Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
DETAILED ACTION
Claims 16-35 are pending.
Claims 16-35 are under examination on the merits.
Objection to the Specification and the Application Data Sheet
As stated in MPEP 201.06, Divisional Applications, “[a] later application for an independent or distinct invention, carved out of a nonprovisional application… and disclosing and claiming only subject matter disclosed in the earlier or parent application, is known as a divisional application… A divisional application is often filed as a result of a restriction requirement made by the examiner.” It is also stated at MPEP 201.06 that possible divisional status corresponds to an application that discloses and claims only subject matter disclosed in a prior, nonprovisional application and appears to claim only subject matter directed to an invention that is independent and distinct from that claimed in said prior, nondivisional application. The instant case is indicated as being a DIV of App. No. 17/140,996. It is noted that a Requirement for Restriction/Election was not issued for App. No. 17/140,996. As such the claimed invention is not the subject matter from of any group from a Requirement for Restriction/Election for App. No. 17/140,996, and the instantly claimed invention does not appear to be a proper divisional of App. No. 17/140,996.
It is noted that this application discloses and claims only subject matter disclosed in prior App. No. 17/140,996, and names the inventor or at least one joint inventor named in the prior application. Accordingly this application may constitute a continuation, and absent any showing that the instant application properly merits divisional status, the instant application is being treated as a continuation. Therefore the application data sheet (ADS), dated 01/05/2024, is objected to, because it indicates that the instant application is a divisional of App. No. 17/140,996. The specification, dated 01/05/2024, is also objected to, because p. 1 of the specification indicates that the instant application is a divisional of App. No. 17/140,996.
It is further noted that since the instant application appears to be a continuation of App. No. 17/140,996, the safe harbor provision of 35 U.S.C. 121 is not applicable in the instant case. As stated in MPEP 201.06, “the protection afforded by section 121 to applications (or patents issued therefrom) filed as a result of a restriction requirement is limited to divisional applications.” Pfizer, Inc. v. Teva Pharmaceuticals USA, Inc., 518 F.3d 1353, 1362, 86 USPQ2d 1001, 1007-1008 (Fed. Cir. 2008).
Objection to the Claims
Claims 17, 18, and 23 are objected to because of the following informalities: The claims recite the term “Fe portion.” It is assumed that this is a typographical error that should read “Fc portion.” Appropriate correction is required.
Claims 22, 28, and 29 recite sequences having the sequence set forth in SEQ ID NO: 2 or 3. The term “having” could be interpreted as “consisting of” or “comprising,” and is being interpreted as “comprising.” Applicant is requested to verify whether the ambiguous term “having” is intended to be “consisting of” or “comprising.”
Claim Rejections
35 U.S.C. 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries set forth in Graham v. John Deere Co., 383 U.S. 1, 148 USPQ 459 (1966), that are applied for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 16, 17, 19-21, and 23-26 are rejected under 35 U.S.C. 103 as being unpatentable over Chen et al. (WO 2011/020024, international publication date: 02/17/2011, in IDS from 05/07/2024), in view of Zhao et al. (PNAS, 110(24): 9879-9884, 2013, in IDS from 05/07/2024).
Chen et al. teach that B7-H7, which is also known as HHLA2, binds to B7-H7CR, which is also known as TMIGD2, see [0007], [0057], and [0072]. Chen et al. also teach “therapeutic agents that modulate one or more immune functions and uses of such therapeutic agents in the prevention, treatment and management of diseases. In one aspect, the therapeutic agents modulate one or more signal transduction pathways induced by the binding of B7-H7 to B7-H7CR… The therapeutic agents can be used in the prevention, treatment and/or management of diseases in which it might be useful to modulate one or more immune functions (e.g., cancer, infectious disease, autoimmune disease, and transplantation rejection).” See [0003]. At [00596]-[00597], Chen et al. teach that the immunostimulatory therapeutic agents of the invention may be administered as an adjuvant in combination with an antigen as a means of enhancing immune function in the treatment of cancer, and Chen et al. also teach that immunostimulatory therapeutic agents of the invention may be administered to cancer patients to increase the proliferation and/or effector function of one or more immune cell populations in a patient.
