DETAILED ACTION
The present application is being examined under the pre-AIA first to invent provisions.
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed 9/2/25 in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 9/2/25 has been entered.
Claims 28-30, 33-37, 39-40 have been amended.
Claims 41-45 have been added.
Claims 27-45 are pending.
Claim 35 is withdrawn from further consideration pursuant to 37 CFR 1.14209 as being drawn to a nonelected invention.
Newly submitted claim 45 is directed to an invention that is independent or distinct from the invention originally claimed for the following reasons:
The originally presented invention involves administering i) an antibody that inhibiters interaction of CEACAM1 and its ligands and (ii) an antibody that inhibits interaction of PD1 and its ligands, i.e. administration of two antibodies. Claim 45 recites administering a bispecific antibody with inhibits interaction of CEACAM1 and its ligands and inhibits interaction of P1 and its ligands. This is patentably distinct and involves structurally distinct antibody compositions.
Since applicant has received an action on the merits for the originally presented invention, this invention has been constructively elected by original presentation for prosecution on the merits. Accordingly, claim 45 is withdrawn from consideration as being directed to a non-elected invention. See 37 CFR 1.142(b) and MPEP § 821.03.
To preserve a right to petition, the reply to this action must distinctly and specifically point out supposed errors in the restriction requirement. Otherwise, the election shall be treated as a final election without traverse. Traversal must be timely. Failure to timely traverse the requirement will result in the loss of right to petition under 37 CFR 1.144. If claims are subsequently added, applicant must indicate which of the subsequently added claims are readable upon the elected invention.
Should applicant traverse on the ground that the inventions are not patentably distinct, applicant should submit evidence or identify such evidence now of record showing the inventions to be obvious variants or clearly admit on the record that this is the case. In either instance, if the examiner finds one of the inventions unpatentable over the prior art, the evidence or admission may be used in a rejection under 35 U.S.C. 103 or pre-AIA 35 U.S.C. 103(a) of the other invention.
Claims 27-34, 36-44 are under examination.
The following is a quotation of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), first paragraph:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 27-28, 30, 34-44 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for pre-AIA the inventor(s), at the time the application was filed, had possession of the claimed invention. Specifically, there is insufficient written description to demonstrate that applicant was in possession of the claimed genus of antibodies that inhibit interaction of CEACAM1 and its ligands.
The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice, reduction to drawings, or by disclosure of relevant, identifying characteristics, i.e., structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the applicant was in possession of the claimed genus. See MPEP 2163.
The instant claims are directed to a method of enhancing an immune response in a subject having cancer comprising administering an antibody that inhibits interaction of CEACAM1 and its ligand. This encompasses a large genus of structurally and functionally distinct antibodies, including those that bind to CEACAM1, as well as those that bind to any CEACMA1 ligand. It is noted that claim 28 is included, since one could pick a PD-1 binding antibody, and the claim would still encompass the genus of antibodies that inhibit interaction of CEACAM1 and its ligands from claim 27 (i.e. ligand binding antibodies). Likewise, claim 30 is included since the claim would encompass antibodies that bind to a site on CEACAM1 ligand that interacts with CEACAM1. The claims encompass methods employing a broad genus of structurally different antibodies. For example, the claims would encompass polyclonal or monoclonal antibodies, or fragment thereof, derived from different species, such as human, mouse, or rat that would have different VH and VL sequences. immunogenicity, affinities and avidities, all of which effect the function of each antibody in vivo (see Scott et al., 2012, page 278, in particular). Additionally, antibody variable regions are composed of a heavy and light chain, each involved in providing for binding specificity. Variability in the antigen binding site is achieved by V(D)J recombination via heavy and light chain pairing, with the most diverse regions being the 6 CDR regions in the heavy and light chain. Furthermore, the diversity of the immunoglobulin repertoire is mediated in part by different combination so heavy and light chain V regions that pair to form a unique antibody binding site. See, for example, Rabia, 2018, which teaches that the maximal chemical diversity of antibody CDRs is unimaginably large and is extremely challenging to define the sequence determinant of antibody specificity (see page 4). Furthermore, regarding antibody antagonists, it is noted that the development of candidate antibodies involves a complex process of clinical and preclinical evaluation that include identification of the physical and chemical properties of the antibody (see Scott et al, pages 278-279, of record). The only species of antibodies that function as claimed disclosed by the instant specification are antibodies that bind to CEACAM1. No species of antibodies that bind to any CEACAM1 ligand are disclosed. Therefore, the specification does not disclose a representative number of species.
