is [] vulnerable to
GSH depletion,” and “[cjertain regions of the brain are particularly
susceptible to GSH depletion.” (Hebert 115, emphasis added.) Hebert
states that “[o]ne such region is the substantia nigra responsible for
dopamine production,” that “Parkinson’s disease is caused by the decreased
production of dopamine in the substantia nigra of the brain,” and “[n]ew
salts of glutathione are needed ... for prevention and treatment of conditions
However, Hebert distinguishes its glutathione salts from glutathione. (See
Hebert H 18, 23, and claim 1.)
6 Although Appellants advance certain contentions regarding Sagara (cited at
Hebert 115) and include a copy of Sagara in the Evidence Appendix (see,
e.g., Appeal Br. 6 and n.2), the Examiner relies on Hebert (and not Sagara)
for the Section 102 and 103 rejections. Appellants do not point to anything
in Sagara that contradicts the statement in Hebert (FF 5) for which Sagara is
cited. We rely on Hebert and not Sagara for purposes of this Decision.
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previously described.” (Id. Tflf 15, 18.) Furthermore, the fact that the cited
portion of paragraph 15 of Hebert (see FF 5) appears in the “Background of
the Invention” section is of no moment since it is within the “four comers”
of Hebert. See Advanced Display Sys., Inc. v. Kent State Univ., 212 F.3d
1272, 1282 (Fed. Cir. 2000).
Appellants also argue that claim 1 of Hebert is a composition claim
and claims 7 and 16 are method claims. (Appeal Br. 5.) Thus, according to
Appellants, claims 7 and 16 are indefinite under Section 112. (Id.)
Appellants further argue that the wording of claim 16 of Hebert (relating to
the use of the method of claim 1 to treat neurological conditions such as
schizophrenia) is “non-statutory” and “nonsensical.” (Id. at 6.) Appellants
thus contend that “[rjeliance on these ‘claims’ requires a more than generous
interpretation of what they would convey to the person of ordinary skill in
the art.” (Id.)
We are not persuaded. In considering the disclosure of a reference for
anticipation, it is proper to take into account not only specific teachings of
the reference but also the inferences that one skilled in the art would
reasonably be expected to draw from it. In re Preda, 401 F.2d 825, 826
(CCPA 1968). We thus agree with the Examiner that “one skilled in the art
can discern that while Claim 1 is a product,” the method claims in Hebert
encompass “administering the compounds of Claim 1 for the purpose of
treating” disorders including schizophrenia. (Ans. 8.)
Appellants state in the Reply Brief that the Examiner “argues that
Hebert teaches treating schizophrenia,” but argue that “Hebert does not
provide an enabling disclosure of treatment of schizophrenia.” (Reply Br.
3.) However, that enablement argument is waived because it was not
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presented in the Appeal Brief in response to the Examiner’s position that
Hebert teaches treating schizophrenia, as set forth in the Final Action dated
September 17, 2015, at 9—10. See 37 C.F.R. § 41.37(c)(l)(iv); see also
MPEP § 1205.02.
Accordingly, for the reasons of record and as set forth above, we
affirm the rejection of claim 27 as anticipated by Hebert. Claims 28—36
were not argued separately and fall with claim 27.
Rejection No. 2
Issue
Whether a preponderance of evidence of record supports the
Examiner’s rejection under pre-AIA 35 U.S.C. § 103(a).
Analysis
The Examiner concluded, based on findings regarding the teachings
and suggestions of Halevie-Goldman and Hebert, that:
It would have been obvious to one of ordinary skill in the art to
administer N-acetyl cysteine (NAC) as taught by both Halevie-
Goldman and Herbert [sic] for the benefit of increasing
glutathione levels for the treatment of mental health diseases
such as schizophrenia. One would have been motivated to
administer NAC and would have had a reasonable expectation of
success in treating schizophrenia given that low levels of SAM
and/or glutathione are implicated in the disease.
(Ans. 3-A\ see also FF 1—7.)
We agree with the Examiner’s findings and conclusions, and address
Appellants’ arguments below. We note at the outset, however, that
Appellants advance arguments regarding Hebert (including its reference to
Sagara) in connection with the obviousness rejection (see Appeal Br. 8—9),
but those arguments are deemed to be fully addressed by the anticipation
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finding discussed above. See In re McDaniel, 293 F.3d 1379, 1385 (Fed.
Cir. 2002) (“anticipation is the epitome of obviousness”) (citations omitted).
We thus limit our discussion to Appellants’ arguments regarding Halevie-
Goldman.
Appellants argue that none of the compounds disclosed for use by
Halevie-Goldman, such as L-methionine, are required by the rejected claims.
(Appeal Br. 7.) Furthermore, according to Appellants, in order to arrive at
claim 27, “the skilled person would have to discard the principal
components of the main claims of Halevie-Goldman, while retaining N-
acetylcysteine, despite the clear teachings of Halevie-Goldman that the only
purpose of including N-acetylcysteine in the composition is to aid
conversion of L-methionine to SAMe.” (Id. at 7—8.) Appellants also argue
that Halevie-Goldman “does not teach or suggest that administration of any
amount of N-acetylcysteine alone is effective in treating a neuropsychiatric
disorder.” (Id. at 8 (emphasis added).)
We are not persuaded. Claim 27 uses the transition term
“comprising.” (Appeal Br. 11; Ans. 14.) “The transition ‘comprising’ in a
method claim indicates that the claim is open-ended and allows for
additional steps.” Invitrogen Corp. v. Biocrest Mfg., L.P., 327 F.3d 1364,
1368 (Fed. Cir. 2003). The allowance of additional steps in a method claim
(such as claim 27) is also consistent with Appellants’ use of “comprising,”
as reflected in the Specification. (Spec. 5.)
As properly construed, claim 27 includes the step of administering a
glutathione precursor, but does not exclude the step(s) of administering
additional components or compounds, such as the compounds recited in
claim 1 of Halevie-Goldman (e.g., L-methionine). That is, claim 27 is not
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limited to administration of a glutathione precursor alone as Appellants
contend. Claim 27, as properly construed, thus reads on Halevie-Goldman.7
(FF 6, 7.) Moreover, at least because the Examiner is not proposing to
modify Halevie-Goldman by “discarding] the two main ingredients of the
composition of Halevie-Goldman,” we are not persuaded by Appellants’
argument that such alleged modification “would render [Halevie-Goldman]
unsatisfactory for its intended purpose.” (Reply Br. 5.)
We discern no error in the Examiner’s rejection of claim 27 for
obviousness. Accordingly, we affirm the rejection of claim 27, and claims
28—36 fall with claim 27 because they were not argued separately.
Conclusions
A preponderance of evidence of record supports the Examiner’s
rejections of claim 27 for anticipation and obviousness. Claims 28—36 were
not argued separately and fall with claim 27.
SUMMARY
We affirm the rejections of all claims on appeal.
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
7 We also note that Halevie-Goldman teaches administering up to 200 mg of
N-acetyl-cysteine to treat neuropsychiatric disorders such as schizophrenia.
(Halevie-Goldman 120.) Cf. Spec. 33 (“[A]n oral dosage unit form contains
between about 0.1 pg and 3000 mg of active compound.”).
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