DETAILED ACTION
Applicant’s amendment and Arguments/Remarks received on 23 March 2026 have been entered. Claims 1-14, 18-19, 22-24, 28, and 31 were previously pending in the application. Claims 18-19, 23, and 31 have been cancelled, and new claims 33-35 have been added by Applicant. Claims 1-14, 22, 24, 28, and 33-35 are currently pending in the application. Claims 1, 13, 22, 24, and 28 are independent claims.
The election of Group I, drawn to a method of generating a stem cell (SC), a stem cell produced by the method, a beta cell produced by the method, a second stem cell, and a cell line derived from the second stem cell, remains in effect in the instant application. The following election of species remains in effect in the instant application:
Genes with reduced expression: a. HLA-1, i. Reduced by: 2. Abrogating expression of β2M;
Exogenous construct introduction: b. AAV construct.
Claims 7 and 9 remain withdrawn from consideration as being directed to a nonelected species, there being no allowable generic or linking claim.
Claims 1-6, 8, 10-14, 22, 24, 28, and 33-35 are currently pending and under examination in the instant application. An action on the merits follows.
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA . The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Priority
The present application is a 35 U.S.C. 371 national stage filing of International Application No. PCT/US2020/055123, filed 09 October 2020, which claims priority to U.S. Provisional Application No. 62/913,568, filed 10 October 2019.
Thus, the earliest possible priority for the instant application is 10 October 2019.
Specification
The specification is objected to as failing to provide proper antecedent basis for the claimed subject matter. See 37 CFR 1.75(d)(1) and MPEP § 608.01(o). MPEP § 608.01(o) states: “While an applicant is not limited to the nomenclature used in the application as filed, he or she should make appropriate amendment of the specification whenever this nomenclature is departed from by amendment of the claims so as to have clear support or antecedent basis in the specification for the new terms appearing in the claims. This is necessary in order to insure certainty in construing the claims in the light of the specification... [if] the claims presented late in prosecution do not comply with 37 CFR 1.75(d)(1), applicant will be required to make appropriate amendment to the description to provide clear support or antecedent basis for the terms appearing in the claims provided no new matter is introduced.”
Correction of the following is required: Applicant amended claims 1, 5, 6, 11, 24 to write out the gene names for CR1 (claims 1 and 24), PD-L1 (claim 5), TAP1 (claim 6), and PPP1R12C (claim 11) as well as to correct the gene symbol for PPP1R12C. However, the specification as filed does not recite the full gene names nor the corrected PPP1R12C symbol recited within the amended claims. Accordingly, Applicant must make appropriate amendment to the specification to provide clear support or antecedent basis for these terms.
Claim Objections
The objection to amended claims 1-2, 4-6, 11, and 24 for multiple informalities is withdrawn in view of the amendment to the claims.
Claim Rejections - 35 USC § 112(b)
The rejection of amended, previously presented, and original claims 1-6, 8, 10-14, 22, 24, and 28 under 35 U.S.C. 112(b) as failing to particularly point out and distinctly claim the subject matter which the inventor(s) regards as the invention for multiple issues of indefiniteness is withdrawn over amended and previously presented claims 24 and 28 and maintained over amended, previously presented, and original claims 1-6, 8, 10-14, and 22 in view of Applicant’s amendments to the claims. Claims 2-6, 8, 10-11, 13-14, and 22 are included in this rejection due to their dependence on and/or encompassing of amended claims 1 and/or 12. Applicant's amendments to the claims and arguments have been fully considered but have not been found persuasive in overcoming the rejection for reasons of record as discussed in detail below.
Applicant amended independent claim 1 to remove “stem” form line 1, to recite “a stem cell (SC)” in line 2, and “the SC” in line 4. Applicant additionally amended claim 12 to recite “the modified SC” in lines 1-2. Although the amendment partially addresses the issue of antecedent basis for “the stem cell” previously recited in claim 12, it also introduces additional issues of antecedent basis. Claim 1 still recites “a wild-type SC” in line 2. As such, recitation of “the SC” in claim 1 line 4 lacks antecedent basis in that claim 1 has two prior recitations of SCs. Additionally, recitation of “the modified SC” in claim 12 lines 1-2 lacks antecedent basis because neither claim 1 nor claim 12 have any prior recitation of any modified SC. Additionally, it is unclear whether the modified stem cell comprises only the reduced expression of HLA-I or whether the modified stem cell recited in amended claim 12 is meant to also comprise the exogenous constructs recited in claim 1 lines 4-6. As such, the metes and bounds of the claim still cannot be determined.