The instant application has not provided a sufficient description showing possession of the necessary functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the applicant was in possession of the genus of antibodies encompassing various structures, specificities and functions. Further, the Court has interpreted 35 U.S.C. §112, first paragraph, to require the patent specification to “describe the claimed invention so that one skilled in the art can recognize what is claimed. Enzo Biochem, Inc. v. Gen-Probe Inc, 63 USPQ2d 1609 and 1618 (Fed. Cir. 2002).
In evaluating whether a patentee has fulfilled this requirement, our standard is that the patent’s “disclosure must allow one skilled in the art ‘to visualize or recognize the identity of’ the subject matter purportedly described.” Id. (quoting Regents of Univ. of Cal. v. Eli Lilly & Co., 43 USPQ2d 1398 (Fed Cir. 1997)).
Vas-Cath Inc. v. Mahurkar, 19 USPQ2d 1111, makes clear that "applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention. The invention is, for purposes of the 'written description' inquiry, whatever is now claimed." (See page 1117.) The specification does not "clearly allow persons of ordinary skill in the art to recognize that [he or she] invented what is claimed." (See Vas-Cath at page 1116.)
Also, it is noted that the Court has held that the disclosure of screening assays and general classes of compounds was not adequate to describe compounds having the desired activity: without disclosure of which peptides, polynucleotides, or small organic molecules have the desired characteristic, the claims failed to meet the description requirement of § 112. See University of Rochester v. G.D. Searle & Co., lnc., 69 USPQ2d 1886,1895 (Fed. Cir. 2004).
Meeting the written description threshold requires showing that the applicant was in “possession” of the claimed invention at the time of filing. Vas-Cath, 935 F.2d at 1563-1564. Support need not describe the claimed subject matter in exactly the same terms as used in the claims. Eiselstein v. Frank, 52 F.3d 1035, 1038 (Fed. Cir. 1995). This support cannot be based on obviousness reasoning – i.e., what the written description and knowledge in the art would lead one to speculate as to modifications the inventor might have envisioned, but failed to disclose. Lockwood v. American Airlines, Inc., 107 F.3d 1565, 1572 (Fed. Cir. 1997). Ariad points out, the written description requirement also ensures that when a patent claims a genus by function, the specification recites sufficient materials to accomplish that function - a problem that is particularly acute in biological arts." Ariad, 598 F.3d at 1352-3. Note the following Court Decisions regarding the written description of antibodies in the context of the current claims.
Given the claimed broadly class of antibodies, in the absence of sufficient disclosure of relevant identifying characteristics, the patentee must establish “a reasonable structure-function correlation” either within the specification or by reference to the knowledge of one skilled in the art with functional claims. AbbVie Deutschland GmbH & Co. v. Janssen Biotech, Inc. (Fed. Cir. 2014) and the specification at best describes plan for making antibodies with the “limitations above” and then identifying those that satisfy claim limitations, but mere “wish or plan” for obtaining claimed invention is not sufficient. Centocor Ortho Biotech Inc. v. Abbott Laboratories, 97 USPQ2d 1870 (Fed. Cir. 2011). There is insufficient written description of the required kind of structure-identifying information about the corresponding makeup of the claimed antibodies to demonstrate possession. Also, see Amgen Inc. v. Sanofi, Aventisub LLC, No. 2017-1480 (Fed. Cir. 2017). Thus, one of skill in the art would conclude that the specification fails to provide adequate written description to demonstrate that Applicant was in possession of the claimed genus. See Eli Lilly, 119 F. 3d 1559, 43, USPQ2d 1398.
The following is a quotation of 35 U.S.C. 103(a) which forms the basis for all obviousness rejections set forth in this Office action:
(a) A patent may not be obtained though the invention is not identically disclosed or described as set forth in section 102 of this title, if the differences between the subject matter sought to be patented and the prior art are such that the subject matter as a whole would have been obvious at the time the invention was made to a person having ordinary skill in the art to which said subject matter pertains. Patentability shall not be negatived by the manner in which the invention was made.
