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
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 05/26/2026 has been entered. Applicant's amendment and response filed on 05/26/2026 has been received and entered into the case.
Amendments
In the reply filed on 05/26/2026, Applicant has amended claims 1-2, 8, 13 and 26-27.
Claim Status
Claims 1-2, 6-13 and 26-27 are pending.
Claims 26-27 have been withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to non-elected inventions, there being no allowable generic or linking claim.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 without traverse in the reply filed on 08/05/2025.
Claims 1-2 and 6-13 are considered on the merits.
Terminal Disclaimers
The terminal disclaimer filed on 02/25/2026 disclaiming the terminal portion of any patent granted on this application which would extend beyond the expiration date of any patent granted on pending reference application 19/073,872 has been reviewed and is accepted. The terminal disclaimer has been recorded.
The rejections of record are withdrawn.
New Claim Objections
Claim 13 is objected to because of the following informalities: Applicant is advised that should claim 10 be found allowable, claim 13 will be objected to under 37 CFR 1.75 as being a substantial duplicate thereof. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 706.03(k).
Withdrawn Claim Rejections - 35 USC § 112
The prior rejection of claim 13 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for insufficient antecedent basis is withdrawn in light of Applicant’s amendment to claim 13.
Withdrawn Claim Rejections - 35 USC § 103
The prior rejection of claims 1-2 and 8-9 under 35 U.S.C. 103 as being unpatentable over Nagy et al., (WO 2018/227286 A1. Prior art of record) in view of Braud et al., (US 2009/0074756A1. Prior art of record) and NCBI alignment (NCBI TNFSF10 alignment with SEQ ID NO: 4. P. 1-5. Prior art of record) is withdrawn in light of Applicant’s amendment to claim 1 to recite new limitation that the set of heterologous transgenes that reduce NK cell-mediated cytotoxicity consists of two or three recited genes, which is not taught by Nagy.
The prior rejection of claims 6-7 under 35 U.S.C. 103 as being unpatentable over Nagy et al., (WO 2018/227286 A1. Prior art of record) in view of Braud et al., (US 2009/0074756A1. Prior art of record), NCBI alignment (NCBI TNFSF10 alignment with SEQ ID NO: 4. P. 1-5. Prior art of record), and Elefanty et al (WO 2016/074016 A1. Prior art of record) is withdrawn in light of Applicant’s amendment to claim 1 to recite new limitation that the set of heterologous transgenes that reduce NK cell-mediated cytotoxicity consists of two or three recited genes, which is not taught by Nagy.
The prior rejection of claims 10-13 under 35 U.S.C. 103 as being unpatentable over Nagy et al., (WO 2018/227286 A1. Prior art of record) in view of Braud et al., (US 2009/0074756A1. Prior art of record), NCBI alignment (NCBI TNFSF10 alignment with SEQ ID NO: 4. P. 1-5. Prior art of record), and Schrepfer (WO 2023/019226 A1. Cited in IDS 06/30/2025) is withdrawn in light of Applicant’s amendment to claim 1 to recite new limitation that the set of heterologous transgenes that reduce NK cell-mediated cytotoxicity consists of two or three recited genes, which is not taught by Nagy.
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 and 8-9 are rejected under 35 U.S.C. 103 as being unpatentable over El Haddad et al., (J Immunol. 2011;187(5):2252-2260) in view of Braud et al., (US 2009/0074756A1. Prior art of record), Xie et al., (Transplantation. 2003;76(11):1556-1559), Nagy et al., (WO 2018/227286 A1. Prior art of record) and NCBI alignment (NCBI TNFSF10 alignment with SEQ ID NO: 4. P. 1-5. Prior art of record).
With respect to claim 1, El Haddad teaches a role of SERPINB9 in cytotoxic protection of human mesenchymal stem cells (MSCs) against granzyme B-mediated destruction by NK cells to enable allogeneic MSCs to evade host immune responses (see e.g., title and abstract). El Haddad teaches overexpression of transgenic PI-9 (i.e., SERPINB9) following retroviral transduction protected MSCs against NK cell killing (see e.g., abstract and p. 2256, last para – p. 2257, para 1, also see Fig 6). Thus, El Haddad teaches a genetically modified stem cell (i.e., human MSCs) comprising a heterologous transgene SERPINB9 that reduces NK cell-mediated cytotoxicity of the genetically modified stem cell, thus teaches claim 1 preamble and limitation (ii).
