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
Amendments
In the reply filed 11/20/2025, Applicant has amended claims 1-2 and 11, newly canceled claims 5-6, and added new claims 30-31.
Claim Status
Claims 1-2, 8-9, 11-12, 14-17, 20-24, 26-27 and 29-31 are pending.
Claims 14-17, 20-24, 26-27 and 29 have been withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to non-elected inventions, there being no allowable generic or linking claim. Election was made with traverse in the reply filed on 02/25/2025.
Claims 1-2, 8-9, 11-12 and 30-31 are considered on the merits.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 11/20/2025 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner. The corresponding signed and initialed PTO form 1449 has been mailed with this action.
Withdrawn Claim Objections
The prior objection to claims 1-2 because of grammatical error is withdrawn in light of Applicant’s amendment to the claims.
New Claim Objections
Claim 1 is objected to because of the following informalities:
Claim 1, last line, recites the phrase “the a γδT cell”, which contains a typographical error. It is recommended to change to “the γδT cell”.
Appropriate correction is required.
Withdrawn Claim Rejections - 35 USC § 112
The prior rejection of claims 1-2, 8-9 and 11-12 under 35 U.S.C. 112(b) is withdrawn in light of Applicant’s amendment to the claims.
Withdrawn Claim Rejections - 35 USC § 102 and 103
The prior rejections of claims 1-2, 8-9 and 11-12 under 35 U.S.C. 102 and 103 over Numbenjapon, Zhang and Collins are withdrawn in light of Applicant’s amendment to claim 1 to recite a new limitation a γδT cell, that is not taught by Numbenjapon.
New Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claims 1-2, 11-12 and 30-31 are rejected under 35 U.S.C. 102 (a)(1) as being anticipated by Deniger et al. (Clin Cancer Res; 2014;20(22): 5708-19), as evidenced by Tremblay-McLean et al. (BMC Immunol. 2019 January;20:8, p. 1-13) and Uniprot (Q29983, MICA-human, downloaded on 2/6/2026, downloaded from https://www.uniprot.org/uniprotkb/Q29983/entry, p. 1-11).
With respect to claim 1, Deniger teaches a method to propagate γδT cells from a population of negatively selected peripheral blood mononuclear cells isolated from heathy volunteers for γδT cell cancer immunotherapy in humans (see e.g., abstract and p. 5709, right col., para “Propagation of γδT cells”), thus teaches the preamble.
In regard to claim 1 (a), Deniger teaches artificial antigen-presenting cells (aAPC) derived from K562 cells are used to expand human γδT cells to clinical scale (see e.g., abstract) and teaches the irradiated K562-derived aAPCs (clone #4) are genetically modified to coexpress CD19, CD64, CD86, CD137L, and a membrane-bound mutein of IL15 (mIL15) (e.g., p. 5709, left col., last para). Thus, Deniger teaches providing an aAPC comprising a cell membrane (i.e., K562 cell-derived aAPC).
In regard to wherein the aAPC expresses an NKG2D ligand, Deniger teaches the K562-derived aAPCs express endogenous MHC class-I chain-related protein A and B (MICA/B) which are ligands for NKG2D (p. 5717, left col, para 2). Furthermore, Tremblay-McLean discloses expression of NKG2D ligands on cell lines including K562 and evidences that K562 expresses a higher intensity of ligands for NKG2D including MIC-A, MIC-B and ULBP-2 (e.g., abstract, Table 2, “Panel 1”, Fig 1a and Fig 2a). Thus, Deniger evidenced by Tremblay-McLean teaches the K562-derived aAPCs express an NKG2D ligand such as MICA.
In regard to wherein the aAPC comprises the NKG2D ligand on the cell membrane, Uniprot evidences that human MICA is a membrane-bound protein (p. 1, para “Function”) that contains a transmembrane domain (see p. 3, para “Features”), thus evidences that the NKG2D ligand MICA is on the cell membrane.
In regard to claim 1 (b), Deniger teaches the population of negatively selected PBMCs are cocultured with γ-irradiated aAPCs (clone #4) for 22 days that results in the robust numeric expansion of γδT cells with a yield of >109 γδT cells from <106 total initiating cells (Fig. 1B) (p. 5710, left col, last para – right col, para 1). Thus, Deniger teaches contacting the isolated immune cell population with an effective amount of the aAPC to expand the γδT cell to an amount effective for immunotherapy.
With respect to claim 2, as stated supra, Deniger evidenced by Tremblay-McLean teaches the K562-derived aAPCs express an NKG2D ligand comprising MICA.
