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
This action is in response to the papers filed June 2, 2026.
Claim Amendments
Applicant’s amendment to the claims filed 06/02/2026 is acknowledged.
Claims 3-10, 13-14, 17-21, 24, 27-29, 32-42, 47-49, 52-79, 81-88 have been cancelled.
Claims 1-2, 11-12, 15-16, 22-23, 25-26, 30-31, 43-46, 50-51, and 80 are pending and under examination.
Election/Restrictions
The following is a summary of the restriction/election requirements in the present application. See, the Requirement of Requirement/Election mailed 04/11/2025.
In the reply filed 09/11/2025, applicant elected, without traverse, the invention of Group 1, drawn to a modified cell, a population of cell comprising thereof, and a pharmaceutical composition comprising thereof. Applicant further elected an NK cell lacking endogenous expression of CD3, possessing endogenous expression of NKp30, NKp44, NKp46 and CD158b, having an exogenous nucleic expression construct encoding a CD16 protein, and exhibiting a loss of function of TGFβR2 and CISH; and wherein the disease is breast cancer.
Priority
The instant application 17/430,382 was filed on 08/12/2021. This application is a national stage of international application PCT/US2020/018443 filed 02/14/2020, claiming priority based on U.S. Provisional Patent Applications 62/943,649, filed 12/04/2019, 62/841,684, filed 05/01/2019, 62/841,066 filed 04/30/2019, and 62/806,457 filed 02/15/2019.
Withdrawal of Prior Rejections/Objections
Rejections and/or objections not reiterated from the previous Office action mailed 01/02/2026 are hereby withdrawn. The following rejections and/or objections are either newly applied or are reiterated and are the only rejections and/or objections presently applied to the instant application.
Regarding the previous rejection of claims 2, 31, 45-46, 50-51, and 80 are rejected under 35 U.S.C. 112(a), for lack of written description for an NK cell having a rearranged TCR locus, the rejection is withdrawn because the claims have been amended to recite an induced NK cell obtained by reprogramming a T cell. See, pages 10-13 of applicant’s reply.
Claim Objections
Claim 50 is objected to because of the following informalities:
Claim 50, in line 4, includes the typographical error “more than more than.”
Appropriate action is required. Applicant should review the claims for typographical errors.
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.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 30 and 80 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by US 2018/0273903 A1 to Zhang et al.
This rejection is newly applied, necessitated by amendment.
Zhang discloses genetically-modified (GM) natural killer (NK) cells lacking expression of TGFBR2 and/or function thereof. See, e.g., Abstract.
The modified NK cells further comprise an exogenous nucleic acid expression construct encoding a CD16 protein. The CD16 protein is a modified CD16 protein resistant to ADAM17 cleavage and having higher affinity for IgG than wildtype CD16. See, e.g., paragraphs 2, 11, 96.
Accordingly, Zhang anticipates claim 30.
Regarding dependent claim 80, Zhang teaches that the CD16 coding sequence is under control of a heterologous promoter. See, e.g., paragraphs 2, 11, 96.
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.
Claims 45-46, 50-51 and 80 are rejected under 35 U.S.C. 103 as being unpatentable over US 2018/0155717 A1 to Valamehr et al.; in view of Baek et al. (2013) “Ex vivo expansion of natural killer cells using cryopreserved irradiated feeder cells” Anticancer Research, 33(5), 2011-2019.
This rejection is newly applied, necessitated by amendment.
VALAMEHR discloses the genomic engineering of induced pluripotent stem cells (iPSCs) and derivative cells with stable and functional genome editing. See, Abstract.
