Ex Parte Pfleger et al

Patent Trial and Appeal Board

Jan 8, 2018

13833230 (P.T.A.B. Jan. 8, 2018)

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.
13/833,230 03/15/2013 BRIAN FREDERICK PFLEGER 09820.515-P120377US02 9267
60961 7590 01/10/2018
Intellectual Property Dept./Dewitt Ross & Stevens
Wisconsin Alumni Research Foundation
2 East Mifflin Street,
Suite #600
Madison, WI 53703-2865
EXAMINER
EKSTROM, RICHARD C
ART UNIT PAPER NUMBER
1652
NOTIFICATION DATE DELIVERY MODE
01/10/2018 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):
IP-DOCKET @ dewittross.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte BRIAN FREDERICK PFLEGER and DANIEL E. AGNEW
Appeal 2016-007913
Application 13/833,2301
Technology Center 1600
Before FRANCISCO C. PRATS, ROBERT A. POLLOCK, and
DAVID COTTA, Administrative Patent Judges.
COTTA, Administrative Patent Judge.
DECISION ON REQUEST FOR REHEARING
Appellants filed a Request for Reconsideration of our Decision of
October 17, 2017 (“Decision”) affirming the Examiner’s obviousness
rejections. We have jurisdiction under 35 U.S.C. § 6(b). Appellants present
several arguments for our reconsideration. We have reconsidered our
Decision in light of Appellants’ positions, and have found no errors.
1 According to Appellants, the real party in interest is the Wisconsin Alumni
Research Foundation. App. Br. 2.
Appeal 2016-007913
Application 13/833,230
ANALYSIS
The claims on appeal are directed to “a recombinant cell for
producing polyhydroxyalkanoate [PHA] . . . wherein gene products of genes
fadA and fadl; fadB and fadJ; or fadA,fadI, fadB and fadJ are functionally
deleted due to genetic modification of the genes.” App. Br., Claim Appx. 1.
We affirmed the Examiner’s rejection of claims 1—6, 8, 10—14, 16, and 17
under 35 U.S.C. § 103(a) as obvious over the combination of Li,2 Pfleger,3
Hein,4 Nelson,5 GenBank,6 Wang,7 and Rehm8 and the Examiner’s rejection
of claims 1—6, 8, and 10—17 over the same art plus Rehm 2011,9 In relevant
part, we found:
Pfleger discloses fadA, fadB, fadl and fadJ as among a
finite group of genes, the functional deletion of which increases
the production of fatty acid. FF10. Rehm and Li disclose that
2 Li et al., A Novel-Designed Escherichia Coli for the Production of Various
Polyhydroxyalkanoates from Inexpensive Substrate Mixture, 75 Appl.
Microbiol Biotechnol, 1103-1109 (2007) (“Li”).
3 Pfleger et al., US Patent Publication No. 2011/0165637 Al, published
July 7, 2011 (“Pfleger”).
4 Hein et al., US Patent No. 7,968,325 B2, issued June 28, 2011 (“Hein”).
5 Nelson et al., Complete Genome Sequence and Comparative Analysis of
the Metabolically Versatile Pseudomonas Putida KT2440, 4(12)
Environmental Microbiology 799-808 (2002).
6 GenBank Accession No. AAN66388.1 (“GenBank”).
7 Wang et al., Development of a New Strategy for Production of Medium-
Chain-Length Polyhydroxyalkanoates by Recombinant Escherichia Coli Via
Inexpensive Non-Fatty Acid Feedstocks, 78(2) Applied and
Environmental Microbiology 519-527 (2012) (“Wang”).
8 Rehm, Heterologous Expression of the Acyl-Acyl Carrier Protein
Thioesterase Gene from the Plant Umbellularia Californica Mediates
Polyhydroxyalkanoate Biosynthesis in Recombinant Escherichia Coli, 55
Appl. Microbiol Biotechnol 205-209 (2001) (“Rehm”).
9 Rehm et al., US Patent Publication No. 2011/0124516 Al, published
May 26, 2011 (“Rehm 2011”).
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Appeal 2016-007913
Application 13/833,230
fatty acid is a precursor in the production of PHAmcl in E. coli.
FF4, FF5, FF9. Rehm and Li also disclose that inhibiting P-
oxidation of fatty acid is necessary for E. coli to produce PHA.
