DETAILED ACTION
Notice of Pre-AIA or AIA Status
The text of those sections of Title 35, U.S. Code not included in this action can
be found in a prior Office action.
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
This action is in response to the papers filed on 06/18/2026. Claims 1-81 are currently pending as per claims filed on 06/18/2026. Claims 1-23, 28, 39, 56, 71, and 77-79 have been amended by Applicants’ amendment filed on 06/18/2026. No claims were newly added or canceled.
Applicant’s election without traverse of Group 1, claims 1-22, 29, 77-79 in the reply filed on 01/26/2026 was previously acknowledged.
Applicant’s further election without traverse of the following species was previously acknowledged:
Species 1:
• an amino acid sequence of the disrupted B2M gene as set forth in SEQ ID NO: 12 (Claim 3);
• the target nucleotide sequence as set forth in SEQ NO: 17 (within SEQ ID NO:1) to which a gRNA binds (Claim 18);
• and the gRNA sequence as set forth in SEQ ID NO: 18 (Claims 19-22)
Species 2:
• MAD7 (Claims 13 and 16)
Claims 14-15 were previously withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected species, there being no allowable generic or linking claim.
Claim 23-28, 30-76 and 80-81 were previously withdrawn from further consideration by Applicants pursuant to 37 CFR 1.142(b), as being drawn to a nonelected subject invention, there being no allowable generic or linking claim.
Claims 28-29 are withdrawn from consideration by the examiner as being dependent on withdrawn claim 23.
Therefore, claims 1-13, 16-22, and 77-79 are under examination to which the following grounds of rejection are applicable. Claims 1 is an independent claim.
Claim Objections
The amendment to the claims filed on 6/18/2026 does not comply with the requirements of 37 CFR 1.121(c) because claims 28 and 29 are not identified as withdrawn claims relative to the immediate prior version of claims 28-29 , filed on 01/26/26. Amendments to the claims filed on or after 01/26/26must comply with 37 CFR 1.121(c) which states:
(c) Claims. Amendments to a claim must be made by rewriting the entire claim with all changes (e.g., additions and deletions) as indicated in this subsection, except when the claim is being canceled. Each amendment document that includes a change to an existing claim, cancellation of an existing claim or addition of a new claim, must include a complete listing of all claims ever presented, including the text of all pending and withdrawn claims, in the application. The claim listing, including the text of the claims, in the amendment document will serve to replace all prior versions of the claims, in the application. In the claim listing, the status of every claim must be indicated after its claim number by using one of the following identifiers in a parenthetical expression: (Original), (Currently amended), (Canceled), (Withdrawn), (Previously presented), (New), and (Not entered). 2) Only claims having the status of “currently amended,” or “withdrawn” if also being amended, shall include markings. If a withdrawn claim is currently amended, its status in the claim listing may be identified as “withdrawn-currently amended.” Specifically, claim 24 should be amended to recite “Currently amended”
Any further claim amendments must comply with 37 CFR 1.121(c) or they may not be entered.
Priority
The instant application claims domestic benefit to US provisional patent application number 63/357,922 filed on 07/21/2022. Thus, the earliest possible priority for the instant application is 07/21/2022.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 06/18/2026 was filed after the mailing date of the office action on 03/18/2026. The submission is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Response to Arguments
Withdrawn objections/rejection in response to Applicants’ arguments or
Amendment
Claim Objections
In view of Applicants’ amendment of claim 56, the claim objections have
been withdrawn.
Claim Rejections - 35 USC § 112 (b)
In view of Applicants’ amendment of claim 5, 6, 9, and 77, the claim rejections have been withdrawn.
Claim Rejections - 35 USC § 101
In view of Applicants’ amendment of claims 1-13, 16-22, and 77-79, the claim rejection has been withdrawn.