Claims 27-34, 36-37, 39-44 are rejected under 35 U.S.C. 103(a) as being unpatentable over Curran et al. (2010, IDS) and US 2009/0217401, in view of WO 2010/125571 (IDS).
Curran et al. teach the treatment of cancer comprising the administration of an anti-PD-1 blocking antibody (see particularly 4276, column 1). The reference further teaches that the administration of two blocking antibodies can provide synergistic results compared to the administration of just a single antibody blocking agent (see particularly the paragraph spanning pages 4275, the Abstract, and the Discussion). The reference further suggest that the most effective combination therapies would likely function through “distinct nonredundant mechanisms” (see particularly page 4275 , column 2). Further, the authors suggest that combination therapy is superior to single therapy because it may avoid “…the upregulation of the unblocked pathway (see particularly page 4279, column 2). The authors conclude:
“To allow tumor-infiltrating T cells the capacity to expand, kill, and produce inflammatory cytokines within the tumor microenvironment appears to require simultaneous blockade of multiple negative costimulatory receptors.”
Curran teaches that blockade of PD-1 increases proliferation of CD8 and CD4 T cells.
Likewise, the ‘401 publication teaches anti-PD-1 blocking antibody for treatment of cancer, and teaches that combined immunotherapy with anti-PD-1 blocking antibodies and other antibodies (See abstract and page 1, in particular). The ‘401 publication teaches that the antibodies inhibit tumor growth by stimulating an anti-tumor immune response (see page 4, in particular). The ‘401 publication teaches using the anti-PD-1 antibody alone, or in combination with other antibodies (see page 27, in particular). The ‘401 publication particularly teaches combining anti-PD-1 with other immune stimulatory therapeutic antibodies, such as anti-CTLA-4, and that doing so can results in synergism (See page 30, in particular). The ‘401 publication teaches PD-1 antibodies raised against the extracellular portion of human PD-1 (it would bind to. SEQ ID NO: 1, which is the human PD-1 sequence) and that the antibodies inhibit binding of PD-1 ligands (See page 34, 36
The references differ from the claimed invention only in that they do not teach administration of an anti-CEACAM1 antibody as the second blocking antibody.
WO 2010/125571 teaches the administration of a CEACAM1 blocking antibody for the treatment of cancer (see particularly, page 12). WO 2010/125571 teaches that CEACAM1 is an inhibitory receptor for activated T cells, including tumor infiltrating lymphocytes, and that the antibodies augment T cell activity (see page 4 and 12, in particular). WO 2010/125571 teaches the antibody inhibits and binds to homophilic interaction sites in the N-domain of human CEACAM1, including positions 43, 44, 63, and 82, see page 12, in particular (i.e. it would bind to amino acid residues within 35-140 of SEQ ID NO: 32 which is a human CEACAM1 sequence).
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was made to combine the administration of the anti-PD-1 antibody of Curran et al. and the ‘401 publication with the anti-CEACAM1 antibody of WO 2010/125571 for the effective treatment of cancer. The combining of known equivalents, in this case anti-cancer agents, for the same purpose, e.g., the treatment of cancer, has long been held obvious, see In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069 (CCPA 1980) and MPEP 2144.06 and would have fallen well within the purview of the ordinarily skilled artisan at the time of the invention. Moreover, Curran et al. and the ‘401 publication also teaches that the combining of agents can have synergistic results compared to the administration of a single anti-cancer agent, thus, rendering the combination therapy of the claims further obvious (see, particularly the author’s conclusion).
Claim 44 is included since the ‘401 publication specifically exemplifies synergistic treatment of tumors with only PD1 and another immunostimulatory antibody (CTLA-4) and substituting said CTLA-4 antibody with anti0CEACAM1 would be obvious, since WO 2010/12557 teach that the anti-CEACAM1 antibody is an equivalent substitute for the anti-CTLA-4 antibody, i.e. they are both non-redundant immunostimulatory antibodies which block immune inhibitory receptors.
Applicant’s arguments filed 9/2/25 have been fully considered, but they are not persuasive.