A somatic source cell is reprogrammed into an iPSC, and the iPSC is differentiated into a hematopoietic lineage cell, whereby genetic imprints are incorporated into the iPSCs either through reprogramming a selected source cell that is donor-, disease- or treatment response-specific, or through introducing genetically modified modalities into the iPSCs via genomic editing. The term “genetic imprint” includes genetic or epigenetic information that contributes to preferential therapeutic attributes in a source cell or iPSC and is retainable in the source cell-derived iPSC and/or the iPSC-derived hematopoietic lineage cell. Genetic imprints include, for example, a prearranged monospecific TCR, e.g., from a viral specific T cell or invariant natural killer T cell; trackable and desirable genetic polymorphisms, e.g., homozygous for a point mutation that encodes for the high-affinity CD16 receptor in selected donors; and predetermined HLA requirements, i.e., selected HLA-matched donor cells exhibiting a haplotype with increased population. Preferential therapeutic attributes include, for example, improved engraftment, trafficking, homing, viability, self-renewal, persistence, immune response regulation and modulation, survival, and cytotoxicity of a derived cell, and may further include antigen targeting receptor expression, HLA presentation or lack thereof, resistance to tumor microenvironment, induction of bystander immune cells and immune modulations, improved on-target specificity with reduced off-tumor effect, and resistance to treatment, e.g., chemotherapy. See, par. 127, 219-220 (par. 219, “the iPSC for differentiation comprises genetic imprints conveying desirable therapeutic attributes in effector cells, which genetic imprints are retained and functional in the differentiated hematopoietic cells derived from said iPSC”).
The iPSC-derived, genome-engineered hematopoietic lineage cell comprise, for example, a T cell receptor (TCR) and/or a high affinity non-cleavable CD16 (hnCD16). See, par. 28.
The somatic source cell used to generate the iPSC includes, for example, a T cell (par. 7, 113, 332-333), and the differentiated hematopoietic cell derived from said iPSC includes, for example, a natural killer (NK) cell (par. 21, 24, 29, 192). The NK cell does not express endogenous CD3 and does express endogenous genes encoding NKp30 and NKp46. See, par. 116.
In the working examples, iPSCs were used to generate induced NK (iNK) cells comprising a hnCD16, whereby the hnCD16-expressing iNK cells possessed enhanced cytokine produced induced by CD16 stimulation. See, par. 75-79, 323-336. CD16 is a transmembrane protein expressed by NK cells and facilitates antibody-dependent cell-mediated cytotoxicity (ADCC), which is the mechanism of NK cell mediated lysis of target cells. The hnCD16 variant is used because wild-type CD16 has low affinity and is subject to proteolytic cleavage See, par. 148, 328.
Valamehr further provides a composition comprising at least 104 or 3×107 derived hematopoietic lineage cells (par. 236), and the derived hematopoietic lineage cells have about 50%, 60%, 70% 80%, 90%, 95%, 98%, 99% or 100% NK cells (par. 233).
Valamehr does not expressly teach that the NK cell expresses endogenous genes NKp44 and CD158b, as instantly claimed in claim 45.
BAEK is relevant prior art for teaching that NKp30, NKp44, NKp46 and CD158b are surface markers of NK cells. See Abstract; pg. 2013-2014, bridging paragraph; Figure 4.
Therefore, prior to the effective filing date of the instantly claimed invention, it would have been prima facie obvious to one of ordinary skill in the art to modify the invention of Valamehr by selecting NK cells endogenously expressing NKp30, NKp44, NKp46 and CD158b, as taught by Baek, with a reasonable expectation of success because Valamehr teaches the gene-modifed NK cells, and NKp30, NKp44, NKp46 and CD158b are surface markers endogenously expressed by NK cells.
For these reasons, claim 45 would have been prima facie obvious over the cited references.
Regarding dependent claim 46, Valamehr discloses that reprogramming factors for generating iPSCs may be introduced in the form of a polypeptide or non-episomal vector (par. 179), and, therefore, the differentiated hematopoietic lineage cell or iNK cell would not harbor episomal expression constructs encoding a reprogramming factor in such embodiments, as instantly claimed.
Regarding dependent claim 50, Valamehr discloses that reprogramming factors for generating iPSCs may be introduced in the form of a polypeptide (par. 179), and, therefore, the differentiated hematopoietic lineage cell or iNK cell would not express a reprogramming factor from an exogenous nucleic acid construct in such embodiments, as instantly claimed.
Regarding dependent claim 51, Valamehr discloses the reprograming factor is OCT-4 and SOX-2. See, par. 179.