With respect to claim 11 directed to the cell membrane further comprising a ligand that binds a co-stimulatory molecule on T cells, and claim 12 directed to the co-stimulatory molecule comprising CD28 or 4-1BB, as stated supra, Deniger teaches the K562-derived aAPCs (clone #4) are genetically modified to coexpress CD86 and CD137L (e.g., p. 5709, left col., last para), thus teaches the cell membrane further comprises a ligand that binds a co-stimulatory molecule CD28 or 4-1BB (i.e., CD86 being a ligand that binds CD28, and CD137L being a ligand that binds 4-1BB).
With respect to claim 30 directed to the cell membrane further comprising a ligand that binds IL15R, as stated supra, Deniger teaches the K562-derived aAPCs (clone #4) are genetically modified to coexpress a membrane-bound mutein of IL15 (mIL15) (e.g., p. 5709, left col., last para), thus teaches the cell membrane of the aAPC further comprises a ligand that binds IL15R.
With respect to claim 31 directed to the aAPC being derived from a K-562 cell line, as stated supra, Deniger teaches the K562-derived aAPCs (e.g., abstract), thus teaches the aAPC is derived from a K-562 cell line.
Accordingly, Deniger, as evidenced by Tremblay-McLean and Uniprot, anticipates instant claims.
Response to Traversal:
Applicant’s arguments filed on 11/20/2025 are acknowledged.
Applicant argues that the amendment to claims reciting a new limitation of a γδT cell overcomes the prior anticipation rejection by Numbenjapon, and obviousness rejection over Numbenjapon in view of Zhang or Collins (Re marks, p. 7-10).
Applicant’s arguments have been fully considered and they are persuasive. Therefore, the prior rejections have been withdrawn. However, as necessitated by amendment, a new ground of rejection has been made by Deniger, as evidenced by Tremblay-McLean and Uniprot as discussed above. Specifically, Deniger teaches a method for expanding γδT cells by coculturing with K562-derived aAPCs.
New Claim Rejections - 35 USC § 103
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 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.
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.
Claims 1-2, 8-9, 11-12 and 30-31 are rejected under 35 U.S.C. 103 as being unpatentable over Deniger et al. (Clin Cancer Res; 2014;20(22): 5708-19), as evidenced by Tremblay-McLean et al. (BMC Immunol. 2019 January;20:8, p. 1-13) and Uniprot (Q29983, MICA-human, downloaded on 2/6/2026, downloaded from https://www.uniprot.org/uniprotkb/Q29983/entry, p. 1-11), and in view of Olive et al., (US 2016/0090420 A1).
Claims 1-2, 11-12 and 30-31 are anticipated by Deniger, as evidenced by Tremblay-McLean and Uniprot, thus are made obvious.
Claim 8 is directed to the aAPC further expressing a scFv antibody that binds a T cell inhibitory molecule. Claim 9 is directed to the T cell inhibitory molecule comprising BTLA.
However, Deniger, Tremblay-McLean and Uniprot are silent on the aAPC further expressing one scFv antibody that binds BTLA.
Olive teaches an antagonist of the BTLA/HVEM interaction for use in therapy, wherein said antagonist increases the proliferation of Vγ9Vδ2 T cells (see e.g., abstract). Olive teaches said antagonist is chosen from antibodies directed against BTLA and fragments thereof (e.g., [0016]), and teaches said fragment of the antibody is chosen scFv fragment (e.g., by molecular biology techniques) (e.g., [0018]), thus teaches a scFv antibody that binds BTLA and increases γδT cell proliferation.
Therefore, it would have been obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method for expanding γδT cells using the engineered aAPC disclosed by Deniger, as evidenced by Tremblay-McLean and Uniprot, by combining engineering the aAPC to further express a scFv antibody that binds BTLA as taught by Olive with a reasonable expectation of success. Since Deniger aims to expand γδT cells for cancer immune therapy (e.g., abstract), and since Olive teaches a scFv antibody that binds BTLA to block the BTLA/HVEM interaction increases the proliferation of γδT cells that can be used in therapy of tumors (see e.g., abstract, [0012]-[0014] and [0016]-[0018]), one of ordinary skill in the art would have had a reason to combine engineering Deniger’s aAPC to further express a scFv antibody that binds BTLA as taught by Olive in order to increase the proliferation of γδT cells for cancer immune therapy.
Hence, the claimed invention as a whole was prima facie obvious to a person of ordinary skill before the effective filing date of the claimed invention in the absence of evidence to the contrary.