However, El Haddad only discloses a single transgene SERPINB9 that reduces NK cell-mediated cytotoxicity, but is silent on a set of transgenes that reduce NK cell-mediated cytotoxicity consisting of SERPINB9, CLEC2D and optionally TRAIL.
Braud teaches modulating cells to express LLT1 (also known as CLEC2D) for reducing organ and bone marrow transplantation rejection (e.g., abstract, [0045] and reference claim 54) and teaches expression of LLT1 in graft cells, such as porcine endothelial cells in case of porcine xenotransplantation, may directly protect sensitive graft cells from human NK cell-mediated xenogeneic cytotoxicity (e.g., [0063]). Braud teaches in working examples that various NK cell targets, such as 293T, C1R, K562, Hela, 721.221, and P815 cell lines, are transfected to express LLT1 ([0189], see Fig 11), which induces down-regulation of CD161 (see Example 3 in page 8) and inhibits NK cell-mediated cytotoxicity (see Examples 4-5 in p. 9 and Figs 7 and 12-14). Thus, Braud teaches genetically modifying various types of cells to express a heterologous transgene CLEC2D that reduces NK cell-mediated cytotoxicity in claim 1 (i).
Xie teaches TRAIL gene transfer in a corneal transplantation model in which the mean graft survival times are 22 days in Ad-TRAIL group compared to 17.7 days in control group and there are more apoptotic cells in the graft of the Ad-TRAIL group than in other groups (e.g., abstract and p. 1557, right col, para 1 and Fig 5). Xie teaches TRAIL plays an important role in corneal-allograft rejection and may be used to prolong the survival of allografts (e.g., abstract). Thus, Xie teaches genetically modifying cornea cells to express a heterologous transgene TRAIL that “induces apoptosis of inflammatory cells in the corneal graft” (p. 1559), related to claim 1 (iii).
Furthermore, Nagy teaches enhancing allograft tolerance by genetically modifying a human stem cell (p. 42, para 2) or an induced pluripotent stem (iPS) cells (p. 42, last para) with a combination of heterologous transgenes for providing a local immunosuppression in an allogeneic host (e.g., abstract, p. 7, para 2). Nagy teaches the heterologous transgenes comprises Serpin B9 to protect against leukocyte-mediated apoptosis (e.g., p. 7, para 3 and p. 28, last para-p. 29, 1st para, consistent with El Haddad’s teaching of SERPINB9 protecting MSCs against NK cell killing) and Tnfsf10 (i.e., TRAIL) to induce apoptosis in graft attacking leukocytes (p. 28, para 2, consistent with Xie’s teaching of TRAIL inducing apoptosis of inflammatory cells in graft). Thus, Nagy suggests a genetically modified stem cell comprising a set of heterologous transgenes that reduce NK cell-mediated cytotoxicity.
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 genetically modified stem cell comprising a SERPINB9 transgene to protect against NK cell killing to evade host immune responses disclosed by El Haddad, by combining a heterologous CLEC2D transgene as taught by Braud and a heterologous TRAIL transgene as suggested by Xie to obtain the stem cell comprising a set of heterologous transgenes that reduce NK cell-mediated cytotoxicity to evade allorejection as suggested by Nagy with a reasonable expectation of success. Since El Haddad teaches genetically modifying stem cells by a SERPINB9 transgene to protect against NK cell killing to evade host immune responses, since Braud teaches expression of LLT1 (CLEC2D) in graft cells directly protects sensitive graft cells from NK cell-mediated cytotoxicity and transfecting cells with LLT1 (CLEC2D) inhibits NK cell-mediated cytotoxicity (see above), since Xie teaches TRAIL gene transfer in a corneal graft prolongs the survival of allografts and induces apoptosis of inflammatory cells in the corneal graft (see above), and since Nagy suggests that genetically modifying a stem cell with a combination of heterologous transgenes such as SERPINB9 and TRAIL induces apoptosis in graft attacking leukocytes and enhances allograft tolerance (see above), one of ordinary skill in the art would have had a reason to genetically modify the stem cell with a set of heterologous transgenes consisting of SERPINB9 (taught by El Haddad), CLEC2D (taught by Braud) and TRAIL (taught by Xie) as suggested by Nagy in order to more efficiently reduce NK cell-mediated cytotoxicity to evade host immune responses.