At [00617]-[00618], Chen et al. teach that various forms of cancer, including breast cancer and leukemia, may be treated with immunostimulatory therapeutic agents. Importantly at [0013], Chen et al. teach that a therapeutic agent of the invention may be a fusion protein comprising the extracellular domain of B7-H7CR and the Fc domain of an antibody, and at [0022], Chen et al. teach that said antibody may be a human antibody of the IgG1 subtype. See also [00238], which teaches B7-H7CR/IgG1 Fc region fusion proteins. Further Chen et al. teach that B7-H7CR comprises an IgV domain, see [0072]. Additionally at [00615], Chen et al. teach that therapeutic agents of the invention may be administered in combination with radiation therapy.
Therefore Chen et al. teach the treatment of cancer in a subject comprising administering to the subject an amount of a fusion protein comprising an IgV-like domain of a TMIGD2 sufficient to treat the cancer, wherein said fusion protein comprising an IgV-like domain of a TMIGD2 comprises an Fc portion of an IgG immunoglobulin, including a human IgG1 immunoglobulin; however Chen et al. do not teach or suggest the treatment of an HHLA2-bearing tumor a subject comprising administering to the subject an amount of a fusion protein comprising an IgV-like domain of a TMIGD2 sufficient to treat the HHLA2-bearing tumor, wherein said fusion protein comprising an IgV-like domain of a TMIGD2 comprises an Fc portion of an IgG immunoglobulin, including a human IgG1 immunoglobulin. This deficiency is remedied by Zhao et al.
Zhao et al. teach that HHLA2 is a unique B7 family member that is expressed on various immune cells, and Zhao et al. further teach that a putative receptor for HHLA2 is expressed on T cells, see Abstract and paragraph bridging p. 9881. At p. 9882, Zhao et al. teach that HHLA2-Ig fusion molecules are capable of inhibiting the T cell receptor-mediated proliferation of T cells, including both CD4+ and CD8+ T cells, and Zhao et al. further teach that the treatment of CD4+ and CD8+ T cells with HHLA2-Ig fusion molecules significantly reduced the production of seven T cell-associated cytokines, including IFN-γ, TNF-α, IL-5, IL-10, IL-13, IL-17A, and IL-22, suggesting that HHLA2 is capable of suppressing cytokine production induced by T cell receptor signaling in T cells. Zhao et al. also teach that the HHLA2/HHLA2 receptor coinhibitory pathway may present a new strategy for treating cancers, see Abstract, and although Zhao et al. do not specifically indicate that HHLA2 is expressed on tumors, Zhao et al. teach that “[f]urther study will also be required to determine whether HHLA2 is expressed on nonhematopoietic cells and tumors.” Zhao et al. additionally teach that other B7 family members, such as B7x, have inhibitory functions, because B7x is aberrantly expressed on many types of human cancers and is typically associated with disease progression and poor prognosis, see p. 9879.