Response to Traversal:
Applicant’s arguments filed on 11/20/2025 are acknowledged and have been discussed above.
Withdrawn Double Patenting Rejections
The prior double patenting rejections set forth in the Office action mailed on 05/20/2025 have been withdrawn in light of Applicant’s amendment to recite a new limitation a γδT cell.
New Double Patenting Rejections
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 USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The 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/process/file/efs/guidance/eTD-info-I.jsp.
Claims 1-2, 8-9, 11-12 and 30-31 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3 and 10-17 of US Patent No. 11,524,988 (‘988) in view of Deniger et al. (Clin Cancer Res; 2014;20(22): 5708-19) and Olive et al., (US 2016/0090420 A1). Although the claims at issue are not identical, they are not patentably distinct from each other.
Reference claims in ‘988 recite a method for producing chimeric antigen receptor (CAR) T cells comprising a) providing a substrate having an exposed surface and a polypeptide disposed on the surface of the substrate, wherein the polypeptide comprises a heparin binding domain and one or more single chain variable fragments (scFv) comprising a CD3 or CD28 antigen recognition domain that selectively binds a T cell, and wherein the heparin binding domain and the scFv are present in the same polypeptide; and b) co-culturing T cells, viral vectors encoding chimeric antigen receptors, and an amount of substrate effective to stimulate T cells (reference claim 1, related to instant claim 1), wherein the substrate comprises an artificial antigen presenting cell (aAPC) comprising a cell line containing on its lipid membrane the polypeptide and one or more scFvs (reference claim 3), wherein the antigen recognition domain binds CD3 receptors and CD28 receptors (reference claims 10-11, related to instant claims 11-12), wherein the substrate further contains on its surface an scFv comprising an antigen recognition domain that selectively binds a co-stimulatory molecule on T-cells comprising 4-1BB (reference claims 12-13, related to instant claims 11-12), wherein the immune effector cells are γδT cells (reference claims 16-17, related to instant claim 1). It is noted that the patented claims encompass a method of expanding the γδT cells.
However, patented claims are silent on the aAPC expressing an NKG2D ligand MICA on the membrane in instant claims 1-2, or a scFv antibody that binds BTLA in instant claims 8-9, or a ligand that binds IL15R in instant claim 30 or the aAPC being derived from a K-562 cell line in instant claim 31.
Deniger teaches a method to propagate γδT cells from a population of negatively selected PBMCs isolated from heathy volunteers by coculturing with artificial antigen-presenting cells (aAPC) to expand to clinical scale for γδT cell cancer immunotherapy (see e.g., abstract and p. 5709, right col., para “Propagation of γδT cells”). Deniger teaches aAPCs are derived from K562 tumor cells (related to instant claim 31) and are genetically modified to coexpress CD86, CD137L, and a membrane-bound mutein of IL15 (mIL15) (e.g., p. 5709, left col., last para, related to instant claim 30). Deniger teaches the K562-derived aAPCs express endogenous MHC class-I chain-related protein A and B (MICA/B) which are ligands for NKG2D (p. 5717, left col, para 2, related to instant claims 1-2).
Olive teaches an antagonist of the BTLA/HVEM interaction for use in therapy, wherein said antagonist increases the proliferation of γδ T cells (see e.g., abstract). Olive teaches said antagonist is chosen from antibodies directed against BTLA and fragments thereof (e.g., [0016]), and teaches said fragment of the antibody is chosen scFv fragment (e.g., by molecular biology techniques) (e.g., [0018]), thus teaches a scFv antibody that binds BTLA, related to instant claims 8-9.
Therefore it would have been obvious for one of ordinary skill in the art before the effective filing date to have recited a method of producing, encompassing expanding, γδ T cells using aAPCs cited in the reference claims of ‘988, by choosing the K562-derived aAPC endogenously expressing an NKG2D ligand MICA on the cell membrane and engineered to express a membrane-bound mutein of IL15 that binds IL15R as taught by Deniger and further engineering the aAPC to express a scFv antibody that binds BTLA as suggested by Olive with a reasonable expectation of success. Since Deniger reduces to practice the usage of the engineered K562-derived aAPC in expanding γδ T cells (see e.g., abstract) and since Olive teaches a scFv BTLA antibody increases the proliferation of γδ T cells (see e.g., abstract), one of ordinary skill in the art would have had a reason to choose the aAPC of Deniger and to further engineer to express a scFv BTLA antibody as suggested by Olive in order to obtain γδ T cells for immune therapy.
Since the instant application claims obvious over cited patent claims, in view of Deniger and Olive, said claims are not patentably distinct.