Applicant argues that the amendments to claims 1 and 12 are such that claim 12 now clearly and unambiguously references the modified SC antecedent in claim 1. However, although claim 1 reciting modifying a stem cell, it does not recite a modified stem cell per se. Additionally, it is unclear whether the modified stem cell comprises only the reduced expression of HLA-I or whether the modified stem cell recited in amended claim 12 is meant to also comprise the exogenous constructs recited in claim 1 lines 4-6. Therefore, Applicant’s arguments do not overcome a finding of indefiniteness under 35 U.S.C. 112(b) for claims 1-6, 8, 10-14, and 22, and the rejection is maintained.
**The following new rejection is necessitated by amendments to the claims.**
Amended claim 11 is newly rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 11 now recites, “targets a site of AAV integration” in line 2, which is indefinite because it is unclear whether the modified AAVS is targeting a site which already has an AAV integration or whether the modified AAVS is targeting a site for AAV integration. As such, the metes and bounds of the claim cannot be determined.
Claim Interpretation
Amended claims 1 and 24 have been amended to recite the gene name for CR1, “complement C3b/C4b receptor 1 (Knops blood group) (CR1)”, wherein “complement C3b/C4b receptor 1 (Knops blood group)” is the gene name and “(CR1)” is the abbreviated gene symbol. As such, the use of a parenthetical around “Knops blood group” is considered definite in that it is a part of the gene name itself.
Claim Rejections - 35 USC § 102
The rejection of amended, previously presented, and original 1-3, 5-6, 8, 12-13, 22, 24, and 28 under 35 U.S.C. 102(a)(2) as being anticipated by Schrepfer [US20230025289A1, published 26 January 2023, filed 24 August 2020, with priority to U.S. Provisional Application No. 62/891,180, filed 23 August 2019], is withdrawn in view of Applicant’s claims which now recite “introducing exogenous constructs into the SC to express immune evasion genes comprising complement C3b/C4b receptor 1 (Knops blood group) (CR1) and one or more of CD46, CD55, CD59, and HLA-E single chain trimer”, wherein the U.S. Provisional Application No. 62/891,180 does not disclose expression of CR1, CD46, CD55, nor CD59 in the modified stem cell.
Claim Rejections - 35 USC § 102/103
Amended claims 1, 4, 6, 12-13, 22, 24, 28, and 34 are rejected under 35 U.S.C. 102(a)(1) as anticipated by or, in the alternative, under 35 U.S.C. 103 as obvious over Ayares [US20110038841A1, published 17 February 2011].
Regarding claims 1, 4, 6, 13, 24, and 34 Ayares teaches a method of generating a stem cell comprising a) modifying a stem cell (SC) to reduce expression relative to a wild-type SC [0202, 0205-0207] of HLA-I by abrogating expression of β2M [0174]; and b) introducing exogenous constructs into the SC to express immune evasion genes comprising two or more of CR1, CD46, CD55, CD59, and HLA-E [0039, 0104, 0106, 0121, 0136-0137, 0148-0151, 0158, 0184, 0188-0189, 0249].
Regarding claims 12 and 22, Ayares teaches genetically modifying embryonic stem cells as a preferred cell type [0205-0207], genetically modified animals produced via the use of embryonic stem cells [0202], and the transplantation of beta cells from the genetically modified animal [0101, 0136, 0276]. Therefore, Ayares teaches differentiating the modified stem cell to a beta cell.
Regarding claim 28, Ayares teaches cell lines obtained from the genetically modified cell [0243, 0337].
Accordingly, by teaching all of the limitations of claims 1, 4, 6, 12-13, 22, 24, 28, and 34 as written, Ayares anticipates the instant invention as claimed.