FF1 (disclosing that “blockage of fatty acid beta-oxidation
pathway at fadB or fadA site is need[ed]” for “[production of
PHAmcl”)? FF6 (disclosing that after investigating “wild-type
E. coli and various fad mutants . . . only when the P-oxidation
pathway was impaired PHAmcl accumulation from gluconate
was observed”). Finally, Li discloses a fadA mutant that
produces PHA (FF2-4) and Rehm discloses a fadB mutant that
produces PHA. FF7 & FF8.
To the skilled artisan, these teachings would have
suggested increasing the production of fatty acids and/or
inhibiting the P-oxidation of fatty acids as a way to increase the
production of PHA. More specifically, these teachings would
have suggested functionally deleting any of the genes identified
by Pfleger, including fadl and fadJ as a way to increase the
production of PHA. See KSR Int’l Co. v. Teleflex Inc., 550 U.S.
398, 421 (2007) (“When there is a design need or market
pressure to solve a problem and there are a finite number of
identified, predictable solutions, a person of ordinary skill has
good reason to pursue the known options within his or her
technical grasp. If this leads to the anticipated success, it is
likely the product not of innovation but of ordinary skill and
common sense. In that instance the fact that a combination was
obvious to try might show that it was obvious under § 103.”).
Decision 8—9.
Appellants argue that the Decision failed to consider that “the record
to date shows no previously known or suspected role offadl and/or fadJ in
P-oxidation, and the alleged obviousness based on such an alleged role is
improper.” Req. Reh’g 2. We are not persuaded because, our decision does
not depend upon the skilled artisan knowing or suspecting the “role offadl
and fadJ in P-oxidation.” Rather, we found that the combined art suggested
increasing the production of fatty acids as one way to increase the
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Application 13/833,230
production of PHA. As discussed in the Decision, Pfleger discloses fadA,
fadB, fadl, and fadJ as among a finite group of genes, the functional deletion
of which increases the production of fatty acid. Decision 8—9; FF10.
Appellants argue that the Decision “offered no findings of fact or any
other evidence to counter” their argument that the prior art teaches that
deleting fadE disrupts PHA production, and thus the person of ordinary skill
in the art would not have been able to predict that deleting fadl and/or fadJ
would have the opposite effect. Req. Reh’g. 3. We disagree. The Decision
expressly addressed this argument:
We acknowledge Appellants’ argument that Li
demonstrates that deletion of one of the genes identified in
Pfleger — fadE — actually disrupts PHA production. However,
when the prior art is considered as a whole, we find that the
negative example of fadE is insufficient to counter the
expectation created by the two positive examples in which the
deletion of genes identified by Pfleger (fadA and fadB)
increased PHA production, particularly in view of the general
suggestion in the art (discussed above) to increase production of
fatty acids and/or inhibit the B-oxidation of fatty acids as a way
to increase the production of PHA.
Decision 9—10.
Appellants request that we designate the rejection as a New Ground.
Req. Reh’g. 4. Under the Administrative Procedure Act, an applicant for a
patent who appeals a rejection to the Board is entitled to notice of the factual
and legal bases upon which the rejection was based. 5 U.S.C. § 554(b)(3).
When the Board relies upon a new ground of rejection not relied upon by the
examiner, the applicant is entitled to reopen prosecution or to request a
rehearing. See 37 C.F.R. § 41.50(b). The Board need not recite and agree
with the examiner’s rejection in haec verba to avoid issuing a new ground of
rejection. “[T]he ultimate criterion of whether a rejection is considered
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Application 13/833,230
‘new’ in a decision by the [B]oard is whether [applicants] have had fair
opportunity to react to the thrust of the rejection.” In re Kronig, 539 F.2d
1300, 1302-03 (CCPA 1976) (finding no new ground of rejection when the
Board relied on the same statutory basis and the same reasoning advanced
by the examiner).
We have reviewed the Decision and the Examiner’s rejection and find
both to have the same general thrust. In finding the claimed recombinant
cell obvious, the Decision and the Examiner’s rejection rely upon the same
teachings from the same prior art references. In particular, we note that both
the Decision and the Examiner’s rejection recognize fatty acid as a precursor
in the production of PHA (Decision 9; FF4, FF5, and FF9; Final Act. 9 (Li
“describes the production of polyhydroxyalkanoates in recombinant cells via
a fatty acid intermediate”)) and both recognize the desirability of increasing
the availability of fatty acids as a way to increase production of PHA.
Decision 8—9; Final Act. 9 (explaining that it would have been obvious to
delete any combination of fadA, fadl, fadB, and fadJ in part because
“Pfleger teaches that inhibiting the activity of any of fadA, fadl, fadB and
fadJ, which are all involved in fatty acid beta-oxidation, is desirable for
increasing cellular production of fatty acids.”). That the Decision articulates
the conclusions drawn from these findings differently than does the
Examiner’s rejection does not change the thrust of the rejection. In re
Kronig, 539 F.2d at 1302—03.