One of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to combine the teachings of Chen et al. and Zhao et al. to develop a method of treating an HHLA2-bearing tumor a subject comprising administering to the subject an amount of a fusion protein comprising an IgV-like domain of a TMIGD2 sufficient to treat the HHLA2-bearing tumor, wherein said fusion protein comprising an IgV-like domain of a TMIGD2 comprises an Fc portion of an IgG immunoglobulin, including a human IgG1 immunoglobulin. One of ordinary skill in the art would have been motivated to do so, because Chen et al. teach the treatment of cancer in a subject comprising administering to the subject an amount of a fusion protein comprising an IgV-like domain of a TMIGD2 sufficient to treat the cancer, wherein said fusion protein comprising an IgV-like domain of a TMIGD2 comprises an Fc portion of an IgG immunoglobulin, including a human IgG1 immunoglobulin. Furthermore based upon the teachings of Zhao et al., one of ordinary skill in the art would have been motivated to screen cancer patients, including breast cancer patients, for HHLA2-expressing tumors, because 1) Zhao et al. suggests or invites one of ordinary skill in the art to perform said screening - “[f]urther study will also be required to determine whether HHLA2 is expressed on nonhematopoietic cells and tumors,” and 2) Zhao et al. teach that at least some inhibitory B7 family members are aberrantly expressed on tumors and are associated with disease progression and a poor prognosis. Furthermore upon the determination that a tumor in a cancer patient expressed HHLA2, one of ordinary skill in the art would reason that said tumor could be treated with the B7-H7CR/IgG1 Fc region fusion protein of Chen et al. (or with a combination of said fusion protein and an additional anti-cancer therapy), because said B7-H7CR/IgG1 Fc region fusion protein would reasonably be expected to bind HHLA2 expressed on said tumor, thus interfering with the interaction of HHLA2 on said tumor with B7-H7CR (the HHLA2 receptor) on CD4+ and CD8+ T cells. Based upon the references cited, this interference would be expected to enhance the proliferation and cytokine production of CD4+ and CD8+ T cells, thus providing an anti-cancer effect. The invention of Chen et al. and Zhao et al. meets the limitations of claims 16 and 17.
With respect to claims 19 and 20, at [0022], Chen et al. teach that fusion proteins of the invention may comprise an Fc region of the human IgG1 subtype.
With respect to claim 21, at [00615], Chen et al. teach that fusion proteins of the invention may be administered in combination with radiation therapy.
With respect to claim 23, at [0067], Chen et al. teach a human B7-H7CR (SEQ ID NO: 5), which appears to be identical to the instant SEQ ID NO: 4; however Chen et al. teach a second human B7-H7CR isoform that differs from SEQ ID NO: 5 in that said second isoform lacks amino acid residues 186-189 of SEQ ID NO: 5. By preparing a B7-H7CR/IgG1 Fc region fusion protein for use in treating cancer, wherein the B7-H7CR component of said B7-H7CR/IgG1 Fc region fusion protein comprises the second B7-H7CR isoform of Chen et al., the resultant B7-H7CR/IgG1 Fc region fusion protein would comprise an IgV-like domain of a TMIGD2 (B7-H7CR ) but not comprise the instant SEQ ID NO: 4, thus meeting the limitations of claim 23.
With respect to claim 24, given that the invention of Chen et al. and Zhao et al. may be used to treat humans having HHLA2-bearing tumors, one of ordinary skill in the art would reason that said HHLA2-bearing tumors express human HHLA2.
With respect to claims 25 and 26, at [00617]-[00618], Chen et al. teach that various forms of cancer, including breast cancer and leukemia, may be treated with fusion proteins of the invention.
Therefore the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective filing date of the invention, as evidenced by the references.
Claim 18 is rejected under 35 U.S.C. 103 as being unpatentable over Chen et al. (WO 2011/020024, international publication date: 02/17/2011, in IDS from 06/07/2021) and Zhao et al. (PNAS, 110(24): 9879-9884, 2013, in IDS from 06/07/2021) as applied to claims 16, 17, 19-21, and 23-26, and further in view of Chamberlain et al. (US PG PUB 2007/0122406, publication date: 05/31/2007, in IDS from 06/07/2021).
The teachings of Chen et al. and Zhao et al. are detailed above. Although these references teach or suggest a method of treating an HHLA2-bearing tumor a subject comprising administering to the subject an amount of a fusion protein comprising an IgV-like domain of a TMIGD2 sufficient to treat the HHLA2-bearing tumor, wherein said fusion protein comprising an IgV-like domain of a TMIGD2 comprises an Fc portion of an IgG immunoglobulin, including a human IgG1 immunoglobulin, these references do not teach or suggest a method of treating an HHLA2-bearing tumor a subject comprising administering to the subject an amount of a fusion protein comprising an IgV-like domain of a TMIGD2 sufficient to treat the HHLA2-bearing tumor, wherein said fusion protein comprising an IgV-like domain of a TMIGD2 comprises an Fc portion of an IgG immunoglobulin, including a human IgG1 immunoglobulin, wherein the C-terminal residue of the IgV-like domain of a TMIGD2 of the fusion protein is fused via a peptide bond to an N-terminal residue of an Fc portion of an IgG. This deficiency is remedied by Chamberlain et al.
