Ex Parte Oh et al

Patent Trials and Appeals Board

Jun 5, 2019

14484599 - (D) (P.T.A.B. Jun. 5, 2019)

UNITED STA TES p A TENT AND TRADEMARK OFFICE
APPLICATION NO. FILING DATE
14/484,599 09/12/2014
32425 7590 06/07/2019
NORTON ROSE FULBRIGHT US LLP
98 SAN JACINTO BOULEVARD
SUITE 1100
AUSTIN, TX 78701-4255
FIRST NAMED INVENTOR
SangKon Oh
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
ATTORNEY DOCKET NO. CONFIRMATION NO.
BHCSP0067USC1/1000206279 4245
EXAMINER
TIJEDES, AMYE
ART UNIT PAPER NUMBER
1644
NOTIFICATION DATE DELIVERY MODE
06/07/2019 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):
aoipdocket@nortonrosefulbright.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte SANGKON OH,
JACQUES F. BANCHEREAU, GERARD ZURAWSKI,
HIDEKI UENO, and LING NI 1
Appeal2018-006451
Application 14/484,599
Technology Center 1600
Before ERIC B. GRIMES, ROBERT A. POLLOCK, and
ELIZABETH A. LA VIER, Administrative Patent Judges.
GRIMES, Administrative Patent Judge.
DECISION ON APPEAL
This is an appeal under 35 U.S.C. § 134(a) involving claims to a
method for decreasing Th2 cell responses, or increasing Th 1 7 cell responses,
in a subject with an autoimmune condition, which have been rejected for
indefiniteness, for lack of adequate written description, and provisionally for
obviousness-type double patenting. We have jurisdiction under 35 U.S.C.
§ 6(b).
We affirm.
1 Appellants identify the Real Party in Interest as BAYLOR RESEARCH
INSTITUTE. Br. 1.
Appeal2018-006451
Application 14/484,599
STATEMENT OF THE CASE
The Specification states that
[ t ]he present invention describes compositions and methods for
enhancing pathogen-specific T cell responses using human
dendritic cells. The method describes an anti-Dectin-1-specific
antibody or binding fragment thereof fused with one or more
antigens, that may be used in the presence or absence of TLR2
ligands to enhance Th 1 and Th 1 7 cell responses and at the same
time decrease Th2 cell responses. Methods for treating
pathogenic infections using the compositions described herein
are also presented that drive the immune response to a Thl and
Thl 7 helper T cells responses.
Spec. ,r 7.
Claims 20, 21, 40, 42, 44, 56, 57, and 59 are on appeal. Claims 20 and
56 are representative and read as follows:
20. A method for reducing Th2 cell responses in a human subject having
an autoimmune condition, the method comprising administering a
therapeutically effective amount of a pharmaceutical composition
comprising an anti-Dectin-1-specific antibody or antigen-binding fragment
thereof and one or both of P. gingivalis lipopolysaccharide and Pam3CSK4.
56. A method for increasing Thl 7 cell responses in a human subject
having an autoimmune condition, the method comprising administering a
therapeutically effective amount of a pharmaceutical composition
comprising an anti-Dectin-1-specific antibody or antigen-binding fragment
thereof and one or both of P. gingivalis lipopolysaccharide and Pam3CSK4.
The claims stand rejected as follows:
Claim 57 under 35 U.S.C. § 112, second paragraph, as indefinite
(Ans. 3);
Claims 20, 21, 40, 42, 44, 56, 57, and 59 under 35 U.S.C. § 112, first
paragraph, for lack of adequate written description (Ans. 4); and
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Appeal2018-006451
Application 14/484,599
Claims 20, 21, 40, 42, 44, 56, 57, and 59, provisionally, for
obviousness-type double patenting based on claims 58---60, 62---64, and 68-
73 of Application 14/264,967, in view of Chandran2 (Ans. 7).