Furthermore, regarding the amino acid sequences of the transgenes, Braud teaches the human LLT1 (CLEC2D) amino acid sequence in [0180] and reference SEQ ID NO: 2, which is 100% identical to instant SEQ ID NO: 2 in claim 1 (i) (see below).
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Nagy teaches a human SERPINB9 amino acid sequence (p. 38, reference SEQ ID NO: 8) that is 100% identical to the instant SEQ ID NO: 6 in claim 1 (ii) (see below).
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NCBI alignment demonstrates the human TNFSF10 (i.e., TRAIL) amino acid sequence (NCBI Reference Sequence NP_003801.1, see NCBI alignment, p. 3-5) is 100% identical to the instant SEQ ID NO: 4 (see NCBI alignment, p. 1-2) in claim 2.
Accordingly, one of ordinary skill in the art would have chosen the amino acid sequences of human CLEC2D taught by Braud, human SERPINB9 taught by Nagy, and human TRAIL taught by NCBI alignment to genetically modifying the human stem cell of El Haddad with a reasonable expectation of success. One of ordinary skill in the art would have had a reason to do so in order to develop MSC-based therapies for human diseases (El Haddad, abstract).
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With respect to claim 8 directed to the modified stem cell being at least 20% less susceptible to natural killer cell-mediated cytotoxicity as compared to a wild-type stem cell, El Haddad teaches overexpression of SERPINB9 reduces NK cell mediated killing by about 50% (see middle bars in Fig 6B attached). Braud teaches a 28.3% lysis decrease is observed for CLEC2D-expressing 293T cells by NK cells with respect to control cells ([0195], Example 4, and Fig 7).
Accordingly, one of ordinary skill in the art would have expected that the genetically modified stem cell comprising a set of heterologous transgenes that reduce NK cell-mediated cytotoxicity that consists of SERPINB9 and CLEC2D and optionally TRAIL, suggested by El Haddad in view of Braud, Xie, Nagy and NCBI alignment, would have had at least 20% less susceptible to NK cell-mediated cytotoxicity as compared to a wild-type stem cell.
With respect to claim 9 directed to the stem cell comprising a human pluripotent stem cell, Nagy teaches the genetically modified stem cell may be a human stem cell (p. 42, para 2) and an induced pluripotent stem (iPS) cell (p. 42, last para).
Accordingly, one of ordinary skill in the art would have substituted the human mesenchymal stem cell of El Haddad with a human pluripotent stem cell as suggested by Nagy with a reasonable expectation of success. Since El Haddad aims to use stem cells to provide therapeutic benefit for a variety of human disorders (e.g., abstract) and since Nagy suggests using a human stem cell (p. 42, para 2) or an induced pluripotent stem (iPS) cell (p. 42, last para) that are of use in cell-based therapies (p. 43, para 1), one of ordinary skill in the art would have had a reason to substitute a human pluripotent stem cell for the human mesenchymal stem cell in order to differentiate the pluripotent stem cell to a variety of cells to provide therapeutic benefit for a variety of human disorders.
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 05/26/2026 are acknowledged.
Applicant argues that by amendment to claim 1, the claims are now interpreted as while the claimed cells can comprise other components, with respect to the set of transgenes that primarily reduce NK cell-mediated cytotoxicity, the cells contain just two or optionally three transgenes, i.e., SERPINB9 and CLEC2D and optionally TRAIL (Remarks, p. 6). However, prior art Nagy requires eight transgenes and with combining CLEC2D taught by Braud, a total of no less than nine transgenes is required for successful immune evasion in the combined teachings. Thus, a person of ordinary skill would have reasonably been dissuaded from not including all the transgenes that were taught to be necessary for immune evasion. That is, the person of ordinary skill would have had motivation based on the teachings of Nagy and Braud to add transgenes to Nagy. Therefore, the person would not remove them (Remarks, p. 8).
