Ex Parte Gervais et al

Patent Trial and Appeal Board

Jul 16, 2013

12157284 (P.T.A.B. Jul. 16, 2013)

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.
12/157,284 06/09/2008 Francine Gervais 117734 - 03501 6682
76426 7590 07/17/2013
McCarter & English/ Neurochem
265 Franklin Street
Boston, MA 02110
EXAMINER
CRUZ, KATHRIEN ANN
ART UNIT PAPER NUMBER
1629
MAIL DATE DELIVERY MODE
07/17/2013 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 FRANCINE GERVAIS and LOUIS R. LAMONTAGNE
__________

Appeal 2012-002886
Application 12/157,284
Technology Center 1600
__________

Before TONI R. SCHEINER, JEFFREY N. FREDMAN,
and ERICA A. FRANKLIN, Administrative Patent Judges.

FREDMAN, Administrative Patent Judge.

DECISION ON APPEAL
This is an appeal1 under 35 U.S.C. § 134 involving claims to a method
for providing neuroprotection for conditions induced by amyloid-β (Aβ)
peptides or proteins by administering 3-amino-1-propanesulfonic acid or a
salt thereof, which have been rejected for obviousness. We have jurisdiction
under 35 U.S.C. § 6(b). We affirm-in-part.

1 Appellants identify the Real Party in Interest as Bellus Health
Inc. (see App. Br. 1).
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Statement of the Case
Background
The Specification teaches a method of “inhibiting Aβ-induced
neuronal cell death [by] contacting a neuronal cell with an Aβ-interferer,
such that neuronal cell death is inhibited. The Aβ-interferer can interfere
with the ability of the Aβ peptide to form amyloid fibrils and/or with the
ability of the Aβ peptide to bind to a cell surface molecule” (Spec. 3, ¶ 1).
The Specification discloses that the method is drawn to administering 3-
amino-1-propanesulfonic acid as the Aβ-interferer (Spec. 3, ¶ 2, lines 8-10).
The Claims
Claims 1-4, 7 and 8 are on appeal. Claim 1 is representative and reads
as follows:
1. A method for providing neuroprotection against
neurodegeneration, neuronal cell toxicity, neuronal cell
death, neuronal cell loss, or senility, in each case induced by
amyloid-β peptides or proteins, comprising administering 3-
amino-1-propanesulfonic acid or a pharmaceutically
acceptable salt thereof to a subject in need thereof.

The Issue
The Examiner rejected claims 1-4, 7 and 8 under 35 U.S.C. § 103(a)
as obvious based on Kisilevsky2 and Panula-Lehto3 (Ans. 5-7).
The Examiner finds “Kisilevsky . . . [teaches] methods and
compositions useful for the treatment of amyloidosis and amyloid deposition

