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Patent Trials and Appeals Board

Apr 22, 2021

2020006045 (P.T.A.B. Apr. 22, 2021)

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.
14/917,643 03/09/2016 Koichi INANO 0760-0463PUS1 1312
2292 7590 04/22/2021
BIRCH STEWART KOLASCH & BIRCH, LLP
8110 Gatehouse Road
Suite 100 East
Falls Church, VA 22042-1248
EXAMINER
HILL, MYRON G
ART UNIT PAPER NUMBER
1648
NOTIFICATION DATE DELIVERY MODE
04/22/2021 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):
mailroom@bskb.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
__________

BEFORE THE PATENT TRIAL AND APPEAL BOARD
__________

Ex parte KOICHI INANO,
TAKASHI MIYAZAWA, and OSAMU ISHIKAWA
__________

Appeal 2020-006045
Application 14/917,643
Technology Center 1600
__________

Before JEFFREY N. FREDMAN, DEBORAH KATZ, and
DAVID D. COTTA, Administrative Patent Judges.

FREDMAN, Administrative Patent Judge.

DECISION ON REQUEST FOR REHEARING
Appellants request rehearing of the decision entered February 12, 2021
(“Decision”) that entered new grounds of rejection under 35 U.S.C. § 103(a) over
Walls, Bucher (1989), and Maher.
We deny the requested relief.