Applicant’s arguments have been fully considered and they are persuasive. Therefore, the prior rejection over Nagy and Braud has been withdrawn. However, as necessitated by amendment, a new ground of rejection is made over El Haddad in view of Braud, Xie and Nagy as discussed above. Specifically, El Haddad teaches a genetically modified stem cell comprising a single transgene SERPINB9 that reduces NK cell-mediated cytotoxicity to the stem cell. Braud is cited to teach CLEC2D transgene reduces NK cell-mediated cytotoxicity in a variety of cell types and Xie is cited to teach TRAIL transgene induces apoptosis of inflammatory cells in the corneal graft and prolongs the survival of allografts. Nagy is cited to suggest a stem cell can be genetically modified with a set of heterologous transgenes such as SERPINB9 and TRAIL to induce apoptosis of graft-attacking leukocytes and to evade allorejection. Thus, one of ordinary skill in the art would have had a reason to combine the teachings of El Haddad, Braud, Xie and Nagy to obtain a genetically modified stem cell comprising a set of heterologous transgenes that reduce NK cell-mediated cytotoxicity that consists of SERPINB9 as taught by El Haddad, CLEC2D as taught by Braud and optionally TRAIL as taught by Xie, as suggested by Nagy in order to more efficiently reduce NK cell killing and to evade allorejection.
Furthermore, regarding Nagy requiring eight transgenes vs. only two or three in the instant claims, Applicant is reminded that although Nagy teaches a combination of eight transgenes including PD-L1, HLA-G, CD47, CD200, FASLG, Ccl21b, Mfge8, and SerpinB9 (see e.g., abstract), those eight transgenes do not function the same. In other words, the transgenes function on different types of immune cells to avoid allorejection (see e.g., Table 1 in p. 36 of Nagy). According to the teaching of Nagy, the targets of the transgenes are: PD-L1 (T cells and macrophages), HLA-G (NK cells), CD47 (macrophages and killer T cells), CD200 (macrophages), FASLG (CD8+ T cells), Ccl21b (antigen presenting cells), Mfge8 (macrophages), and SerpinB9 (granzyme/perforin inhibition taught by Nagy, likely cytotoxic T cells and NK cells) (see Table 1 in p. 36). Therefore, the eight transgenes of Nagy actually comprise a set of heterologous transgenes that reduce NK cell-mediated cytotoxicity that consists of only two genes, HLA-G and SerpinB9, with the only difference being HLA-G vs. CLEC2D in the instant claims.
Applicant further argues that the data disclosed in the present specification show the utility of the claimed genetically modified stem cells. Since a prima facia case of obviousness does not exist against the present claims for at least the reasons discussed above, the data are not needed to overcome a rejection, thus there is no requirement that the claims must be commensurate in scope with these data (Remarks, p. 9).
Applicant’s arguments have been fully considered but they are not persuasive because, as discussed above, a new ground of rejection has been made over El Haddad in view of Braud, Xie, Nagy and NCBI alignment, thus a prima facia case of obviousness does exist against the present claims.
Claims 6-7 are rejected under 35 U.S.C. 103 as being unpatentable over El Haddad et al., (J Immunol. 2011;187(5):2252-2260) in view of Braud et al., (US 2009/0074756A1. Prior art of record), Xie et al., (Transplantation. 2003;76(11):1556-1559), Nagy et al., (WO 2018/227286 A1. Prior art of record) and NCBI alignment (NCBI TNFSF10 alignment with SEQ ID NO: 4. P. 1-5. Prior art of record), as applied to claim 1 above, and further in view of Elefanty et al (WO 2016/074016 A1. Prior art of record).
Claims 6-7 are directed to expression of the heterologous CLEC2D and SERPINB9 being driven by a promoter of an endogenous GAPDH gene.
However, El Haddad, Braud, Xie, Nagy and NCBI are silent on CLEC2D and SERPINB9 being driven by a promoter of an endogenous GAPDH gene.
Elefanty teaches targeted integration of exogenous nucleic acids into the locus of a constitutively expressed gene such as GAPDH gene (abstract and Fig 1). Elefanty teaches replacing the genomic stop codon of the constitutively expressed gene with an in-frame translation interruption-reinitiation signal that operably links the constitutively expressed gene with the exogenous nucleic acid (i.e., the exogenous nucleic acid is driven by the promoter of the endogenous constitutively-expressed gene GAPDH gene, see p. 7, lines 24-26 and Fig 1), related to claims 6 and 7. Elefanty teaches experiments with GT-GFP (exogenous GFP being targeted integrated into GAPDH locus and being driven by endogenous GAPDH promoter, see Fig 1) hESCs indicated that this line maintained robust GFP expression when cells were differentiated into hematopoietic mesoderm and endothelial-like cells. Cells comprising this vector also generated neural, cardiomyocyte and pancreatic cell types that retained high levels of reporter expression (p. 39, last para).