Alternatively, it would have been obvious to make the selection of the combination of abrogating expression of β2M to induce MHC class I deficiency and introduction of exogenous constructs to express CR1 and one or more or all of CD46, CD55, and CD59 from the teachings of Ayares to disrupt β2M to induce MHC class I deficiency in a stem cell [0174] and to express two or more different complement regulators, including selecting from the limited number of specifically recited complement inhibitors CR1, CD55, CD46, and CD59 [0158]. Further, Ayares teaches that CR1 appears to be functionally the most important regulator of complement activation in rodents [01148]; that host cells are protected from their own complement by membrane-bound complement regulatory proteins like DAF/CD55, MCP/CD46, and CD59 [0150]; and that inhibition of complement using sCR1 has been shown to prevent or delay rejection [0150]. Therefore, an ordinarily skilled artisan at the time of filing the instant application would have been motivated to express CR1 and one or more or all of CD55, CD46, and CD59 in a stem cell modified to have reduced expression of HLA-I via disrupted expression of β2M to protect the cells from complement-mediated rejection.
Therefore, given the teachings of Ayares to modify stem cells by disrupting expression of β2M; to modify cells to express CR1; to modify cells to express two or more of CR1, CD46, CD55, CD59, and HLA-E; and the motivation taught by Ayers to express CR1 and one or more of CD55, CD46, and CD59 in a stem cell with reduced expression of HLA-I via disrupted expression of β2M to protect the cells from complement-mediated rejection; it would have been prima facie obvious to an ordinarily skilled artisan at the time of filing the instant application to modify the method of Ayares to combine reduced expression of HLA-I via disrupted expression of β2M in a stem cell and expression of CR1 and one or more or all of CD55, CD46, and CD59 in the modified stem cell with a reasonable expectation of success.
Claim Rejections - 35 USC § 103
The rejection of amended and previously presented claims 1, 4, 10, 11, and 14 under 35 U.S.C. 103 as being unpatentable over Schrepfer [US20230025289A1, published 26 January 2023, filed 24 August 2020, with priority to U.S. Provisional Application No. 62/891,180, filed 23 August 2019]; in view of Oceguera-Yanez et al. [2016, Methods, 101, 43-55, published online 18 December 2015]; and Gornalusse et al. [2017, Nature Biotechnology, 35(8), 765-775], is withdrawn in view of Applicant’s claims which now recite “introducing exogenous constructs into the SC to express immune evasion genes comprising complement C3b/C4b receptor 1 (Knops blood group) (CR1) and one or more of CD46, CD55, CD59, and HLA-E single chain trimer”, wherein the U.S. Provisional Application No. 62/891,180 does not disclose expression of CR1, CD46, CD55, nor CD59 in the modified stem cell.
Amended, previously presented, original, and new claims 1-6, 8, 10-14, 22, 24, 28, and 33-35 are newly rejected under 35 U.S.C. 103 as being unpatentable over Ayares [US20110038841A1, published 17 February 2011]; in view of Schrepfer [US20230025289A1, published 26 January 2023, filed 24 August 2020, with priority to U.S. Provisional Application No. 62/891,180, filed 23 August 2019]; Gornalusse et al. [2017, Nature Biotechnology, 35(8), 765-775]; and Oceguera-Yanez et al. [2016, Methods, 101, 43-55, published online 18 December 2015].
Regarding claims 1, 4, 6, 13, 24, and 34 Ayares teaches a method of generating a stem cell comprising a) modifying a stem cell (SC) to reduce expression relative to a wild-type SC [0202, 0205-0207] of HLA-I by abrogating expression of β2M [0174]; and b) introducing exogenous constructs into the SC to express immune evasion genes comprising two or more of CR1, CD46, CD55, CD59, and HLA-E [0039, 0104, 0106, 0121, 0136-0137, 0148-0151, 0158, 0184, 0188-0189, 0249]. Further, Ayares teaches that CR1 appears to be functionally the most important regulator of complement activation in rodents [01148]; that host cells are protected from their own complement by membrane-bound complement regulatory proteins like DAF/CD55, MCP/CD46, and CD59 [0150]; and that inhibition of complement using sCR1 has been shown to prevent or delay rejection [0150]. Therefore, an ordinarily skilled artisan at the time of filing the instant application would have been motivated to express CR1 and one or more or all of CD55, CD46, and CD59 in a stem cell modified to have reduced expression of HLA-I via disrupted expression of β2M to protect the cells from complement-mediated rejection.