2 Kisilevsky et al., WO 96/28187 A1, published September 19, 1996.
3 Panula-Lehto et al., Effects of taurine, homotaurine and GABA on
hypothalamic and striatal dopamine metabolism, 346 ARCHIVES OF
PHARMACOLOGY 57-62 (1992).
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in subjects . . . [and] subjects susceptible to amyloidosis” (Ans. 5). The
Examiner finds that Kisilevsky teaches “amyloid proteins and diseases that
are to be treated include b-amyloid [diseases] (Alzheimer’s disease, Downs
syndrome etc…)” (Id.). The Examiner finds “therapeutic compounds useful
in the invention include . . . 3-amino-1-propanesulfonic acid (Id.).
However, the Examiner finds Kisilevsky “does not expressly teach that 3-
amino-1-propanesulfonic acid (homotaurine) is more effective than taurine”
(Ans. 6).
The Examiner finds that Panula-Lehto teaches “homotaurine is more
effective than taurine in altering the striatal Dopamine . . . [and] taurine
tends to reduce neuronal excitability, thereby mimicking the structurally
related inhibitory neurotransmitters Y-aminobutyric acid (GABA) and
glycine . . .” (Ans. 6). Furthermore, the Examiner finds “homotaurine is a
potent GABAA and had a more potent effect on dopamine than GABA and
taurine . . .” (Id.).
The Examiner finds “[i]t would have been obvious to one of ordinary
skills in the art at the time of the invention to employ 3-amino-1-
propanesulfonic acid (homotaurine) for providing neuroprotection against
neurodegeneration, neuronal cell toxicity, neuronal cell death, neuronal cell
loss, decreased neuronal cell communication or senility” (Ans. 6).
Furthermore, the Examiner finds “[o]ne would have been motivated to
employ 3-amino-1-propanesulfonic acid (homotaurine) providing
neuroprotection against neurodegeneration because it is known in the art that
homotaurine is more potent than taurine as taught by [Panula-]Lehto” (Id.).
The Examiner finds that it is known in the art and Kisilevsky teaches “that
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homotaurine [is] effective for the treatment of amyloidosis and amyloid
deposition” (Id.).
The issue with respect to this rejection is: Does the evidence of record
support the Examiner’s conclusion that Kisilevsky and Panula-Lehto render
the claims obvious?
Findings of Fact
The following findings of fact (“FF”) are supported by a
preponderance of the evidence of record.
1. Kisilevsky teaches “[t]herapeutic compounds and methods for
inhibiting amyloid deposition in a subject” (Kisilevsky, abstract).
2. Kisilevsky teaches that “the compositions and methods of the
invention are useful for inhibiting amyloidosis in disorders in which amyloid
deposition occurs. The methods of the invention can be used therapeutically
to treat amyloidosis or can be used prophylactically in a subject susceptible
to amyloidosis” (Kisilevsky 2, ll. 3-6).
3. Kisilevsky teaches “Alzheimer’s disease . . . [a]
neurodegenerative disorder, is characterized by congophilic angiopathy,
neuritic plaques and neurofibrillary tangles, all of which have characteristics
of amyloids. In this case . . . formed by the beta protein” (Kisilevsky 1, ll. 6-
7 and 10-13).
4. Kisilevsky teaches “[s]ulfonated substituted aliphatic
compounds contemplated for use in the invention include 3-amino-1-
propanesulfonic acid (XXII, shown as the sodium salt) . . . and
pharmaceutically acceptable salts thereof” (Kisilevsky 12, ll. 11-14).
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5. Kisilevsky teaches that the “sulfated and sulfonated compounds
used in the methods described herein are commercially available (e.g. Sigma
Chemical Co.. St. Louis, MO, or Aldrich Chemical Co.. Milwaukee, WI)
and/or can be synthesized by standard techniques known in the art”
(Kisilevsky 20, ll. 35-36).
6. The Specification teaches “[a] progressive neuronal cell loss
accompanies the deposition of Aβ amyloid fibrins in senile plaques” (Spec.
1, ll. 8-9).
7. The Specification teaches “[i]n yet further preferred
embodiments, the Aβ-interferer is . . . 3-amino-1-propanesulfonic acid, or a
pharmaceutically acceptable salt thereof” (Spec. 3, ll. 8-10).
Principles of Law
The Examiner has the initial burden of establishing a prima facie case
of obviousness under 35 U.S.C. § 103. In re Oetiker, 977 F.2d 1443, 1445
(Fed. Cir. 1992). Once a prima facie case of obviousness has been
established, evidence in support of unexpected properties may be provided
by appellant; however, “[when an] advantage is not disclosed in appellant’s
application” he is “not in a favorable position to urge it as a basis for the
allowance of claims” In re Herr, 50 CCPA 705, 709 (1962) citing In re
Lundberg, 45 CCPA 838 (1958). Further, evidence of undisclosed
advantages must “‘inherently flow’ from what was disclosed in the
specification” In re Davies, 475 F.2d 667, 670 (1973) citing In re Zenitz, 53
CCPA 746 (1964).

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Analysis
Claim 1
Kisilevsky teaches neurodegenerative disorders such as Alzheimer’s
disease have characteristics of amyloids formed by the beta protein (FF 3)
which may be treated by administering 3-amino-1-propanesulfonic acid or a
pharmaceutically acceptable salt thereof (FF 4). Likewise, Appellant’s
Specification teaches the treatment of Aβ amyloids (FF 6) by administering
an interferer, 3-amino-1-propanesulfonic acid, or a pharmaceutically
acceptable salt thereof (FF 7).
Appellants contend that “Kisilevsky’s very broad disclosure does not
render obvious the use of the specific compound (or its salts) to treat the
recited conditions” (App. Br. 2). Appellants contend that Kisilevsky “does
not state that each and every compound useful in the method of the invention
is useful in conjunction with each and every disclosed disease” (App. Br. 4).
We are not persuaded. Kisilevsky is drawn entirely to “[t]herapeutic
compounds and methods for inhibiting amyloid deposition in a subject”
(Kisilevsky, abstract; FF 1). Kisilevsky teaches that “the compositions . . .
of the invention are useful for inhibiting amyloidosis in disorders in which
amyloid deposition occurs” (Kisilevsky 2, ll. 3-6; FF 2). Kisilevsky further
teaches “[s]ulfonated substituted aliphatic compounds contemplated for use
in the invention include 3-amino-1-propanesulfonic acid (XXII, shown as
the sodium salt) . . . and pharmaceutically acceptable salts thereof”
(Kisilevsky 12, ll. 11-14; FF 4).
When Kisilevsky identifies a compound as “contemplated for use in
the invention”, Kisilevsky is clearly and unambiguously identifying a
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compound which will be “useful for inhibiting amyloidosis in disorders in
which amyloid deposition occurs” (Kisilevsky 2, ll. 3-6; FF 2). This is the
entire intent of Kisilevsky (FF 3). We recognize that there are a number of
diseases listed in Kisilevsky, but Kisilevsky is reasonably interpreted as
teaching that the listed compounds will treat “amyloidosis in disorders in
which amyloid deposition occurs” (Kisilevsky 2, ll. 3-6; FF 2). There is no
separate discussion in Kisilevsky suggesting that different compounds treat
different diseases.
Appellants contend “[t]he very broad disclosure of large classes of
compounds and the very broad recitation of the exemplary species within
these classes, in combination with the very broad disclosure of amyloidosis
types and numerous exemplary associated diseases, make clear that
Kisilevsky does not effectively disclose the particular use of 3-amino-1-
propanesulfonic acid or a salt thereof as recited in the claims for treatment of
amyloid-β peptide or protein induced conditions as recited in the claims”
(App. Br. 3). Appellants argue “In re Baird4 is dispositive of the no prima
facie obviousness issue” where “the Federal Circuit held that the mere fact
that a genus encompasses claimed subject matter is not sufficient to establish
prima facie obviousness.” Appellants contend In re Baird is similar to the
Examiner’s position in the case at hand.
We are not persuaded. In Baird, the Federal Circuit found that the
generic formula encompassed “more than 100 million different diphenols,
only one of which is bisphenol A [the compound at issue].” Baird, 16 F.3d at