Chamberlain et al. teach that targeting protein/Fc fusion proteins may be prepared such that the Fc component of said fusion protein is linked to the N- or C-terminus of the targeting protein component, and Chamberlain et al. also teach that said Fc and targeting protein components may be linked via a peptide bond, see [0278].
One of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to combine the teachings of Chen et al. and Zhao et al. with the teachings of Chamberlain et al. to develop a method of treating an HHLA2-bearing tumor a subject comprising administering to the subject an amount of a fusion protein comprising an IgV-like domain of a TMIGD2 sufficient to treat the HHLA2-bearing tumor, wherein said fusion protein comprising an IgV-like domain of a TMIGD2 comprises an Fc portion of an IgG immunoglobulin, including a human IgG1 immunoglobulin, wherein the C-terminal residue of the IgV-like domain of a TMIGD2 of the fusion protein is fused via a peptide bond to an N-terminal residue of an Fc portion of an IgG. One of ordinary skill in the art would have been motivated to do so, because Chen et al. and Zhao et al. teach or suggest a method of treating an HHLA2-bearing tumor a subject comprising administering to the subject an amount of a fusion protein comprising an IgV-like domain of a TMIGD2 sufficient to treat the HHLA2-bearing tumor, wherein said fusion protein comprising an IgV-like domain of a TMIGD2 comprises an Fc portion of an IgG immunoglobulin, including a human IgG1 immunoglobulin, wherein said HHLA2-bearing tumor is a breast cancer tumor. Furthermore based upon the teachings of Chamberlain et al., one of ordinary skill in the art would appreciate that the fusion protein of Chen et al. and Zhao et al. could be prepared such that the Fc component of said fusion is linked to either the N- or C-terminus of the IgV-like domain of a TMIGD2 via a peptide linker, and either preparation would have reasonably been expected to provide a therapeutic benefit to individuals having HHLA2-bearing tumors.
Therefore the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective filing date of the invention, as evidenced by the references.
Claim 27 is rejected under 35 U.S.C. 103 as being unpatentable over Chen et al. (WO 2011/020024, international publication date: 02/17/2011, in IDS from 06/07/2021) and Zhao et al. (PNAS, 110(24): 9879-9884, 2013, in IDS from 06/07/2021) as applied to claims 16, 17, 19-21, and 23-26, and further in view of Bauer et al. (Cancer, 109(9):1721-1728, 2007, in IDS from 06/07/2021).
The teachings of Chen et al. and Zhao et al. are detailed above. Although these references teach or suggest a method of treating an HHLA2-bearing tumor a subject comprising administering to the subject an amount of a fusion protein comprising an IgV-like domain of a TMIGD2 sufficient to treat the HHLA2-bearing tumor, wherein said fusion protein comprising an IgV-like domain of a TMIGD2 comprises an Fc portion of an IgG immunoglobulin, including a human IgG1 immunoglobulin, wherein said HHLA2-bearing tumor is a breast cancer tumor, these references do not teach or suggest a method of treating an HHLA2-bearing tumor a subject comprising administering to the subject an amount of a fusion protein comprising an IgV-like domain of a TMIGD2 sufficient to treat the HHLA2-bearing tumor, wherein said fusion protein comprising an IgV-like domain of a TMIGD2 comprises an Fc portion of an IgG immunoglobulin, including a human IgG1 immunoglobulin, wherein said HHLA2-bearing tumor is a triple negative breast cancer tumor. This deficiency is remedied by Bauer et al.
Bauer et al. teach that triple negative breast cancer accounts for about 12.5% of breast cancer cases, see p. 1723, second column. Bauer et al. also teach that “[r]elative survival for women with triple-negative breast cancer was poorer than for women with other types of breast cancer, with 77% of women surviving 5 years after diagnosis, compared with 93% survival for other breast cancers… Women with triple-negative breast cancer had consistently poorer survival when compared with women with other breast cancers for each stage and race group.” See p. 1724.