Regarding claim 2, Ayares does not teach wherein the immune evasion genes further comprise CD24.
However, Schrepfer teaches a method of generating a stem cell (SC) comprising a) modifying a SC to reduce expression relative to a wild-type SC of HLA-I by abrogating expression of B2M/β2M [abstract, 0138, 0171-0175, claim 5]; and b) introducing exogenous constructs to express immune evasion genes CD24 [0138, 0160, 0198]. Schrepfer further teaches that the hypoimmunogenic cells of the invention have a reduced susceptibility to macrophage phagocytosis and NK cell killing, wherein the cells escape the immune macrophage and innate pathways due to the expression of one or more CD24 transgenes [0304]. Therefore, an ordinarily skilled artisan at the time of filing the instant application would have been motivated to express a CD24 transgene to promote hypoimmunogenicity in a cell for xeno/allogenic transplantation.
Regarding claims 3, 14, 33, and 35 as discussed above, Ayares teaches the motivation to express CR1 and up to all of CD55, CD46, and CD59 in a stem cell modified to have reduced expression of HLA-I via disrupted expression of β2M to protect the cells from complement-mediated rejection. Ayares also teaches wherein the immune evasion genes comprise HLA-E [0039, 0106, 0184], wherein HLA-E is assembled in the ER and transported to the cell surface as a stale trimeric complex consisting of the HLA-E heavy chain, β2-macroglobulin (β2m), and a peptide derived from the leader sequence of some MHC class I molecules [0189]. Additionally, Schrepfer teaches wherein the immune evasion genes further comprise HLA-E heavy chain [0006, 0138], but neither Ayares nor Schrepfer teach that the HLA-E/HLA-E heavy chain is comprised within an HLA-E single chain trimer.
However, Gornalusse teaches that disruption of the Beta-2 microglobulin (B2M) gene eliminates surface expression of all HLA class I molecules, but leaves the cells vulnerable to lysis by natural killer (NK) cells (e.g., a “missing self” response) [abstract]. Gornalusse further teaches that the “missing self” response can be prevented by forced expression of minimally polymorphic HLA-E molecules, including HLA-E single-chain trimers, in pluripotent stem cells (PSCs) such that the HLA-engineered PSCs and their differentiated derivatives are not recognized as allogeneic by CD8+ T cells, do not bind anti-HLA antibodies, and are resistant to NK-mediated lysis [abstract]. Gornalusse also teaches that single-chain HLA-E molecules prevent the NK-mediated lysis of B2M-/- cells without stimulating allogeneic T cells, addressing a major problem in the creation of universal donor cells for regenerative medicine application [column 2 ¶ 2]. Gornalusse additionally teaches that HLA-E forms a heterodimer with a B2M subunit and so it is not expressed on the surface of B2M-/- cells, but that B2M-/- cells could be engineered to express HLA-E as a single-chain protein fused to B2M, and thereby create cells that express HLA-E as their only surface HLA class I molecule [column 1 ¶ 2- column 2 ¶ 2, column 4 ¶ 1-2].
Therefore, given the teachings of Gornalusse that HLA-E expression overcomes the missing-self response associated with disruption of B2M expression, and the teaching that the HLA-E single-chain trimer overcomes the lack of surface expression of HLA-E in B2M-/- cells, an ordinarily skilled artisan at the time of filing the instant application would have been motivated to express an HLA-E single-chain trimer in a stem cell modified to reduce expression of HLA-I by abrogating expression of B2M to overcome the missing-self response and protect the cells from NK-mediated lysis in allogenic transplantation applications.
Regarding claim 5, Ayares further teaches to express the immunomodulator PD-L1 [0039, 106, 0184, 0186]; that binding of PD-L1 to PD-1 leads to inhibitory signals in T-cells; PD-1 signaling is required for the suppressive activity of regulatory T cells (Tregs) and the generation of adaptive Treg to involve immunoregulation; and that the transgenic expression of PD-L1 should reduce early T-cell responses initiated via the direct route of sensitization, and also control T cells sensitized to the xenograft through the indirect route that is required to achieve long-lasting tolerance [0186]. Therefore, an ordinarily skilled artisan at the time of filing the instant application would have been motivated to express the immunomodulator PD-L1 in a cell for xeno/allotransplantation to achieve long-lasting tolerance.