I
The Examiner rejects claim 573 as indefinite, on the basis that it is
directed to increasing an allogeneic Thl 7 cell response in a human subject
having an autoimmune condition, but "[i]t is not clear how an allogeneic
response are [sic] increased by administration of said antibody. There is no
recited step or element explaining how the allogeneic response is involved in
the method, i.e. introduction of an alloantigen, introduction of an allogeneic
transplant, etc." Ans. 3. The Examiner finds that "[t]he only mention of
alloantigen response in the instant specification is in paragraph 68 which
describes in vitro experiments" and "does not provide any context for the
present in vivo therapeutic methods." Id.
Br. 2.
Appellants argue that the Specification's paragraph 68 states that
"the inventors observed the induction of allogeneic Thl 7 cell
responses, which were further enhanced by activating DCs with
anti-hDectin-1 mAb or curdlan, a fungal b-glucan ( data not
shown) .... Thus, the specification demonstrates that
administration of the antibody induces allogeneic T cell
responses. For at least these reasons, this claim is clear.
2 Chandran et al., "TLR2 Engagement on Dendritic Cells Promotes High
Frequency Effector and Memory CD4 T Cell Responses," 183 J. Immunol.
7832-7841 (2009).
3 Claim 57 is directed to "[t]he method of claim 56, wherein the Thl 7 cell
responses are allogeneic." Appeal Br. 4.
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Appeal2018-006451
Application 14/484,599
We conclude that the Examiner's rejection is supported by a
preponderance of the evidence. As the Examiner pointed out, claim 57 is
directed to a method of increasing Thl 7 cell responses in a human subject,
where the Thl 7 cell responses are allogeneic, yet the claim does not include
any limitations that would cause any non-endogenous ( allogeneic) Th 17
cells to be present in the human subject.
Appellants point to paragraph 68 of the Specification, which reads (in
relevant part) as follows:
IL-23 and IL-I B secreted by DCs enhanced HAI-specific Thl 7
cell responses, but did not result in the induction ofHAl-
specific Thl 7 cells in vitro. While testing HAI-specific T cell
responses, the inventors also assessed the allogeneic nai"ve
CD4+ T cell responses induced by DCs, as many studies
employ allogeneic systems to test the types of T cell responses
induced in vitro. Indeed, the inventors observed the induction of
allogeneic Th 17 cell responses, which were further enhanced by
activating DCs with anti-hDectin-1 mAb or curdlan, a fungal b-
glucan (data not shown).
Spec. ,r 68.
We agree with the Examiner's reading of this passage as describing an
experiment carried out in vitro, and Appellants do not dispute that
interpretation. Rather, Appellants simply assert that it describes an
allogeneic T cell response, which is true. But claim 57 requires inducing
such a response in a human subject, and Appellants provide no explanation
of how the response observed in a laboratory experiment would be replicated
in a human subject by carrying out the process defined by claim 57.
We therefore affirm the rejection of claim 57 under 35 U.S.C. § 112,
second paragraph, for indefiniteness.
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Appeal2018-006451
Application 14/484,599
II
The Examiner rejects all of the claims on appeal for lack of adequate
written description. The Examiner finds that the Specification does not
adequately describe "[a] method for reducing Th2 cell responses, or a
method of increasing Thl 7 response in a human subject 'having an
autoimmune condition' comprising administering an 'anti-Dectin-specific
antibody or fragment thereof."' Ans. 4. 4
The Examiner finds that the Specification describes a method of
inducing a pathogen-specific Thl 7 response, and a method of reducing Th2
cell responses, by administering an anti-dectin-1 specific antibody fused to
an antigen, but does not describe methods of administering an anti-dectin-1
specific antibody that is not fused to an antigen. Id. at 4--5.
The Examiner also finds that the
specification is clearly directed to methods of increasing THI 7
immunity, or decreasing TH2 cell response for the purpose of
treating pathogenic infections, such as influenza virus infection,
by administration of a composition comprising anti-Dectin-1
specific antibody conjugated/fused to an antigen .... Nowhere
is it contemplated to perform such a method in a subject with an
autoimmune condition.