Appellants argue that the Decision is based on five “new allegations”
and thus constitutes a new ground of rejection. With regard to first alleged
“new allegation,” Appellants argue that the “original rejections are not based
on an alleged ‘general suggestion in the art... to increase production of
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Appeal 2016-007913
Application 13/833,230
fatty acids and/or inhibit the P-oxidation of fatty acids as a way to increase
production of PHA.’” Req. Reh’g 5. This argument is belied by the Appeal
Brief which characterizes the Examiner’s rejection as follows: “[t]he Office
has alleged that any given gene deletion increasing fatty acid production
would ‘reasonably be expected to increase polyhydroxyalkanoate
production.’” App. Br. 7 (emphasis added). This characterization is
consistent with the Examiner’s rejection, but inconsistent with Appellants’
argument that the Examiner’s rejection was not based on a suggestion to
increase fatty acid production.
With respect to second “new allegation,” Appellants contend:
With regard to Allegation 2, the original rejections
merely allege it would have been obvious “to have used any
combination of deletion mutants of fadA, fadl, fadB and fadJ in
the recombinant cells of Li 2007” because “fadA, fadl, fadB
and fadl... are all involved in fatty acid beta-oxidation.” . . . The
original rejections are silent regarding any alleged obviousness
of deleting any other genes identified by Pfleger et al. as a way
to increase the production of PHA.
Req. Reh’g 5. Again, this argument is belied by the statement in the Appeal
Brief that “[t]he Office has alleged that any given gene deletion increasing
fatty acid production would ‘reasonably be expected to increase
polyhydroxyalkanoate production.’” App. Br. 7 (emphasis added).
The other “new allegations” identified by Appellants rely upon the
assertions in the first and second “new allegations” that the Examiner’s
rejection did not rely upon a teaching in the art to increase availability of
fatty acid and did not suggest deleting any of the genes disclosed in Pfleger.
Thus, Appellants contend:
With regard to Allegation 3, the original rejections
merely reference fadA, fadl, fadB and fadJ among the genes
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Application 13/833,230
taught by Pfleger et al. for increasing fatty acid production. The
original rejections do not mention any other genes taught by
Pfleger et al. for increasing fatty acid production or the scope of
any genus of genes taught by Pfleger et al. for increasing fatty
acid production. . . .
With regard to Allegation 4,. . . [t]he original rejections
are completely silent regarding any obvious-to-try rationale
based on an alleged ‘general suggestion in the art. .. to increase
production of fatty acids and/or inhibit the P-oxidation of fatty
acids as a way to increase production of PHA, ’ an allegation
that the art suggests “functionally deleting any of the genes
identified by Pfleger, including fadl and fadJ as a way to
increase the production of PHA,” and an alleged disclosure of
“fadA, fadB, fadl and fadJ as among a finite group of genes.”
With regard to Allegation 5,. . . [t]he original alleged
expectation of success is not based on an alleged “general
suggestion in the art... to increase production of fatty acids
and/or inhibit the P-oxidation of fatty acids as a way to increase
production of PHA” and a two to-one accounting of the three
genes with known function listed in Pfleger et al.
Id.
As discussed in connection with Allegations 1 and 2, we disagree with
Appellants that the Examiner’s rejection did not rely upon a teaching to
increase production of fatty acid and to delete any of the genes identified in
Pfleger. As Allegations 3—5 are premised on Allegations 1—2, we are not
persuaded that they are “new.” Moreover, given that Appellants themselves
understood the Examiner’s rejection to encompass Allegations 1 and 2, we
are not persuaded that Appellants were denied the “opportunity to react to
the thrust of the rejection.” In re Kronig, 539 F.2d at 1302-03. Accordingly,
we deny Appellants’ request that we designate our decision a new ground of
rejection.
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Appeal 2016-007913
Application 13/833,230
SUMMARY
Based on the record before us now and in the original appeal, we have
granted Appellants’ request to the extent that we have reconsidered our
Decision, but we deny Appellants’ request to make any changes in our
Decision. It is our view that Appellants have not identified any points the
Board has misapprehended or overlooked.
The request for rehearing is denied.
No time period for taking any subsequent action in connection with
this appeal may be extended under 37 C.F.R. § 1.136(a)(l)(v).
REQUEST FOR REHEARING DENIED
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