Regarding claim 8, Ayares does not teach wherein modifying comprises genome editing using CRISPR/Cas9 targeted mutation.
Schrepfer teaches wherein the modifying comprises genome editing using CRISPR/Cas9 targeted mutation [0006-0007, 0094, 0116, 0166, 0171, 0174, 0221]. Schrepfer also teaches that CRISPR/Cas is a method useful for inactivation or ablation of MHC class I expression in cells such as pluripotent stem cells [0094] and provides examples of methods utilizing CRISPR/Cas9 for targeting B2M to reduce or ablate expression in target cells [0116, 0171]. Therefore, an ordinarily skilled artisan at the time of filing the instant application would have been motivated to use a CRISPR/Cas9 system to introduce a targeted mutation to modify a stem cell to reduce expression relative to a wild-type SC of HLA-I.
Regarding claims 10-11, Ayares teaches introducing exogenous constructs using an AAV construct as one of several options [0213, 0218-0219].
Gornalusse teaches specifically using AAV-mediated gene editing to knock in HLA-E genes at the B2M locus [abstract, column 2 ¶ 2-column 4 ¶ 1].
Additionally, Schrepfer teaches introducing exogenous constructs via a viral vector, such as a lentiviral vector [0209, 0215] and to introduce the exogenous constructs into a safe harbor locus which allows safe expression of a transgene or an exogenous gene, such as a PPP1R12C (AKA AAVS1) gene [0101, 0186, 0199].
However, Ayares, Gornalusse , and Schrepfer do not teach wherein the AAV construct is a modified AAVS construct that specifically targets a site of endogenous AAV integration located in an intronic region of PPP1R12C.
Oceguera-Yanez teaches that the AAVS1 locus lies within the first intron of the constitutively expressed PPP1R12C gene [column 3 ¶ 3]. Oceguera-Yanez also teaches a method outlining the specific delivery of transgenic elements to the AAVS1 safe-harbor locus in human induced pluripotent stem cells (iPSCs), stimulated by a CRISPR/Cas9 nuclease system [column 3 ¶ 3]. Oceguera-Yanez also teaches using an AAV construct (e.g., donor vector) which is a modified AAVS construct that targets the endogenous AAVS1 locus/ the site of endogenous AAV integration located in an intronic region of PPP1R12C within iPSCs [column 4 ¶ 3-4, Table 1, Figure 2]. Oceguera-Yanez further teaches that using CRISPR/Cas9 nuclease technologies to introduce transgenes into pre-defined loci overcomes random position effects associated with viral or transposon vectors, and that AAVS1 is an exemplary locus within the PPP1R12C gene that permits robust expression of CAG promoter-driven transgenes [abstract]. Oceguera-Yanez also teaches that gene targeting controls transgene copy number such that reporter expression patterns are reproducible and scalable by ~2-fold, and that gene expression is maintained during long-term human iPSC culture and in vitro differentiation along multiple lineages [abstract].
Therefore, given the teachings of Oceguera-Yanez of a modified AAVS construct that targets the AAVS1 locus, and that targeting the AAVS1 locus overcomes random position effects, permits robust expression of transgenes that is maintained during long-term stem cell culture and along multiple differentiation lineages, an ordinarily skilled artisan at the time of filing the instant application would have been motivated to introduce a transgene into a stem cell using a modified AAVS construct that targets the AAVS1 locus within intron 1 of the endogenous PPP1R12C gene of the stem cell to achieve robust transgene expression during long-term culture and/or during differentiation of the stem cell to various lineages.
Regarding claims 12 and 22, Ayares teaches genetically modifying embryonic stem cells as a preferred cell type [0205-0207], genetically modified animals produced via the use of embryonic stem cells [0202], and the transplantation of beta cells from the genetically modified animal [0101, 0136, 0276]. Therefore, Ayares teaches differentiating the modified stem cell to a beta cell.