4 The Examiner also rejects claim 57 for lack of adequate written
description, on the basis that the Specification does not describe "increasing
an 'allogeneic' THI 7 response in a human subject having an autoimmune
condition comprising administering an anti-Dectin-1 specific antibody."
Ans. 4. This rejection is affirmed for the reasons discussed in regard to the
rejection under 35 U.S.C. § 112, second paragraph: the Specification does
not describe producing an allogeneic response in a human subject by
carrying out the recited method.
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Appeal2018-006451
Application 14/484,599
Id. at 5. The Examiner finds that "[t]he Specification does not disclose
administration of said antibodies to a subject having an autoimmune
condition, as presently claimed." Id.
Appellants argue that "support for the subject having an autoimmune
condition can be found at ,r [0038] and [0067] of the filed specification."
Br. 2.
We conclude that the Examiner's rejection is supported by a
preponderance of the evidence. Paragraph 3 8 of the Specification states that
"IL-17-producing Thl 7 CD4+ T cells (Thl 7 cells) ha[ve] been broadly
linked to the pathogenesis of multiple autoimmune diseases. However,
recent compelling evidence indicates that Th 1 7 cells are crucial for
protective immunity against many mucosal and systemic infections." Spec.
,r 38 (reference citations omitted). As the Examiner pointed out (Ans. 5), this
description indicates that Thl 7 cells are linked to the pathogenesis of
autoimmune diseases, not that increasing Thl 7 cell responses is effective in
treating an autoimmune condition, as recited in claim 56.
Appellants also cite paragraph 67 of the Specification as describing
the disputed limitations but do not explain what disclosure in that paragraph
is specifically relied on. See Br. 2. We agree with the Examiner that
[p ]aragraph 67 of the specification discloses that the role of
TLR2 ligands in expansion of THI 7 cells [is] not clearly
elucidated, and discusses other prior art references teaching that
TLR2 can promote regulatory T cells responses that inhibit
autoimmunity in mice. The discussion of a prior art references
teaching that TLR2 can promote regulatory T cell responses
that inhibit autoimmunity in mice does not provide support for
administration [ ofJ dectin-1 antibody and P AM3CSK4 to
reduce TH2 cells and increase TH 1 7 response in human
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Appeal2018-006451
Application 14/484,599
subjects having an autoimmune condition[] as presently
claimed.
Ans. 5.
We therefore conclude that the rejection of claims 20 and 56 for lack
of adequate written description is supported by a preponderance of the
evidence. Claims 21, 40, 42, 44, 57, and 59 fall with claims 20 and 56
because they were not argued separately. 37 C.F.R. § 4I.37(c)(l)(iv).
III
The Examiner provisionally rejects all of the claims on appeal for
obviousness-type double patenting based on the claims of application
14/264,967, in view of Chandran, on the basis that the two sets of claims
are not patentably distinct from each other because the '967
application claims a method of decreasing a Th2 cell response
in a subject with an autoimmune disorder comprising
administering a composition comprising an anti-dectin-1
antibody and a TLR2 ligand. Selecting from the known TLR2
ligands, such as Pam3CSK4, as taught by Chandran et al., as
well as the routes of administration, would be obvious and
routine.
Ans. 7.
Appellants do not present any arguments contesting the merits of the
provisional double patenting rejection. Br. 3. We therefore affirm the
provisional obviousness-type double patenting rejection based on claims 58-
60, 62---64, and 68-73 of application 14/264,967. See Manual of Patent
Examining Procedure§ 1205.02 ("An appellant may, of course, choose not
to present arguments or rely upon particular evidence as to certain claim
rejections; however, such arguments and evidence are waived for purposes
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Appeal2018-006451
Application 14/484,599
of the appeal and the Board may summarily sustain any grounds of
rejections not argued.").
SUMMARY
We affirm all of the rejections on appeal.
TIME PERIOD FOR RESPONSE
No time period for taking any subsequent action in connection with
this appeal may be extended under 3 7 C.F .R. § 1.13 6( a )(1 )(iv).
AFFIRMED
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