Regarding dependent claim 80, Valamehr discloses the exogenous nucleic acid encoding CD16 is under the control of a heterologous promoter. See, par. 19-20.
Claims 1-2, 11-12, 15-16, 22-23, 25-26, 30-31, 43-46, 50-51, and 80 are rejected under 35 U.S.C. 103 as being unpatentable over US 2022/0031749 A1 to Basar et al.; in view of US 2018/0155717 A1 to Valamehr et al.; and Baek et al. (2013) “Ex vivo expansion of natural killer cells using cryopreserved irradiated feeder cells” Anticancer Research, 33(5), 2011-2019.
This rejection is newly applied, necessitated by amendment.
US 2022/0031749 A1 to Basar et al. claims priority to 11/28/2018 based on U.S. Provisional Application No. 62/772,406. The teachings relied upon in this rejection find written support in the priority document.
BASAR teaches natural killer (NK) cells possessing loss-of-function of CISH and TGFβRII, thereby increasing their functionality and enhancing their antitumor cytotoxicity. The NK cells do not express T-cell marker CD3. See paragraphs 6, 10, 15, 32, 35, 119, 279-284; see also paragraphs 4, 8, 13, 113, 235-240 of the priority document for written support.
Basar does not teach that the NK cells express endogenous genes encoding NKp30, NKp44, NKp46 and CD158b, as instantly claimed.
The teachings of BAEK have been provided above and are hereby incorporated by reference.
Therefore, prior to the effective filing date of the instantly claimed invention, it would have been prima facie obvious to one of ordinary skill in the art to modify the invention of Basar by selecting cells endogenously expressing NKp30, NKp44, NKp46 and CD158b, as taught by Baek, with a reasonable expectation of success because Basar teaches the modification of NK cells, and NKp30, NKp44, NKp46 and CD158b are surface markers endogenously expressed by NK cells.
Basar teaches preventing CD16 loss or “shedding” in NK cells by knockout of ADAM17, thereby improving ADCC and cytotoxicity of the NK cells. See, par. 281. However, Basar does not teach the NK cells comprise an exogenous nucleic acid expression construct encoding CD16, as instantly claimed in claim 1.
The teachings of VALAMEHR have been provided above and are hereby incorporated by reference.
Therefore, prior to the effective filing date of the instantly claimed invention, it would have been prima facie obvious to one of ordinary skill in the art to modify the invention of Basar by introducing at least one exogenous nucleic acid expression construct encoding CD16, in view of Valamehr, with a reasonable expectation of success because the hnCD16 variant possesses high-affinity and is resistant to proteolytic cleavage compared to wild-type CD16, and, therefore, the modification would improve ADCC and cytotoxicity of the NK cells.
For these reasons, claim 1 would have been prima facie obvious over the cited references.
Regarding dependent claim 2, Basar teaches the NK cell comprises an insertion of an exogenous nucleic acid construct into a genomic locus harboring a CISH or TGFβRII gene. See, e.g., paragraphs 12, 54; see also paragraphs 10, 52 of the priority document for written support. Valamehr teaches the NK cell is an iNK cell generated from a iPSC derived from a mature T cell. See, e.g., par. 7, 21, 24, 29, 192, 332-333.
Regarding dependent claim 11, Basar teaches the NK cells are derived from pluripotent stem cells. See, e.g., paragraph 120; see also paragraph 114 of the priority document for written support. Valamehr teaches the NK cells are derived from pluripotent stem cells. See, e.g., par. 7, 21, 24, 29, 192, 332-333.
Regarding dependent claim 12, Basar teaches the NK cells are derived from induced pluripotent stem cells or embryonic stem cells. See, e.g., paragraph 120; see also paragraph 114 of the priority document for written support. Valamehr teaches the NK cells are derived from pluripotent stem cells. See, e.g., par. 7, 21, 24, 29, 192, 332-333.
Regarding dependent claim 15, Basar teaches genetically modifying the pluripotent stem cells. See, e.g., paragraph 102; see also paragraph 98 of the priority document for written support. Valamehr teaches genetically modifying the pluripotent stem cells. See, e.g., par. 75-79, 127, 219-220.