Additionally, Schrepfer teaches that the method further comprises differentiating the SC to a β cell [0372-0381], such that the hypoimmunogenic pluripotent cells are differentiated into beta-like cells or islet organoids for transplantation to address type I diabetes mellitus (T1DM), and wherein cell systems are a promising way to address T1DM [0378-0379]. Schrepfer further teaches that once the beta cells are generated by differentiation of a modified stem cell, they can be transplanted [0381]. Therefore, an ordinarily skilled artisan at the time of filing the instant application would have been motivated to specifically induce the hypoimmunogenic stem cells to differentiate into beta cells to use for transplantation cell therapy to treat T1DM.
Regarding claim 28, Ayares teaches cell lines obtained from the genetically modified cell [0243, 0337].
Therefore, given the motivation taught by Ayares to express CR1 and one or more or all of CD55, CD46, and CD59 in a stem cell modified to have reduced expression of HLA-I via disrupted expression of β2M to protect the cells from complement-mediated rejection; the motivation taught by Schrepfer to express a CD24 transgene to promote hypoimmunogenicity in a cell for xeno/allogenic transplantation; the motivation taught by Gornalusse to express an HLA-E single-chain trimer in a stem cell modified to reduce expression of HLA-I by abrogating expression of B2M to overcome the missing-self response and protect the cells from NK-mediated lysis in allogenic transplantation applications; the motivation taught by Ayares to express the immunomodulator PD-L1 in a cell for xeno/allotransplantation to achieve long-lasting tolerance; the motivation taught by Schrepfer to use a CRISPR/Cas9 system to introduce a targeted mutation to modify a stem cell to reduce expression relative to a wild-type SC of HLA-I; the motivation taught by Oceguera-Yanez to introduce a transgene into a stem cell using a modified AAVS construct that targets the AAVS1 locus within intron 1 of the endogenous PPP1R12C gene of the stem cell to achieve robust transgene expression during long-term culture and/or during differentiation of the stem cell to various lineages; and the motivation taught by Schrepfer to specifically induce the hypoimmunogenic stem cells to differentiate into beta cells to use for transplantation cell therapy to treat T1DM; it would have been prima facie obvious to an ordinarily skilled artisan at the time of filing the instant application to modify the method of Ayares to combine reduced expression of HLA-I via disrupted expression of β2M in a stem cell with exogenous expression of CR1, CD24, CD55, CD46, CD59, HLA-E single chain trimer, and PD-L1 within the modified stem cell, to use CRISPR/Cas9 to disrupt expression of β2M, to introduce the transgene(s) into the stem cell using a modified AAVS construct that targets the AAVS1 locus, and to induce the stem cell to differentiate into a beta cell with a reasonable expectation of success.
Insofar as applicant’s arguments apply to this new grounds of rejection, applicant argues that the priority document for Schrepfer, U.S. Provisional Application No. 62/891,180, which is the only document in the Schrepfer filing which predates the effective filing date of the instant application, fails to disclose exogenous expression of CR1, CD46, CD55, or CD59, and as such the relevant disclosure relating to CR1, CD46, CD55, and CD59 in Schrepfer is not prior art against the pending claims and the instant claims are therefore nonobvious over the cited references. However, this is not agreed.
As discussed above, Schrepfer was not relied on for teaching the exogenous expression of CR1, CD46, CD55, or CD59, which is taught by Ayares. Schrepfer was cited for teachings and motivations regarding limitations recited in dependent claims, including the exogenous expression of CD24, the use of CRISPR/Cas9 to disrupt B2M expression, and specifically inducing the hypoimmunogenic stem cells to differentiate into beta cells to use in transplantation cell therapy to treat T1DM. All teachings, suggestions, and motivations of Schrepfer relied on in the instant rejection were disclosed in the U.S. Provisional Application No. 62/891,180 filed 23 August 2019, and as such constitute prior art against the pending claims.
Therefore, Applicant’s arguments do not overcome a finding of obviousness over Ayares, Schrepfer, Gornalusse, and Oceguera-Yanez.
Conclusion
No claim is allowed.
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DR. KATIE L. PENNINGTON
Examiner
Art Unit 1634
/KATIE L PENNINGTON/Examiner, Art Unit 1634
Dr. A.M.S. Wehbé
/ANNE MARIE S WEHBE/Primary Examiner, Art Unit 1634
Prosecution Insights