Ex Parte Daly

Patent Trial and Appeal Board

Nov 28, 2017

11542982 (P.T.A.B. Nov. 28, 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.
11/542,982 10/04/2006 John Daly 109797.000025 4144
7590
BAKER & HOSTETLER LLP
WASHINGTON SQUARE, SUITE 1100
1050 CONNECTICUT AVE. N.W.
WASHINGTON, DC 20036-5304
EXAMINER
MARVICH, MARIA
ART UNIT PAPER NUMBER
1633
NOTIFICATION DATE DELIVERY MODE
11/30/2017 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
following e-mail address(es):
eofficemonitor@bakerlaw.com
edervis @bakerlaw.com
patents @ bakerlaw. com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte JOHN DALY
Appeal 2017-001558
Application 11/542,9821
Technology Center 1600
Before ERIC B. GRIMES, TAWEN CHANG and DAVID COTTA,
Administrative Patent Judges.
COTTA, Administrative Patent Judge.
DECISION ON APPEAL
This is an appeal under 35 U.S.C. § 134 involving claims to a method
for assaying an effect of a test agent on the activity of a non-constitutive
promoter. The Examiner rejected the claims on appeal as obvious under 35
U.S.C. § 103(a).
We reverse.
1 According to Appellant, the real party in interest is Thermo Fisher
Scientific, the exclusive licensee of the Assignee, Gene Stream PTY LTD,
and the Assignee Gene Stream PTY LTD. App. Br. 1.
Appeal 2017-001558
Application 11/542,982
STATEMENT OF THE CASE
The Specification discloses that “[t]here is a need ... to develop
improved vectors and systems for conducting gene expression assays and in
particular post-transcriptional assays as well as assays that permit a more
real-time determination of changes in gene expression.” Spec. 143. The
Specification asserts that the “present invention is predicated in part on the
development of a novel series of constructs and methods which permit inter
alia modulation and determination of transcript stability and/or improved
real-time determination of gene expression.” Id. 144.
Claims 23, 33—37, 39-46, 48 and 50 are on appeal. Claim 23 is
illustrative and reads as follows (with emphasis added to highlight disputed
limitation):
23. A method for assaying an effect of a test agent on the
activity of a non-constitutive promoter in cells of a first type,
the method comprising:
expressing in cells of the first type, in the presence and
the absence of the test agent, a first polynucleotide comprising
the coding sequence of a first polypeptide wherein the first
polynucleotide is in a construct comprising, in operable linkage:
a sequence comprising the non-constitutive promoter, the first
polynucleotide and a nucleic acid sequence encoding a U-rich
and/or AU-rich element that reduces the stability of a transcript
produced from the expression of the first polynucleotide in both
the presence and the absence of the test agent with the proviso
that the construct lacks an element that stabilizes the transcript;
measuring the level or the activity of the first polypeptide
produced from the construct in the presence and the absence of
the test agent; and
comparing the measured level or the measured activity of
the first polypeptide in the presence of the test agent to the
measured level or the measured activity of the first polypeptide
in the absence of the test agent wherein a difference indicates
the effect of the test agent on the non-constitutive promoter;
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Appeal 2017-001558
Application 11/542,982
wherein the non-constitutive promoter, the coding
sequence and the nucleic acid sequence are heterologous to
each other.
App. Br. 9.
The claims stand rejected as follows:
Claims 23, 33—35, 39-45 and 50 were rejected under 35 U.S.C. §
103(a) as unpatentable over the combination of Nunokawa,2 and Ni3 or
Rosen.4
Claims 36, 37, 46 and 48 were rejected under 35 U.S.C.
§ 103(a) as unpatentable over the combination of Nunokawa, Ni or
Rosen, and Kriz5 or Kain.6
ANALYSIS
The same issue is dispositive with respect to both rejections.
Accordingly, we address both rejections together.
In rejecting the pending claims as obvious, the Examiner found that
Nunokawa disclosed a method for assaying an effect of a test agent on the
activity of NF-kB regulated promoters comprising all of the steps of the
claimed method except that it did not disclose using a promoter that was
heterologous to the “first polynucleotide . .. coding sequence” and the “U-
rich and/or AU-rich” “nucleic acid sequence.” Ans. 3—6. With respect to
this requirement, the Examiner found that Nunokawa was not limited to
2 Nunokawa, US Patent No. 6,156,516, issued Dec. 5, 2000 (“Nunokawa”).
3 Ni et al., US Patent No. 5,965,421, issued Oct. 12, 1999 (“Ni”).
4 Rosen et al., US Patent Publication No. 2002/0102638 Al, published Aug
1, 2002 (“Rosen”).
5 Kriz et al., US Patent No. 6,433,252 Bl, issued Aug. 13, 2002 (“Kriz”).
6 Kain et al., US Patent No. 6,306,600 Bl, issued Oct. 23, 2001 (“Kain”).
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Appeal 2017-001558
Application 11/542,982