New Provisional Double Patenting Rejections
Claims 1-2, 8-9, 11-12 and 30-31 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3, 11-13, 15-16 and 19-20 of copending Application No. 18/079,302 (‘302) in view of Deniger et al. (Clin Cancer Res; 2014;20(22): 5708-19) and Olive et al., (US 2016/0090420 A1). Although the claims at issue are not identical, they are not patentably distinct from each other.
Reference claims in ‘302 recite a method for producing chimeric antigen receptor (CAR) T cells comprising a) providing a substrate having an exposed surface and a polypeptide disposed on the surface of the substrate, wherein the polypeptide comprises a heparin binding domain and one or more single chain variable fragments (scFv) comprising an antigen recognition domain that selectively binds an antigen on immune effector cells are disposed in the surface of the substrate; and b) co-culturing immune effector cells, viral vectors encoding chimeric antigen receptors, and an effective amount of substrate (reference claim 1, related to instant claim 1), wherein the substrate comprises an artificial antigen presenting cell (aAPC) comprising a cell line containing on its lipid membrane the polypeptide and one or more scFvs (reference claim 3), wherein the antigen recognition domain binds CD3 receptors, CD28 receptors and 4-1BB (reference claims 11-13, related to instant claims 11-12), wherein the substrate further contains on its surface an scFv selectively binds a coctimulatory molecule on T cells, the costimulatory molecule comprises 4-1BB (reference claims 15-16, related to instant claims 11-12), wherein the immune effector cells are CD3+ T cells, γδT cells (reference claims 19-20, related to instant claim 1). It is noted that the copending claims encompass a method of expanding the γδT cells.
However, copending claims are silent on the aAPC expressing an NKG2D ligand MICA on the membrane in instant claims 1-2, or a scFv antibody that binds BTLA in instant claims 8-9, or a ligand that binds IL15R in instant claim 30 or the aAPC being derived from a K-562 cell line in instant claim 31.
Deniger teaches a method to propagate γδT cells from a population of negatively selected PBMCs isolated from heathy volunteers by coculturing with artificial antigen-presenting cells (aAPC) to expand to clinical scale for γδT cell cancer immunotherapy (see e.g., abstract and p. 5709, right col., para “Propagation of γδT cells”). Deniger teaches aAPCs are derived from K562 tumor cells (related to instant claim 31) and are genetically modified to coexpress CD86, CD137L, and a membrane-bound mutein of IL15 (mIL15) (e.g., p. 5709, left col., last para, related to instant claim 30). Deniger teaches the K562-derived aAPCs express endogenous MHC class-I chain-related protein A and B (MICA/B) which are ligands for NKG2D (p. 5717, left col, para 2, related to instant claims 1-2).
Olive teaches an antagonist of the BTLA/HVEM interaction for use in therapy, wherein said antagonist increases the proliferation of γδ T cells (see e.g., abstract). Olive teaches said antagonist is chosen from antibodies directed against BTLA and fragments thereof (e.g., [0016]), and teaches said fragment of the antibody is chosen scFv fragment (e.g., by molecular biology techniques) (e.g., [0018]), thus teaches a scFv antibody that binds BTLA, related to instant claims 8-9.
Therefore it would have been obvious for one of ordinary skill in the art before the effective filing date to have recited a method of producing, encompassing expanding, γδ T cells using aAPCs cited in the reference claims of ‘302, by choosing the K562-derived aAPC endogenously expressing an NKG2D ligand MICA on the cell membrane and engineered to express a membrane-bound mutein of IL15 that binds IL15R as taught by Deniger and further engineering the aAPC to express a scFv antibody that binds BTLA as suggested by Olive with a reasonable expectation of success. Since Deniger reduces to practice the usage of the engineered K562-derived aAPC in expanding γδ T cells (see e.g., abstract) and since Olive teaches a scFv BTLA antibody increases the proliferation of γδ T cells (see e.g., abstract), one of ordinary skill in the art would have had a reason to choose the aAPC of Deniger and to further engineer to express a scFv BTLA antibody as suggested by Olive in order to obtain γδ T cells for immune therapy.
Since the instant application claims obvious over cited application claims, in view of Deniger and Olive, said claims are not patentably distinct.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims in the copending application have not in fact been patented.
Claims 1-2, 8-9, 11-12 and 30-31 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-4 of copending Application No. 18/866,630 (‘630) in view of Deniger et al. (Clin Cancer Res; 2014;20(22): 5708-19) and Olive et al., (US 2016/0090420 A1). Although the claims at issue are not identical, they are not patentably distinct from each other.