4 In re Baird, 16 F.3d 380 (1994).
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382. In Baird, there was no direction to the specific compound, much less
any indication that the specific compound at issue would function.
By contrast, the case at hand presents a very different situation where
Kisilevsky specifically identifies the 3-amino-1-propanesulfonic acid as an
exemplary compound which is taught to treat amyloid deposition (FF 1-4).
See Perricone v. Medicis Pharm. Corp. 432 F.3d 1368, 1376 (Fed. Cir.
2005) (“This court rejects the notion that one of [14 listed] ingredients
cannot anticipate because it appears without special emphasis in a longer
list.”); see also Merck & Co. v. Biocraft Labs., Inc., 874 F.2d 804, 807 (Fed.
Cir. 1989) (holding that the prior art’s disclosure of a multitude of
combinations failed to render any particular formulation less obvious).
In the instant case, the rejection is obviousness, not anticipation, so it
is only necessary that the teaching of Kisilevsky render obvious the use of 3-
amino-1-propanesulfonic acid as an exemplary compound which is taught to
treat amyloid deposition (FF 1-5). In Gleave, the Federal Circuit expressly
addressed the issue of lists of large numbers of compounds, where the “list
includes more than 1400 sequences.” In re Gleave, 560 F.3d 1331, 1333
(Fed. Cir. 2009). The Court, found that “Wraight expressly lists every
possible fifteen-base-long oligodeoxynucleotide sequence in IGFBP-2, and
under our precedent, this list anticipates Gleave’s claims.” Id. at 1338.
Consequently, we agree with Examiner that Kisilevsky teaches that
homotaurine is “effective for the treatment of amyloidosis and amyloid
deposition in subjects . . . [thus] one of ordinary skills would have [a]
reasonable expectation of success in administering homotaurine for
treatment of neuroprotection against neurodegeneration” (Ans. 6-7). We
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find Examiner has met the burden of establishing a prima facie case of
obviousness.
Appellants contend that the claimed compound, 3-amino-1-
propanesulfonic acid, possesses unexpected properties of superiority which
can overcome a prima facie case of obviousness. The Kong5 Declaration
states that “3-amino-1-propanesulfonic acid (3-APS) protected the involved
neuronal cells against adverse effects of Aβ42 to a significant degree and
that 2-aminoethanesulfonic acid (taurine) showed no protection at all” (Kong
Dec. 1).
Although we find Appellants’ results showing the statistically
significant effect of 3-amino-1-propanesulfonic acid over taurine, a similarly
structured molecule disclosed in the prior art, credible, we do not find the
Declaration overcomes the prima facie case of obviousness established by
the Examiner because the results set forth in Declaration were not identified
and lack descriptive support in the Appellants’ Specification.
Specifically, we do not find any teaching in Appellants’ Specification
that 3-amino-1-propanesulfonic acid would have unexpected properties in
reducing A-induced neuronal cell death relative to taurine for treatment of
Aβ-amyloids. Rather, Appellants’ Specification merely lists both taurine
and 3-amino-1-propanesulfonic acid in a list of compounds (see Spec. 3-4).
Indeed, Appellants’ Specification identifies taurine as “preferred” and
identifies homotaurine as simply “contemplated for use in the invention”
(see Spec. 17-18). Based on the lack of disclosure of the unexpected