One of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to combine the teachings of Chen et al. and Zhao et al. with the teachings of Bauer et al. to develop a method of treating an HHLA2-bearing tumor a subject comprising administering to the subject an amount of a fusion protein comprising an IgV-like domain of a TMIGD2 sufficient to treat the HHLA2-bearing tumor, wherein said fusion protein comprising an IgV-like domain of a TMIGD2 comprises an Fc portion of an IgG immunoglobulin, including a human IgG1 immunoglobulin, wherein said HHLA2-bearing tumor is a triple negative breast cancer tumor. One of ordinary skill in the art would have been motivated to do so, because Chen et al. and Zhao et al. teach or suggest a method of treating an HHLA2-bearing tumor a subject comprising administering to the subject an amount of a fusion protein comprising an IgV-like domain of a TMIGD2 sufficient to treat the HHLA2-bearing tumor, wherein said fusion protein comprising an IgV-like domain of a TMIGD2 comprises an Fc portion of an IgG immunoglobulin, including a human IgG1 immunoglobulin, wherein said HHLA2-bearing tumor is a breast cancer tumor. Furthermore in view of the teachings of Bauer et al., one of ordinary skill in the art would have been motivated to identify and subsequently treat triple negative breast cancer patients having HHLA2-bearing tumors, because one of ordinary skill in the art would recognize the need for methods of treating this aggressive form of breast cancer that is associated with a poor prognosis.
Therefore the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective filing date of the invention, as evidenced by the references.
Nonstatutory Double Patenting
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 16-32 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6 and 8-14 of U.S. Patent No. 10,280,208. Although the claims at issue are not identical, they are not patentably distinct from each other, because both sets of claims encompass a fusion protein comprising an IgV-like domain of a TMIGD2 and methods of treating HHLA2-bearing tumors comprising administering said fusion protein to a subject in need thereof.
Claims 33-35 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6 and 8-14 of U.S. Patent No. 10,280,208, as applied to claims 16-32 in view of Chamberlain et al. (US PG PUB 2007/0122406, publication date: 05/31/2007, in IDS from 06/07/2021).
With respect to claim 33, at [0281], Chamberlain et al. teach that therapeutic proteins may be produced by culturing a host cell transformed with an expression vector that includes a nucleic acid that encodes said therapeutic protein. One of ordinary skill in the art would have thus been motivated to produce nucleic acids that encode the fusion protein of the conflicting claims, as said nucleic acids may be used to produce the fusion protein of the conflicting claims for use in clinical applications.
With respect to claims 34 and 35, at [0314], Chamberlain et al. teach pharmaceutical compositions of therapeutic proteins comprising a pharmaceutically acceptable carrier or excipient. One of ordinary skill in the art would have thus been motivated to prepare a pharmaceutical composition that comprises the fusion protein of U.S. Patent No. 10,280,208 and a pharmaceutically acceptable carrier or excipient, because there would have been a reasonable expectation that said pharmaceutical composition could be useful in treating HHLA2-bearing tumors.
Therefore the invention as a whole is prima facie obvious over the conflicting claims in view of Chamberlain et al.
Claims 16, 17, 19-26, 28, and 29 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6 of U.S. Patent No. 10,882,893 in view of Zhao et al. (PNAS, 110(24): 9879-9884, 2013, in IDS from 05/07/2024).
The conflicting claims recite a fusion protein comprising an IgV-like domain of a TMIGD2 fused to an Fc portion of IgG, wherein said fusion proteins comprises SEQ ID NO: 2 or SEQ ID NO: 3.