Applicant argues that Curran only shows that combination of anti-PD-1 and anti-CTLA-4 improve treatment with Fvax and does not disclose the use of anti-PD-1 and anti-CLTA-4 as a pairwise combination. Applicant argues that a combination of a cancer vaccine and immunomodulating antibodies cannot be considered applicable to a combination of immunomodulating antibodies which are not tested by Curran.
The present claims (with the exception of new claim 44) do not exclude giving a cancer vaccine since the method is a method “comprising” administering the antibodies, which does not exclude unrecited steps or elements.
Regardless, the ‘401 publication exemplifies synergistic tumor treatment with only two antibodies (anti-PD-1 and anti-CTLA-4).
Applicant further argues that present invention demonstrates unexpected results in that a combination of anti-CEACAM1 and anti-PD-1 was more effective than either antibody alone.
The declaration of Inventor Blumberg is not persuasive of unexpected results for several reasons. As explained in the decision by the Patent Trial and Appeal Board of 7/3/25, the results are not unexpected compared to the closest prior art, since Curran (and also the ‘401 publication) demonstrate that pairs of nonredundant immunomodulating antibodies (anti-PD-1 and CTLA-4) achieve synergistic results.
Furthermore, the unexpected results are not commensurate in scope with the instant claims. For example, the asserted unexpected results were with a particular dosing regimen in subjects with a particular type of tumor (3M or CT26), and a single type of anti-CEACAM1 antibody and anti-PD1 antibody, while the present claims broadly encompass any administration regimen at any dose in a subject with any cancer, and with any antibody that inhibits interaction of PD1 and its ligands, and any antibody that inhibits interaction of CEACAM1 and its ligands.
Claims 27-34, 36-37, 39-44 are rejected under 35 U.S.C. 103(a) as being unpatentable over Curran et al (of record) and US 2009/0217404., in view of Ortenberg, March 2012, and Sapoznik, June 2012 (of record).
Curran et al. teach the treatment of cancer comprising the administration of an anti-PD-1 blocking antibody (see particularly 4276, column 1). The reference further teaches that the administration of two blocking antibodies can provide synergistic results compared to the administration of just a single antibody blocking agent (see particularly the paragraph spanning pages 4275, the Abstract, and the Discussion). The reference further suggest that the most effective combination therapies would likely function through “distinct nonredundant mechanisms” (see particularly page 4275 , column 2). Further, the authors suggest that combination therapy is superior to single therapy because it may avoid “…the upregulation of the unblocked pathway (see particularly page 4279, column 2). The authors conclude:
“To allow tumor-infiltrating T cells the capacity to expand, kill, and produce inflammatory cytokines within the tumor microenvironment appears to require simultaneous blockade of multiple negative costimulatory receptors.”
Curran teaches that blockade of PD-1 increases proliferation of CD8 and CD4 T cells.
Likewise, the ‘401 publication teaches anti-PD-1 blocking antibody for treatment of cancer, and teaches combined immunotherapy with anti-PD-1 blocking antibodies and other antibodies (See abstract and page 1, in particular). The ‘401 publication teaches that the antibodies inhibit tumor growth by stimulating the anti-tumor immune response (see page 4, in particular). The ‘401 publication teaches using the anti-PD-1 antibody alone, or in combination with other antibodies (see page 27, in particular). The ‘401 publication particularly teaches combining anti-PD-1 with other immunostimulatory therapeutic antibodies, such as anti-CTLA-4, and that doing so can result in a synergism (See page 30, in particular). The ‘401 publication teaches PD-1 antibodies raised against the extracellular portion of human PD-1 (i.e. SEQ ID NO: 1, which is the human PD-1 sequence) and that the antibodies inhibit binding of PD-1 ligand (See page 34, 36
The references differ from the claimed invention only in that they do not teach administration of an anti-CEACAM1 antibody as the second blocking antibody.
Sapoznik teaches three types of immune modulatory targets that can be treated with antibodies to increase anti-tumor immune responses, namely, CTLA-4, PD-1, and CEACAM1 (See Fig. 1). Sapoznik teaches that CEACAM1 acts as an inhibitory molecules that blocks proliferation of T cells, and that anti-CEACAM1 antibodies that bind to human CEACAM1 act as antagonists to inhibit homophilic CEACAM1 interactions (See page 3-4, in particular). See also Ortenberg which teaches that such CEACAM1 blocking antibodies that inhibit homophilic interactions bind to the N-domain of human CEACAM1 (i.e. to residues within 41-136 of SEQ ID NO: 32, which is represents a human CEACAM1 sequence).