Regarding dependent claim 16, Basar teaches the NK cell comprises an insertion of an exogenous nucleic acid construct into a genomic locus harboring a CISH or TGFβRII gene. See, e.g., paragraphs 12, 54; see also paragraphs 10, 52 of the priority document for written support.
Regarding dependent claim 22, Basar teaches the NK cells are obtained by editing a genomic locus with an RNA-guide endonuclease or a Cas9 nuclease. See, e.g., paragraphs 7, 32, 51; see also paragraphs 5, 30, 49 of the priority document for written support. Valamehr teaches the NK cells are obtained by editing a genomic locus with an RNA-guide endonuclease or a Cas9 nuclease. See, e.g., par. 152, 160.
Regarding dependent claim 23, Basar teaches the NK cells are obtained by editing a genomic locus with an RNA-guide endonuclease or a Cas9 nuclease. See, e.g., paragraphs 7, 32, 51; see also paragraphs 5, 30, 49 of the priority document for written support. Valamehr teaches the NK cells are obtained by editing a genomic locus with an RNA-guide endonuclease or a Cas9 nuclease. See, e.g., par. 152, 160.
Regarding dependent claim 25, since the RNA-guided endonuclease would target the gene copies on both alleles, Basar is found to teach or fairly suggest editing both genomic loci encoding CISH and TGFβRII. In addition, Basar describes “biallelic” genomic modification of the cells. See, e.g., paragraph 72; see also paragraph 66 of the priority document for written support. For these reasons, the limitations of the claim would have been prima facie obvious over the cited references.
Regarding dependent claim 26, Basar does not teach that the different genomic modifications have been edited by a different RNA-guided nuclease, as instantly claimed. Even though product-by-process claims are limited by and defined by the process, determination of patentability is based on the product itself. If the product in the product-by-process claim is the same as or obvious from a product of the prior art, the claim is unpatentable even though the prior product was made by a different process. In re Thorpe, 777 F.2d 695, 698, 227 USPQ 964, 966 (Fed. Cir. 1985). In this case, both the claims and the prior art provide NK cells modified with an RNA-guided nuclease. Therefore, the process of making the claimed NK cell in claim 26 is substantially similar to the product-by-process limitations taught by the prior art. The product-by-process limitations recited by claim 26 are not found to necessarily imply a structure that patentably distinguishes the instantly claimed NK cell from that found in the prior art. For these reasons, the product of claim 26 would have been prima facie obvious over the prior art. The Patent Office bears a lesser burden of proof in making out a case of prima facie obviousness for product-by-process claims because of their peculiar nature than when a product is claimed in the conventional fashion. In re Fessmann, 489 F.2d 742, 744, 180 USPQ 324, 326 (CCPA 1974). Once the examiner provides a rationale tending to show that the claimed product appears to be the same or similar to that of the prior art, although produced by a different process, the burden shifts to applicant to come forward with evidence establishing a nonobvious difference between the claimed product and the prior art product. In re Marosi, 710 F.2d 799, 803, 218 USPQ 289, 292-33 (Fed. Cir. 1983). See MPEP 2113.
The limitations of claims 30-31 are taught or fairly suggested by the cited references, as outlined above.
Claim 43 further recites a population of cells comprising the NK cells. Basar teaches a population of cells comprising the modified NK cell. See, e.g., paragraph 20; see also paragraph 18 of the priority document for written support. Valamehr teaches a population of cells comprising the modified NK cell. See, e.g., par. 233, 236.
Claim 44 further recites a pharmaceutical composition comprising the population of cells. Basar teaches a pharmaceutical composition comprising a population of cells comprising the modified NK cell. See, e.g., paragraph 20; see also paragraph 18 of the priority document for written support. Valamehr teaches a pharmaceutical composition comprising the population of cells. See, e.g., par. 44.
Regarding the additional limitations of claims 45-46, 50-51 and 80, the corresponding teachings of Valamehr have been provided above and are hereby incorporated by reference.