5 Declaration under 37 C.F.R. § 1.132 filed by Xianqi Kong on
Mar. 17, 2009.
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properties in Appellants’ specification, it appears Appellants were not aware
of or in possession of the results disclosed in the Kong Declaration at the
time of filing the application. The en banc Court of Customs and Patent
Appeals concluded that “[when an] advantage is not disclosed in appellant’s
application” he is “not in a favorable position to urge it as a basis for the
allowance of claims” In re Herr, 50 CCPA 705, 709 (1962). While a panel
of the Federal Circuit in Genetics Institute v. Novartis Vaccines and
Diagnostics, 655 F.3d 1291, 1307 (Fed. Cir. 2011) found that “every
property of a claimed compound need not be fully recognized as of the filing
date of the patent application to be relevant to nonobviousness”, even the
Genetics panel recognized that the evidence must be that “which ‘would
inherently flow’ from what was originally disclosed”) (quoting In re Zenitz,
52 CCPA 746, 333 F.2d 924, 927 (1964); see also Davies, 475 F.2d at 670
(1973).
Moreover, allowing post-filing date data that is entirely unsupported
by the Specification to serve as evidence of unexpected results subverts the
quid pro quo inherent in the patent system. 35 U.S.C. § 112, first paragraph
(2012) sets the expectation that the “specification shall contain a written
description of the invention . . . and shall set forth the best mode
contemplated by the inventor or joint inventor of carrying out the invention.”
It is inconsistent with the patent statute itself to advantage an unexpected
result not described in the Specification, whose best mode is therefore not
revealed until well after the application is filed. This situation differs from
other secondary consideration such as commercial success, copying, or
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praise by others, which address the question of whether the marketplace
found the novel invention nonobvious.
The instant situation also differs from the case where the Specification
focused on a single compound, device, or method which was later shown to
inherently have unexpected results. That is the situation where the
unexpected results “would inherently flow” from the Specification. The
originally filed independent claim 1 in Grandparent US application
09/874,543 was drawn to any A-interferer compound with taurine (2-
aminoethanesulfonic acid) listed in claim 10, while homotaurine was listed
in claim 13. There was no recognition in the Specification that homotaurine
was superior to taurine.
Appellants have provided no evidence which would support a finding
that the superiority of homotaurine over taurine in the specific assay
presented in the Kong Declaration “would inherently flow” from any
teaching in the Specification. Indeed, in Knoll, the case relied upon by the
divided Genetics panel for the rule that a property need not be recognized by
the filing date, limited the use of post filing data “to respond to litigation
attacks on validity.” Knoll Pharmaceutical Co., Inc. v Teva Pharmaceuticals
USA, Inc., 367 F.3d 1381, 1385 (Fed. Cir. 2004). This rationale does not
reasonably apply to determinations made within the USPTO prior to
allowance, otherwise postfiling data showing unexpected results not
contemplated by the Specification could be presented in every chemical
case, so long as sufficient numbers of different compounds were tested to
find, post hoc, a compound which provided a different post hoc result in the
assay test being performed.
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We conclude that the unexpected results submitted in the Declaration
fail to overcome the prima facie case of obviousness when these results were
not included in the original application and thus, no properties in the original
disclosure are found to be unobvious or unexpected.
Claims 2 and 3
Appellants contend that claims 2 and 3 differ because they are drawn
separately to the compound and to the sodium salt (see App. Br. 11).
We are not persuaded. As discussed above, where the specific
compound is expressly included in a list, the fact that the Kisilevsky
“discloses a multitude of effective combinations does not render any
particular formulation less obvious. This is especially true because the
claimed composition is used for the identical purpose taught by the prior
art.” Merck, 874 F.2d at 807.
Claim 8
Appellants contend that Kisilevsky is “silent with respect to whether
its compounds would provide effects such as those recited in the claims of
this application which are induced by soluble (not deposited) -amyloid
peptides or proteins” (App. Br. 11).
The Examiner does not specifically address claim 8, nor does the
Examiner identify any teaching in Kisilevsky regarding the effect of the
claimed compounds on soluble -amyloid peptides or proteins. We are
therefore constrained to reverse the rejection of claim 8.
Conclusion of Law
The evidence of record supports the Examiner’s conclusion that
Kisilevsky and Panula-Lehto render claims 1-4 and 7 obvious.
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The evidence of record does not support the Examiner’s conclusion
that Kisilevsky and Panula-Lehto render claim 8 obvious.
SUMMARY
In summary, we affirm the rejection of claims 1-3 under 35 U.S.C.
§ 103(a) as obvious over Kisilevsky and Panula-Lehto. Pursuant to 37
C.F.R. § 41.37(c)(1), we also affirm the rejection of claims 4 and 7, as these
claims were not argued separately.
We reverse the rejection of claim 8 under 35 U.S.C. § 103(a) as
obvious over Kisilevsky and Panula-Lehto.

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-IN-PART

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