DISCUSSION
Appellant asserts several specific errors under 37 C.F.R. § 41.52 that the
Decision: “misapprehended (misinterpreted) the teachings in Walls as they relate to
the binding properties of the B4 monoclonal antibody” (Req. 4) and “misapprehended
the teachings of Bucher” (Req. 5–9). We will address these in order.
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Walls
Appellant contends that
the B4 antibody reacts with influenza B hemagglutinin and not
influenza B M1 protein. Thus, it is respectfully submitted that
the New Ground of Rejection is based on a fundamental
misapprehended point regarding the binding properties of the
B4 antibody of Walls, as well as an important overlooked
disclosure in Walls regarding the actual binding properties of
the B4 antibody.
(Req. 4).
We agree that our statement that “Walls is silent regarding the epitope of the
M1 protein to which the B4 monoclonal antibody binds” (Dec. 12, FF 11) was inartful
and potentially misleading in suggesting that Walls teaches that the B4 antibody binds
the M1 protein. But we did not rely upon Walls to teach or suggest an antibody
against the influenza B M1 protein or more specifically to “the region of the 125th to
248th amino acids of M1” recited in claim 1. Instead, we relied on Bucher (1989) to
suggest using the M1 protein and the specific epitope of the 125th to 248th amino acids
for detection (see, e.g., Dec. 15).
We relied upon Walls to teach that immunoassays for detecting influenza B
were generally known using labeled antibodies and immobilized antibodies as
required by the steps of claim 1 (see Dec. 14). And we did not address which antigens
of influenza B were actually targets of the monoclonal antibodies of Wall, instead
identifying what Wall did not teach. We do note that the portion cited by Appellant
makes it clear that Walls recognized that the influenza matrix antibody would have
been a potential target for the immunoassay because the A2 antibody was targeted to
the influenza A matrix protein (see Req. 4).
We therefore find that while we were unclear, we did not state that Walls taught
an antibody to the influenza B matrix protein but rather that Walls did not teach that
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the B4 antibody, the preferred antibody in Walls, bound to an epitope of the M1
protein, or to an influenza B protein. Therefore, we did not misapprehend the
essential teachings of Walls that immunoassays to influenza A and B viruses using the
claimed general format with monoclonal antibodies to viral proteins would have been
obvious based on the prior art.
Bucher (1989)
Appellant contends “while the Board asserts that Table 3 of Bucher shows
reactivity of monoclonal antibodies with Peptide 5 of the M1 protein of influenza B,
Bucher actually specifically says that none of the tested monoclonal antibodies
showed any reactivity against influenza B” (Req. 5). Appellant contends “it is
submitted that ‘Peptide 5’ described in Bucher is synthesized on the basis of M-
protein of influenza A virus and not the peptide of the M1 protein of influenza B
virus” (Req. 6). Appellant concludes that “it is clear that the Board misapprehended
the teachings of Bucher. Contrary to the Board’s interpretation of Bucher, the
publication does not teach the reactivity of monoclonal antibodies with the M1 protein
of influenza B” (Req. 8).
While we agree that our finding of fact 13 has a typographical error in reciting
“influenza B,” that error is not repeated in our actual analysis (see Dec. 12, 15–16). In
our analysis, we stated:
Bucher (1989) teaches three monoclonal antibodies to the
influenza A virus M1 protein that bind to a peptide 5 (FF 13)
and are therefore targeted to a region in the 125th to 248th
amino acids of M1 of influenza A virus. We further note that
the Specification acknowledges that “[a]mino acid sequences of
B-Ml are known, and described in, for example,
GenBank:AEN79424 (SEQ ID NO: 1)” (FF 2).
(Dec. 15). Thus, we clearly did not misapprehend that peptide 5 binds to the matrix
protein of the influenza A protein, but rather expressly stated that peptide 5 binds a
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region between the 125th and 248th amino acids of the influenza A protein. We then
noted that the corresponding sequence of the influenza B protein was known in the
GenBank database (see Dec. 15).
Indeed, the next sentence of our analysis confirms this, stating “Bucher (1989)
does not teach monoclonal antibodies to the influenza B virus” (Dec. 15). We also
noted, to support a reasonable expectation of success, that “Bucher (1989)
demonstrates the ability to obtain three antibodies to the C-terminal region of the M1
protein of the influenza A virus (FF 13)” (Dec. 16). Thus, it is clear that finding of
fact 13 contained a typographical error and we did not misapprehend that peptide 5 in
Bucher (1989) binds to the M1 protein of influenza A protein, but instead relied upon
that fact.
Appellant contends
Bucher, when properly understood, actually teaches away from
the presently claimed invention. From the portions discussed
above, it is clear that Bucher teaches that none of the tested
antibodies were reactive against influenza B, or at least against
the one tested strain of influenza B. Thus, one skilled in the art
seeking to make a monoclonal antibody against influenza B
would not be encouraged to make an antibody against the
peptides tested in Bucher, including the M1 protein, but rather
would likely be led to seek an antibody against some other
protein from influenza B.
(Req. 9).
We find this argument unpersuasive because Bucher (1989) is drawn to
“monoclonal antibodies [that] were capable of recognizing antigenic differences
among various strains of type A influenza viruses” (Bucher (1989) 3622, col. 1–2).
Thus, Bucher (1989) did not attempt to make antibodies to influenza B virus proteins.
However, Walls did show that influenza B virus proteins were used to generate
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monoclonal antibodies (see Req. 4, citing Walls 908 “Influenza B hemagglutinin (B1
and B4), and influenza B nucleoprotein (B2)” (emphasis omitted)).
We relied on Bucher (1989) to demonstrate two significant points. First, that
“[s]ignificant levels of antibodies to M protein are found after influenza virus
infection or influenza virus vaccination in clinical studies” (Dec. 12, FF 12). Second,
that regarding the C-terminal region of the M1 protein that “it is likely that this region
represents a linear epitope involving residue 231. This region appears to be a
significant B-cell recognition site, with at least 3 of 16 hybridoma lines (Table 3)
showing high reactivity with this site” (Dec. 13, FF 15). In particular, it is the Bucher
(1989) teaching that the C-terminal region of the M1 protein of influenza A protein
has high reactivity that suggests generating monoclonal antibodies for detection of
influenza B using the C-terminal region of the influenza B virus M1 protein.
It therefore would have been obvious to select the C-terminal region of the
influenza B virus protein for use in the Walls immunoassay for influenza B, as noted
in Decision, because “Bucher (1989) teaches the C-terminus of the Ml protein likely
comprises a linear epitope with ‘high reactivity’ (FF 15) that results in sensitive
detection with a peptide portion of the site (FF 14)” and selection of that region for
detection from the Influenza B virus would have been an obvious equivalent with high
reactivity with targeting antibodies (see Dec. 13, 15; FF 15).
As to the specific teaching away argument, a teaching away requires a reference
to actually criticize, discredit, or otherwise discourage the claimed solution. See In re
Fulton, 391 F.3d 1195, 1201 (Fed. Cir. 2004). Appellant does not identify, and we do
not find, any disclosure in the cited prior art that actually criticizes, discredits, or
otherwise discourages generating monoclonal antibodies to the C-terminus of the M1
protein of influenza B virus for the purpose of immunoassays.
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DECISION SUMMARY
We have reviewed the original opinion in light of Appellant’s request, and
while we had an inadvertent error, it did not impact our obviousness analysis and we
find no point of law or fact which we overlooked or misapprehended in arriving at our
decision. Therefore, Appellant’s request is denied with respect to making any
modifications to the decision entering a new ground of rejection.

Outcome of Decision on Rehearing:
Claim 35 U.S.C. § Basis Granted Denied
1–6, 8–12,
19–24
103 Walls, Bucher
(1989)
1–6, 8–12,
19–24
13–18 103 Walls, Bucher
(1989), Maher
13–18

Final Outcome of Appeal after Rehearing
Claim 35 U.S.C.
§
Basis Affirmed Reversed New
Ground
1–6, 8–12,
19–24
103 Walls, Bucher
(1989)
1–6, 8–
12, 19–
24
13–18 103 Walls, Bucher
(1989), Maher
  13–18 

No time period for taking any subsequent action in connection with this appeal
may be extended under 37 C.F.R. § 1.136(a).

REHEARING DENIED