In addition, with respect to claim 46, Basar teaches that the NK cells are reprogrammed to express a CAR or TCR by insertion of a coding vector into the genome. See, e.g., paragraphs 12, 54; see also paragraphs 10, 52 of the priority document for written support. Since the reprogramming factor is integrated into the genome, the vector is not an episomal expression construct. For these reasons, the limitations of the claim are taught or fairly suggested by the cited references.
In addition, with respect to claim 50, Basar teaches genetically modifying the CISH and TGFβRII genomic loci of NK cells without introducing a reprogramming factor from an exogenous nucleic acid construct. See, e.g., paragraphs 279-284; see also, e.g., paragraphs 235-240 of the priority document for written support. Accordingly, the limitations of the claim are taught or fairly suggested by the cited references.
In addition, with respect to claim 51, Basar teaches genetically modifying the CISH and TGFβRII genomic loci of NK cells without introducing a reprogramming factor from an exogenous nucleic acid construct. See, e.g., paragraphs 279-284; see also, e.g., paragraphs 235-240 of the priority document for written support. Accordingly, the limitations of the claim are taught or fairly suggested by the cited references.
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.
Claim 30 is provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over the claims of copending U.S. Application No. 17/786,753 (reference to claim listing filed on 04/23/2026). Although the claims at issue are not identical, they are not patentably distinct from each other because the reference claims anticipate the instant claims. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
The reference claims recite a genetically-engineered cell comprising a genetic edit that results in loss of function of CISH and a genetic edit that results in loss of function of TGFβRII, wherein the genetic edits are made via RNA-guided nucleases. See, claim 30.
The RNA-guided nuclease is a Cas12a variant. See, claim 32.
The genetically engineered cell is differentiated into a natural killer (NK) cell (claim 92); the cell does not express endogenous CD8 (claim 93); the cell expresses an endogenous natural cytotoxicity receptor (claim 93).
The cell is further engineered to express an exogenous nucleic acid encoding CD16. See, claim 94.
Therefore, instant claim 30 is anticipated by the reference claims.
Claims 1, 11-12, 15-16, 22-23, 25-26, 43-44 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over the claims of copending U.S. Application No. 17/786,753 (reference to claim listing filed on 04/23/2026), as applied above; in view of Baek et al. (2013) “Ex vivo expansion of natural killer cells using cryopreserved irradiated feeder cells” Anticancer Research, 33(5), 2011-2019. Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been prima facie obvious over the reference claims and secondary references. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
This rejection is newly applied, necessitated by amendment.
The features of the reference claims have been provided above and are hereby incorporated by reference.
The reference claims do not recite the NK cells express endogenous genes encoding NKp30, NKp44, NKp46 and CD158b, as instantly claimed.
The teachings of BAEK have been provided above and are hereby incorporated by reference.
Therefore, prior to the effective filing date of the instantly claimed invention, it would have been prima facie obvious to one of ordinary skill in the art to modify the invention of the reference claims by selecting cells endogenously expressing NKp30, NKp44, NKp46 and CD158b, as taught by Baek, with a reasonable expectation of success because the reference claims recite the modification of NK cells, and NKp30, NKp44, NKp46 and CD158b are surface markers endogenously expressed by NK cells.
Therefore, instant claims 1 would have been prima facie obvious over the reference claims.
Regarding instant claims 11-12, 15-16, the reference claims recite the NK cell is derived from a human pluripotent stem cell or a human induced pluripotent stem cell (iPSC). See, claims 30, 90, 92, 94.
Regarding instant claims 22-23, the reference claims recite the genetic edits are made via RNA-guided nucleases (claim 30), wherein the RNA-guided nuclease is a Cas12a variant (claim 32).
Regarding instant claim 25, since the RNA-guided endonuclease would target the gene copies on both alleles, the reference claim is found to teach or fairly suggest editing both genomic loci encoding CISH and TGFβRII.
