Ex Parte Matsuyama

Patent Trial and Appeal Board

Mar 14, 2017

13679439 (P.T.A.B. Mar. 14, 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
www.uspto.gov
APPLICATION NO. FILING DATE FIRST NAMED INVENTOR ATTORNEY DOCKET NO. CONFIRMATION NO.
13/679,439 11/16/2012 Shigemi Matsuyama CWR-019245US CON-1 9748
68705 7590 03/16/2017
TAROLLI, SUNDHEIM, COVELL & TUMMINO, LLP
1300 EAST NINTH STREET
SUITE 1700
CLEVELAND, OH 44114
EXAMINER
KAUFMAN, CLAIRE M
ART UNIT PAPER NUMBER
1646
NOTIFICATION DATE DELIVERY MODE
03/16/2017 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 SHIGEMI MATSUYAMA1
Appeal 2016-003978
Application 13/679,439
Technology Center 1600
Before ERIC B. GRIMES, RYAN H. FLAX, and
DEVON ZASTROW NEWMAN, Administrative Patent Judges.
GRIMES, Administrative Patent Judge.
DECISION ON APPEAL
This is an appeal under 35U.S.C. § 134 involving claims to a
pharmaceutical composition, which have been rejected as being directed to
patent-ineligible subject matter. We have jurisdiction under 35 U.S.C.
§ 6(b).
We affirm.
1 Appellant identifies the Real Party in Interest as Case Western Reserve
University. (Appeal Br. 2.)
Appeal 2016-003978
Application 13/679,439
STATEMENT OF THE CASE
The Specification states that the “cellular attrition observed in most
degenerative conditions is apoptotic in nature.” (Spec.213.) “Bax is . . .
involved in regulating programmed cell death. Bax plays a key role in the
intrinsic pathway of apoptosis.” {Id. 14.)
The Specification discloses “a method of inhibiting apoptosis in a cell.
The method includes administering to the cell a therapeutically effective
amount of cell penetrating peptide (CPP). The CPP consists of about 5 to
about 41 amino acids and is substantially homologous to a portion of the C-
terminal region of interferon gamma receptor 2 (IFNyR2).’’ {Id. 1 5.) “An
‘effective amount’ or ‘therapeutically effective amount’ of CPP
administered to a cell is the amount of the CPP effective to mitigate Bax
mediated apoptosis in the cell.” {Id. 133.)
Claims 36, 38-40, 42, and 43 are on appeal. Claim 36 is the only
independent claim and reads as follows:
Claim 36: A pharmaceutical composition comprising:
a synthetic peptide for inhibiting apoptosis in a cell
consisting of about 5 to about 41 amino acids of SEQ ID NO: 1; and
a pharmaceutically acceptable carrier.
DISCUSSION
The Examiner has rejected all of the claims on appeal under 35 U.S.C.
§ 101 on the basis that they are directed to patent-ineligible subject matter;
specifically, “a law of nature/natural principle.” (Ans. 2.) The Examiner
2 Our citations are to the “Clean Specification” filed Feb. 12, 2013.
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finds that natural products are not patent-eligible, and a “fragment of a
natural product which does not possess[] properties different than those it
possesses when part of the full-length protein (aside from size) may also be
considered a natural product.” (Id.) The Examiner finds that “the claimed
peptide is part of the Bax-inhibiting domain of IFNyR2 and naturally has the
property of inhibiting Bax-mediated apoptosis both as a fragment and as part
of IFNyR2,” and therefore is not patentable subject matter. (Id.)
We agree with the Examiner that claim 36 is not patent-eligible
subject matter. Claim 36 is directed to composition comprising a carrier and
a peptide that is a fragment of the naturally occurring IFNyR2 protein. Thus,
Association for Molecular Pathology v. Myriad Genetics, Inc., 133 S.Ct.
2107 (2013), is controlling. In Myriad, the Court considered claims directed
to isolated DNA encoding the BRCA1 polypeptide and fragments of at least
15 nucleotides of that DNA. Id. at 2113.
The Court held that “Myriad did not create anything. To be sure, it
found an important and useful gene, but separating that gene from its
surrounding genetic material is not an act of invention.” Id. at 2117. “Myriad
found the location of the BRCA1 and BRCA2 genes, but that discovery, by
itself, does not render the BRCA genes ‘new . . . composition^] of matter,’
§ 101, that are patent eligible.” Id. “Nor are Myriad’s claims saved by the
fact that isolating DNA from the human genome severs chemical bonds and
thereby creates a nonnaturally occurring molecule.” Id. at 2118.
The same analysis applies here. Claim 36 is directed to fragments of a
naturally occurring protein, separated from the rest of the protein. Appellant
has identified certain peptides, with naturally occurring amino acid
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Application 13/679,439
sequences, that have the property of inhibiting Bax-mediated apoptosis, but
this property does not render the peptides new compositions of matter that are
patent-eligible. Rather, claim 36 is directed to products of nature.3
Appellant argues that the
claimed composition modifies the structure of the naturally
occurring IFNyR2 peptide by only using a fragment, the
IFNyR2296-337 domain (SEQ ID NO: 1), of the full-length peptide.
The synthetic peptide has a markedly different structure than
IFNyR2 in that it only has about 5 to about 41 amino acids of
SEQ ID NO: 1, whereas IFNyR2 has 337 amino acids.
(Br. 6—7.) Appellant argues that “[t]he synthetic peptides involve the
creation of a new compound, unlike the isolated DNA that coded for a
BRCA1 polypeptide in [Myriad].” (Id. at 10.)
This argument is not persuasive because the Myriad Court expressly
held that the isolated BRCA genes were not patent-eligible even though
isolating the DNA required severing chemical bonds. Myriad, 133 S.Ct. at
2118. The same conclusion would follow even if the peptide were
manufactured rather than isolated from the whole protein. See also In re
BRCA1- and BRCA2-based Hereditary Cancer Test Patent Litigation, 11A
F.3d 755, 760 (Fed. Cir. 2014) (“The Supreme Court held ineligible claims