The teachings of Zhao et al. are detailed above. Based upon the teachings of Zhao et al., one of ordinary skill in the art would have been motivated to screen cancer patients, including breast cancer patients, for HHLA2-expressing tumors, because 1) Zhao et al. suggests or invites one of ordinary skill in the art to perform said screening - “[f]urther study will also be required to determine whether HHLA2 is expressed on nonhematopoietic cells and tumors,” and 2) Zhao et al. teach that at least some inhibitory B7 family members are aberrantly expressed on tumors and are associated with disease progression and a poor prognosis. Furthermore upon the determination that a tumor in a cancer patient expressed HHLA2, one of ordinary skill in the art would reason that said tumor could be treated with the fusion protein of the conflicting claims (or with a combination of said fusion protein and an additional anti-cancer therapy), because said fusion protein would reasonably be expected to bind HHLA2 expressed on said tumor, thus interfering with the interaction of HHLA2 on said tumor with B7-H7CR (the HHLA2 receptor) on CD4+ and CD8+ T cells. Based upon the references cited, this interference would be expected to enhance the proliferation and cytokine production of CD4+ and CD8+ T cells, thus providing an anti-cancer effect.
Therefore the invention as a whole is prima facie obvious over the conflicting claims in view of Zhao et al.
Claim 18 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6 of U.S. Patent No. 10,882,893 in view of Zhao et al. (PNAS, 110(24): 9879-9884, 2013, in IDS from 05/07/2024), as applied to claims 16, 17, 19-21, and 23-26, and further in view of Chamberlain et al. (US PG PUB 2007/0122406, publication date: 05/31/2007, in IDS from 06/07/2021).
The teachings of Chamberlain et al. are detailed above. Based upon the teachings of Chamberlain et al., one of ordinary skill in the art would appreciate that the fusion protein of the conflicting claims and Zhao et al. could be prepared such that the Fc component of said fusion is linked to either the N- or C-terminus of the IgV-like domain of a TMIGD2 via a peptide linker, and either preparation would have reasonably been expected to provide a therapeutic benefit to individuals having HHLA2-bearing tumors.
Therefore the invention as a whole is prima facie obvious over the conflicting claims in view of Zhao et al. and Chamberlain et al.
Claim 27 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6 of U.S. Patent No. 10,882,893 in view of Zhao et al. (PNAS, 110(24): 9879-9884, 2013, in IDS from 05/07/2024), as applied to claims 16, 17, 19-21, and 23-26, and further in view of Bauer et al. (Cancer, 109(9):1721-1728, 2007, in IDS from 06/07/2021).
The teachings of Bauer et al. are detailed above. In view of the teachings of Bauer et al., one of ordinary skill in the art would have been motivated to identify and subsequently treat triple negative breast cancer patients having HHLA2-bearing tumors, because one of ordinary skill in the art would recognize the need for methods of treating this aggressive form of breast cancer that is associated with a poor prognosis.
Therefore the invention as a whole is prima facie obvious over the conflicting claims in view of Zhao et al. and Bauer et al.
Statutory Double Patenting
A rejection based on double patenting of the “same invention” type finds its support in the language of 35 U.S.C. 101 which states that “whoever invents or discovers any new and useful process... may obtain a patent therefor...” (Emphasis added). Thus, the term “same invention,” in this context, means an invention drawn to identical subject matter. See Miller v. Eagle Mfg. Co., 151 U.S. 186 (1894); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Ockert, 245 F.2d 467, 114 USPQ 330 (CCPA 1957).
A statutory type (35 U.S.C. 101) double patenting rejection can be overcome by canceling or amending the claims that are directed to the same invention so they are no longer coextensive in scope. The filing of a terminal disclaimer cannot overcome a double patenting rejection based upon 35 U.S.C. 101.
Claims 30-35 are rejected under 35 U.S.C. 101 as claiming the same invention as that of claims 1-6 of U.S. Patent No. 10,882,893. This is a statutory double patenting rejection.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to NELSON B MOSELEY II whose telephone number is (571)272-6221. The examiner can normally be reached on M-F, 9:00-6:00 EST.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Samira Jean-Louis, can be reached at 571-270-3503. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/NELSON B MOSELEY II/Primary Examiner, Art Unit 1642
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