Regarding instant claim 26, the reference claims do not recite that the different genomic modifications have been edited by a different RNA-guided nuclease, as instantly claimed. Even though product-by-process claims are limited by and defined by the process, determination of patentability is based on the product itself. If the product in the product-by-process claim is the same as or obvious from a product of the prior art, the claim is unpatentable even though the prior product was made by a different process. In re Thorpe, 777 F.2d 695, 698, 227 USPQ 964, 966 (Fed. Cir. 1985). In this case, both the instant claims and the reference claims provide NK cells modified with an RNA-guided nuclease. Therefore, the process of making the claimed NK cell in claim 26 is substantially similar to the product-by-process limitations taught by the reference claims. The product-by-process limitations recited by claim 26 are not found to necessarily imply a structure that patentably distinguishes the instantly claimed NK cell from that found in the reference claims. For these reasons, the product of claim 26 would have been prima facie obvious over the reference claims.
Regarding instant claims 43-44, since the reference claims teach making the genetically modified cells or NK cells induced therefrom, the reference claims are found to also teach or fairly teach a population of said cells and a composition comprising said population of claims. Regarding the limitation of a “pharmaceutical” composition, the limitation is directed to an intended use that is not found to necessarily result in a structural difference which patentable distinguishes the instantly claimed composition from that taught or fairly suggested from the reference claims.
Claims 2, 31, 45-46, 50-51 and 80 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over the claims of copending U.S. Application No. 17/786,753 (reference to claim listing filed on 04/23/2026); and Baek et al. (2013) “Ex vivo expansion of natural killer cells using cryopreserved irradiated feeder cells” Anticancer Research, 33(5), 2011-2019, as applied above; in further view of US 2018/0155717 A1 to Valamehr et al. Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been prima facie obvious over the reference claims and secondary references. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
This rejection is newly applied, necessitated by amendment.
The features of the reference claims, and teachings of Baek, have been provided above and are hereby incorporated by reference.
The reference claims do not recite that the human pluripotent stem cell or iPSC was derived from a mature T cell, as instantly claimed
The teachings of Valamehr have been provided above and are hereby incorporated by reference.
Therefore, prior to the effective filing date of the instantly claimed invention, it would have been prima facie obvious to one of ordinary skill in the art to modify the invention of the reference claims by using an iPSC derived from a mature T cell, in view of Valamehr, with a reasonable expectation of success because such a reprogramming process would provide genetic imprints from the source T cell and retain preferential therapeutic attributes, such as improved engraftment and antigen targeting receptor expression.
The additional limitations of claims 2, 31, 45-46, 50-51 and 80 have been addressed above.
Accordingly, claims 2, 31, 45-46, 50-51 and 80 would have been prima facie obvious over the cited references.
Response to Arguments
Applicant’s remarks filed 06/02/2026 have been carefully considered, but are not found persuasive.
Applicant argues that the claimed invention provides unexpected and improved properties, e.g., enhanced tumor killing. The argument shows figures/data without providing any support or description of any experiment. See, pages 20-23 of the reply.
Arguments presented by the applicant cannot take the place of evidence in the record. In re Schulze, 346 F.2d 600, 602, 145 USPQ 716, 718 (CCPA 1965) and In re De Blauwe, 736 F.2d 699, 705, 222 USPQ 191, 196 (Fed. Cir. 1984). Examples of statements which are not evidence and which must be supported by an appropriate affidavit or declaration include statements regarding unexpected results, commercial success, solution of a long-felt need, inoperability of the prior art, invention before the date of the reference, and allegations that the author(s) of the prior art derived the disclosed subject matter from the inventor or at least one joint inventor. MPEP 716.01(c).
As presented, the alleged unexpected and improved properties of the claimed invention cannot be evaluated. There is no description of how the figures/data were generated, and there is no means of determining which claims should the reconsidered in light of the alleged secondary considerations, if any. The remainder of the arguments are moot or otherwise obviated by the new grounds of rejection set forth in this action.
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 nonprovisional extension fee (37 CFR 1.17(a)) 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 mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to JAMES J GRABER whose telephone number is (571)270-3988. The examiner can normally be reached Monday-Thursday: 9:00 am - 4:00 pm.
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/JAMES JOSEPH GRABER/Examiner, Art Unit 1631
Prosecution Insights