Copending claims in ‘630 recite a method of providing anti-cancer immunity in a subject by administering an effective amount of an NKG2D-expressing immune effector cells genetically modified to express an anti-CD33 CAR or other CARs, wherein at least 70% of the immune effector cells express detectable NKG2D (reference claims 1-2), wherein at least 70% of the immune effector cells are selected from a γδ T cell (reference claim 3, related to instant claim 1), wherein the immune effector cells have been expanded with artificial antigen presenting cells (aAPCs) (reference claim 4, related to instant claims 1-2 and 11-12).
However, copending claims are silent on the aAPC expressing an NKG2D ligand MICA on the membrane in instant claims 1-2, or a scFv antibody that binds BTLA in instant claims 8-9, or containing one ligand that binds a co-stimulatory molecule 4-1BB in instant claims 11-12, or a ligand that binds IL15R in instant claim 30 or the aAPC being derived from a K-562 cell line in instant claim 31.
Deniger teaches a method to propagate γδT cells from a population of negatively selected PBMCs isolated from heathy volunteers by coculturing with artificial antigen-presenting cells (aAPC) to expand to clinical scale for γδT cell cancer immunotherapy (see e.g., abstract and p. 5709, right col., para “Propagation of γδT cells”). Deniger teaches aAPCs are derived from K562 tumor cells (related to instant claim 31) and are genetically modified to coexpress CD86, CD137L (i.e., 4-1BBL), and a membrane-bound mutein of IL15 (mIL15) (e.g., p. 5709, left col., last para, related to instant claims 11-12 and 30). Deniger teaches the K562-derived aAPCs express endogenous MHC class-I chain-related protein A and B (MICA/B) which are ligands for NKG2D (p. 5717, left col, para 2, related to instant claims 1-2).
Olive teaches an antagonist of the BTLA/HVEM interaction for use in therapy, wherein said antagonist increases the proliferation of γδ T cells (see e.g., abstract). Olive teaches said antagonist is chosen from antibodies directed against BTLA and fragments thereof (e.g., [0016]), and teaches said fragment of the antibody is chosen scFv fragment (e.g., by molecular biology techniques) (e.g., [0018]), thus teaches a scFv antibody that binds BTLA, related to instant claims 8-9.
Therefore it would have been obvious for one of ordinary skill in the art before the effective filing date to have recited a method encompassing expanding γδ T cells using aAPCs cited in the reference claims of ‘630, by choosing the K562-derived aAPC endogenously expressing an NKG2D ligand MICA on the cell membrane and engineered to express a 4-1BBL that binds 4-1BB and a membrane-bound mutein of IL15 that binds IL15R as taught by Deniger and further engineering the aAPC to express a scFv antibody that binds BTLA as suggested by Olive with a reasonable expectation of success. Since Deniger reduces to practice the usage of the engineered K562-derived aAPC in expanding γδ T cells (see e.g., abstract) and since Olive teaches a scFv BTLA antibody increases the proliferation of γδ T cells (see e.g., abstract), one of ordinary skill in the art would have had a reason to choose the aAPC of Deniger and to further engineer to express a scFv BTLA antibody as suggested by Olive in order to obtain γδ T cells for providing anti-cancer immunity.
Since the instant application claims obvious over cited application claims, in view of Deniger and Olive, said claims are not patentably distinct.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims in the copending application have not in fact been patented.
Response to Traversal:
Applicant’s arguments filed on 11/20/2025 are acknowledged.
Applicant requests that the double patenting rejections be held in abeyance until allowable claims are found. This is not found persuasive. Applicant is reminded that a complete response to a nonstatutory double patenting (NSDP) rejection is either a reply by applicant showing that the claims subject to the rejection are patentably distinct from the reference claims, or the filing of a terminal disclaimer. Such a response is required even when the nonstatutory double patenting rejection is provisional. See MPEP 804.I.B.1. As necessitated by amendment, the prior rejections have been withdrawn and a new ground of rejection has been made over the cited patent and applications in view of Deniger and Olive as discussed above.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any extension fee pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the date of this final action.
No claims are allowed.
Examiner Contact Information
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Jianjian Zhu whose telephone number is (571)272-0956. The examiner can normally be reached M - F 8:30AM - 4PM (EST).
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, James Douglas (Doug) Schultz can be reached on (571) 272-0763. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/JIANJIAN ZHU/Examiner, Art Unit 1631
/JAMES D SCHULTZ/Supervisory Patent Examiner, Art Unit 1631