using the disclosed 5’ HiNOS promoter. Final Act.7 3. Instead, “any NfKb
containing promoter can be used.” Id. at 6. The Examiner further found that
both Ni and Rosen disclosed promoters that were heterologous to the first
polynucleotide coding sequence and the U-rich and/or AU-rich nucleic acid
sequence disclosed in Nunokawa. Id. The Examiner then concluded that the
skilled artisan would have found it obvious to “use the promoters of Ni or
Rosen et al with the methods of Nunokawa” because “Nunokawa et al teach
that it is within the ordinary skill of the art to screen compounds that affect
NF-KB . . . and because Ni and Rosen et al teach such promoter for said
same purpose.” Id. at 7. The Examiner further concluded “it is routine in
the art to substitute well known components in related methods.” Id.
Appellant argues, inter alia, that “Nunokawa does not teach or
suggest that any other promoter, other than its hiNOS promoter, could
function in the method described therein, and the Examiner does not provide
any evidence to the contrary.” App. Br. 2. Appellant asserts that
Nunokawa’s hiNOS promoter requires the cooperation of the 3’ and 5’
flanking regions in order to regulate expression. Accordingly, Appellant
contends that “[a] skilled person in the art.. . would not expect that one
could substitute the 5’ flanking region from a completely different, i.e.,
heterologous, gene and recreate the same cooperation.” Id. at 4. More
specifically, Appellant contends that “the skilled person in the art would
assume . . . that the sequence differences between one promoter (comprising
an NF-KB recognition sequence) and another different promoter (also
comprising a NF-KB recognition sequence) would prevent recreation of the
cooperation that Nunokawa requires.” Id.
1 Office Action mailed Oct. 2, 2015 (“Non-Final Act.”).
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Application 11/542,982
As stated in In re Oetiker, 977 F.2d 1443, 1445 (Fed. Cir. 1992):
“[T]he examiner bears the initial burden ... of presenting a prima facie case
of unpatentability.” Appellant has persuaded us that the Examiner has not
carried the burden of establishing that the claimed invention would have
been obvious over the cited art.
Nunokawa discloses a “method for screening and evaluating a
synthetic compound or naturally occurring compound which inhibits an
activation of NF-kB” using a “gene having a sequence which regulates the
expression of human inducible nitric oxide synthase (hiNOS) gene.”
Nunokawa col. 1,11. 6—12. To replicate NF-kB regulation in vivo,
Nunokawa created a construct comprising the hiNOS gene, a portion of the
5’ UTR of the hiNOS gene, and a portion of the 3’ UTR of the hiNOS gene.
Id. at col. 11,11. 5—22. Constructs that lacked both the 5’ UTR and the 3’
UTR did not recreate proper regulation of expression of the hiNOS gene. Id.
at col. 10,1. 65 — col. 11,1. 4. Nunokawa thus discovered that it was critical
to include both the 5 ’ UTR and the 3 ’ UTR because “expression regulation
of a hiNOS gene is carried out by the upstream portion containing the 5’-
UTR and the downstream portion containing the 3’-UTR in corporation [sic,
cooperation].” Id. at col. 11,11. 11—15 (emphasis added); see also, id. at col.
5,11. 28—35 (explaining that insertion of a region containing the 3 ’-UTR and
the 3’-flanking region of the hiNOS gene downstream of the reporter gene in
an expression vector “drived [sic, drove] the promoter of the hiNOS gene”
and that “the inserted region was found to participate in strong expression in
corporation [sic, cooperation] with the promoter region containing the NF-
kB recognition region.”)
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Application 11/542,982
Given Nunokawa’s teaching that proper regulation of expression of
the hiNOS gene is carried out by 3’ and 5’ regions acting in cooperation, we
agree with Appellant that the skilled artisan “would not expect that one
could substitute the 5' flanking region from a completely different, i.e.,
heterologous, gene and recreate the same cooperation.” App. Br. 4. As
Appellant explains, “the three dimensional structure would not be the same,
and the 5’ sequences that interact with 3’ sequences would likely be absent.”
Id. As the Examiner has not provided persuasive evidence that the skilled
artisan would reasonably expect the cooperation between 3 ’ and 5 ’ regions
to continue in the manner disclosed in Nunokawa if the promoters disclosed
in Ni and Rosen were substituted for Nunokawa’s hiNOS promoter, we
reverse the Examiner’s rejection of claims 23, 33—37, 39-46, 48 and 50.
SUMMARY
For the reasons set forth herein, we reverse the Examiner’s rejection
of claims 23, 33—35, 39-45 and 50 obvious over the combination of
Nunokawa, and Ni or Rosen and of claims 36, 37, 46 and 48 as obvious over
the combination of Nunokawa, Ni or Rosen, and Kriz or Kain.
REVERSED
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