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 genetically modified stem cell comprising a set of transgenes that reduce NK cell-mediated cytotoxicity that consists of CLEC2D and SERPINB9 suggested by El Haddad in view of Braud, Xie, Nagy and NCBI, by substituting the retroviral transduction with targeted integration into the locus of GAPDH gene such that the heterologous transgenes are driven by the promoter of the endogenous GAPDH gene as suggested by Elefanty with a reasonable expectation of success. Since Elefanty teaches hESCs comprising exogenous GFP driven by endogenous GAPDH promoter maintain robust GFP expression when cells are differentiated into hematopoietic mesoderm, endothelial-like cells, neural, cardiomyocyte and pancreatic cell types (p. 39, last para), one of ordinary skill in the art would have had a reason to targeted integrate the heterologous CLEC2D and SERPINB9 nucleic acids into the endogenous GAPDH locus as suggested by Elefanty in order to achieve constitutive robust expression of the CLEC2D and SERPINB9 products during multiple generations and differentiation.
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 05/26/2026 are acknowledged and have been discussed above.
Claims 10-13 are rejected under 35 U.S.C. 103 as being unpatentable over El Haddad et al., (J Immunol. 2011;187(5):2252-2260) in view of Braud et al., (US 2009/0074756A1. Prior art of record), Xie et al., (Transplantation. 2003;76(11):1556-1559), Nagy et al., (WO 2018/227286 A1. Prior art of record) and NCBI alignment (NCBI TNFSF10 alignment with SEQ ID NO: 4. P. 1-5. Prior art of record), as applied to claim 1 above, and further in view of Schrepfer (WO 2023/019226 A1. Cited in IDS 06/30/2025).
However, El Haddad, Braud, Xie, Nagy and NCBI are silent on the genetically modified stem cell further comprising a genetic modification that results in reduced T cell-mediated killing in claims 10 and 13, nor teach the genetic modification comprising a deletion of a B2M gene and a deletion of a CIITA gene in claims 11 and 12.
Schrepfer teaches genetically modified cells for allogeneic cell therapy that avoid detection by the recipient's immune system (abstract and [0004]). Schrepfer teaches the engineered cell comprising modifications that increase expression of one or more tolerogenic factors such as SERPINB9 (see e.g., [0005] and [0041]) and reduce expression of one or more MHC class I molecules such as B2M knocked out ([0011]-[0017]) and one or more MHC class II molecules such as CIITA knocked out ([0026]-[0032]), related to claims 11 and 12. Schrepfer teaches the engineered cells (hypoimmunogenic cells) are protected from T cell-mediated adaptive immune rejection (e.g., [0354] and [0327]), thus teaches the genetic modifications result in reduced T cell-mediated killing as compared to a wild-type stem cell, related to claims 10 and 13.
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 genetically modified stem cell comprising a set of heterologous transgenes that reduce NK cell-mediated cytotoxicity suggested by El Haddad in view of Braud, Xie, Nagy and NCBI, by combining genetic modifications comprising deletion of B2M gene and CIITA gene resulting in reduced T cell-mediated killing as suggested by Schrepfer with a reasonable expectation of success. Since Nagy suggests a combination of heterologous transgenes functioning to reduce NK cell-, T cell- and macrophage-mediated cytotoxicity to avoid allorejections (see Table 1 in p. 36), and since Schrepfer teaches genetically modified cells comprising deletion of B2M gene and CIITA gene are protected from T cell-mediated adaptive immune rejection (e.g., [0354] and [0327]), one of ordinary skill in the art would have had a reason to combine genetic modifications comprising deletion of B2M gene and CIITA gene as suggested by Schrepfer in order to further protect the stem cell from T cell-mediated killing to enhance allograft tolerance.
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 05/26/2026 are acknowledged and have been discussed above.
Withdrawn Provisional Double Patenting Rejections
The prior rejection of claims 1-2 and 6-13 on the ground of nonstatutory double patenting as being unpatentable over copending Application No. 19/073,872 is withdrawn in light of the terminal disclaimer filed on 02/25/2026 disclaiming the terminal portion of any patent granted on this application which would extend beyond the expiration date of any patent granted on pending reference application 19/073,872.
Conclusion
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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/JIANJIAN ZHU/Examiner, Art Unit 1631