directed to segments as short as 15 nucleotides, the same length as the
primer claims at issue here, suggesting that even short strands identical to
3 Claim 36 recites a “synthetic” peptide but “[a]s the Supreme Court made
clear, neither naturally occurring compositions of matter, nor synthetically
created compositions that are structurally identical to the naturally occurring
compositions, are patent eligible.” In re BRCA1- and BRCA2-based
Hereditary Cancer Test Patent Litigation, 11A F.3d 755, 760 (Fed. Cir.
2014).
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Appeal 2016-003978
Application 13/679,439
those found in nature are not patent eligible.”). The logic of the Myriad
Court also applies when the naturally occurring product is a fragment of a
protein rather than a gene.
Appellant also argues that the claimed composition comprises a
carrier in addition to the peptide, and that “pharmaceutically acceptable
carriers comprise excipient[s] and auxiliaries that facilitate processing of the
active agents into preparations that can be used pharmaceutically. The
carrier modifies the properties of the peptide so that it is easier for
processing and administration to a subject.” (Br. 8, citing Spec. 151.)
Appellant argues that “since the carrier modifies the properties of the
synthetic peptide so that it is easier for processing and administration to a
subject, the claimed composition has markedly different characteristics than
the naturally occurring IFNyR2 peptide and is not a ‘product of nature.’”
(Id. at 10.)
This argument is also unpersuasive. The Specification states that
“[t]he pharmaceutical compositions of the present invention can include
pharmaceutically acceptable carriers comprising excipients and auxiliaries
that facilitate processing of the active agents into preparations that can be
used pharmaceutically.” (Spec. 1 51, emphasis added.) Thus, the
Specification does not define “pharmaceutically acceptable carriers” to
require excipients and auxiliaries, but only states that they are possible
components of a carrier.
The Specification also states that “[fjormulations for parenteral
administration include aqueous solutions of the active compounds in water-
soluble form, for example, water-soluble salts and alkaline solutions.” (Id.
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Application 13/679,439
at | 52, emphasis added.) Thus, the broadest reasonable interpretation of a
“pharmaceutically acceptable carrier,” read in light of the Specification,
includes water—the carrier in the case of an aqueous solution. We agree
with the Examiner (Ans. 4) that combining the naturally occurring peptide
recited in claim 36 with water would not result in a composition with
markedly different properties from those of the peptide itself, and does not
render the composition of claim 36 patent-eligible.
Finally, Appellant argues that the peptide recited in claim 36 “has
different properties than those of the naturally occurring IFNyR2 that can be
attributed to the structural changes.” (Br. 11.) Appellant argues that “[t]he
naturally occurring IFNyR2 peptide can participate in JAK/STAT signaling
while the synthetic peptide cannot.” (Id.)
These arguments are not persuasive, because they are not supported
by the evidence provided by Appellant’s Specification. With regard to
JAK/STAT signaling, the Specification states that
[t]o confirm that IFNyR2 does not require Jak2-mediated
signaling for Bax inhibition, human cell lines lacking IFNyR2
and Jak2[ ]were examined. . . . IFNyR2296-337 and IFNyR2wild
type were both able to inhibit etoposide-induced [i.e., Bax-
mediated] apoptosis in these cells, but IFNyR21.295 could not
(Fig. 2B-E). These results support the hypothesis that IFNyR2
can rescue cells from apoptosis independent of Jak2-mediated
signal transduction.
(Spec. 1 87.) “IFNyR2296-337” is the peptide of SEQ ID NO: 1. (Id. 130.)
Thus, the Specification states that both the full-length (wild-type) IFNyR2
and the peptide corresponding to SEQ ID NO: 1 both inhibit Bax-mediated
apoptosis in cells lacking Jak2; i.e., independent of JAK/STAT signaling.
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Application 13/679,439
Appellant also argues that “the new peptide demonstrates increased
inhibition of Bax-mediated apoptosis compared to the natural product.” (Br.
11.) Appellant points specifically to the results shown in Figures 2B—E, 4A,
and 7C—E. (Id.)
Again, the evidence provided in the Specification does not support
Appellant’s argument. Figures 2B—2E relate to the experiments done in
cells lacking Jak2, and are discussed above. Regarding Figure 4A, the
Specification states that “IFNyR2wild type as well as IFNyR2296-337 were
able to inhibit apoptosis induced by Bim overexpression.” (Spec. 1 89.)
Regarding Figures 7C—E, the Specification states that “IFNyR2296-337-GFP as
well as IFNyR2wild type-GFP (Fig. 7C and D) inhibited STS-induced Bax
activation. . . . The inhibition of Bax activation by IFNyR2296-337-GFP as
well as IFNyR2 wild type-GFP was statistically significant (Fig. 7E).”
(Spec. 195.) Thus, the Specification states that the results for the full-length
IFNyR2 and those for the peptide of SEQ ID NO: 1 were comparable, not
that those for the peptide were significantly different from those for the full-
length protein.
In summary, we agree with the Examiner that the claimed
composition is not markedly different from a naturally occurring product.
We therefore affirm the rejection of claim 36 under 35 U.S.C. § 101. Claims
38-40, 42, and 43 have not been argued separately and therefore fall with
claim 36. 37 C.F.R. § 41.37(c)(l)(iv).
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Application 13/679,439
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
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