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was made to combine the administration of the anti-PD-1 antibody of Curran et al. and the ‘401 publication with the anti-CEACAM1 antibody of Sapoznik and Ortenberg for the effective treatment of cancer. The combining of known equivalents, in this case anti-cancer agents, for the same purpose, e.g., the treatment of cancer, has long been held obvious, see In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069 (CCPA 1980) and MPEP 2144.06 and would have fallen well within the purview of the ordinarily skilled artisan at the time of the invention. Moreover, Curran et al. and the ‘401 publication also teaches that the combining of agents can have synergistic results compared to the administration of a single anti-cancer agent, thus, rendering the combination therapy of the claims further obvious (see, particularly the author’s conclusion).
Claim 44 is included since the ‘401 publication specifically exemplifies synergistic treatment of tumors with only PD1 and another immunostimulatory antibody (CTLA-4) and substituting said CTLA-4 with anti-CEACAM1 would be obvious, since Sapoznik and Ortenberg teach that the anti-CEACAM1 antibody is an equivalent substitute for the anti-CTLA-4 antibody, i.e. they are both non-redundant immunostimulatory antibodies which block immune inhibitor receptors.
Claim 38 is rejected under 35 U.S.C. 103(a) as being unpatentable over Curran et al. 2010, US 2009/0328401, and WO 2010/125571 or over Curran et al, US 2009/0217404, Ortenberg, March 2012, and Sapoznik, June 2012 as applied to claims 27, 37 above, and further in view of Lin, 2008
The combined teachings of the cited references are discussed above.
They do not explicitly teach that the PD-1 antibody binds to an amino acid residue corresponding to any of amino acid residues 41-136 of SEQ ID NO: 1.
Lin teaches that the PD-1 residues that interact with its ligand include positions 64-136 of human PD-1 (see Table 1).
Therefore, it would have been obvious to a person of ordinary skill in the art at the time the invention was made to apply the teachings of Lin to the PD-1 antibody made obvious above. As Curran and the ‘401 publication specifically teaches that the anti-PD-1 blocking antibody blocks ligand binding and binds to the extracellular portion of human PD-1 (i.e. SEQ ID NO: 1), it would be obvious that the antibodies would bind in the region of PD-1 responsible for interaction with said ligand, i.e. within amino acid positions 64-136 of human PD-1 as taught by Lin.
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 27-34, 36-44 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 49-50, 52, 61-62 of copending Application No. 18/842,534 or claims 105, 108-109 of copending Application No. 18/952,149, in view of US 2009/0217401 and Lin, 2008
The co-pending applications claim a method of treating cancer in a subject in need thereof comprising administering to the subject a CEACAM1 antibody having certain specifically identified CDRs with defined SEQ ID Nos, and a checkpoint inhibitor, such as an PD-1 inhibitor. It would be obvious use a PD-1 antibody as the PD-1 inhibitor taught by the ‘401 publication and Lin for the same reason set forth above. The function of binding to residues 35-140 of SEQ ID NO: 32 and blocking ligands is an inherent property of the anti-CEACAM1 antibodies claimed in the copending applications.
This is a provisional nonstatutory double patenting rejection.
Claims 27-34, 36-44 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 20-22 of U.S. Patent No. 12,173,066, in view of US 2009/0217401 and Lin, 2008.
The ‘066 patent claims a method of reducing tumor growth in a subject in need thereof comprising administering to the subject a CEACAM1 antibody having CDRs of SEQ ID NO:9,2,10,4,5, and 11 and a checkpoint inhibitor, such as an PD-1 inhibitor. It would be obvious use a PD-1 antibody as the PD-1 inhibitor taught by the ‘401 publication and Lin, and that the method would enhance the immune response for the same reason set forth above. The function of binding to residues 35-140 of SEQ ID NO: 32 and blocking ligands is an inherent property of the anti-CEACAM1 antibodies claimed in the ‘066 patent.
No claim is allowed.
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Amy E. Juedes
Patent Examiner
Technology Center 1600
/AMY E JUEDES/Primary Examiner, Art Unit 1644