Maintained and/or modified rejections in response to Applicants’ arguments or
Amendment
Claim Rejections - 35 USC § 103
Claims 1-13, 16-22, and 77-79 remain rejected under 35 U.S.C. 103 as being unpatentable over Izhar et al (US Patent Application No: US 20240042025 A1; as cited in office action mailed 03/18/2026), and further in view of Watanabe et al (Stem Cells and Translational Medicine, 2017, pages 34-44; as cited in office action mailed 03/18/2026), Das et al (US Patent Application No: US 20230248825 A1; as cited in office action mailed 03/18/2026), Pulé et al (US Patent Application No: US 20200255494 A1; as cited in office action mailed 03/18/2026), Lee et al (US Patent Application No: US 20220175839 A1; as cited in office action mailed 03/18/2026), Fry et al (WO Publication No: WO/2023/183313 – too large to attach to file wrapper; as cited in office action mailed 03/18/2026), Ando et al (US Patent Application No: US 20220339194 A1; as cited in office action mailed 03/18/2026), Barghetti (US Patent Application No: US 20230235362 A1; as cited in office action mailed 03/18/2026), and Donohoue (US Patent Application No: US 20250027078 A1; as cited in office action mailed 03/18/2026) as evidenced by Wikipedia Beta-2 Microglobulinpp. (pp1-6 downloaded March 13, 2026; as cited in office action mailed 03/18/2026). This rejection has been modified as necessitated by applicant's amendment filed on 06/18/2026.
Regarding claim 1, Izhar teaches knocking out (i.e. disrupting) the B2M gene in cells, which can be isolated from a subject, to minimize the immunogenicity of CAR-T cells such that an allogeneic adoptive transfer strategy can be implemented in which universal CAR cells derived from cells from healthy donors can be applied to treat multiple patients (para 005 and 0149). Izhar teaches “the cell is a lymphocyte, a T cell, a T regulatory cell, a B cell, a natural killer (NK) cell, a macrophage, a stem cell, or a fibroblast, blood cell, hepatocyte, keratinocyte, or any other cell type capable of being reprogrammed to an induced pluripotent stem cell (iPSC)” (claim 25) and inactivating a B2M allele in a cell and “in some embodiments, the cell is an iPSC” (para 0013).
However, Izhar does not teach that the cells are iPSCs which have been generated by reprogramming γδ T cells.
Watanabe teaches a method of generating iPSCs from γδ T cells using the Yamanaka factors OCT4, SOX2, KLF4, and c-MYC (page 35, right col, Generation of iPSCs from Human γδ T Cell Culture, para 1) and they can provide a therapeutic cell source for novel adoptive cell therapies as they exhibit anti-tumor activity (page 1 Introduction; page 35, left col, para 3).
It would have been prima facie obvious to one of ordinary skill, in the art at the time of the effective filing date, to modify the teachings of disrupting the B2M gene in cells such as T cells from Izhar with the teachings of reprogramming γδ T cells to become iPSCs from Watanabe to generate a population of iPSCs with a disrupted B2M gene. One would be motivated to do so since iPSCs are self-renewing and therefore one would have a regenerative cell source/consistent supply of cells to use for B2M gene disruption and, subsequently, use as a cell therapy source. As reprogramming cells into iPSCs and gene editing iPSCs are known techniques in the art, one would have a reasonable expectation of success.
Regarding claim 2, the teachings of Izhar and Watanabe render obvious claim 1.
However, Izhar and Watanabe do not teach wherein the disrupted B2M gene comprises a deletion of at least a portion of the nucleotide sequence of SEQ ID NO: 1 or of about or at least about 5-100% of the nucleotide sequence of SEQ ID NO: 1.
Das teaches a nucleotide sequence of SEQ ID NO: 48 identifying the B2M gene. When comparing the nucleotide of SEQ ID NO: 48 with the claimed nucleotide of SEQ ID NO:1 or a mutated form with a deletion of at least a portion of the sequence set forth in SEQ ID NO: 1 as recited in claim 2, a portion of the instant SEQ ID NO:1 is identical the nucleotide of SEQ ID NO: 48.
See sequence alignment below – shown are only positions 1-179 of SEQ ID NO: 48. Red box = SEQ ID NO:1; Green Box = reference application SEQ ID NO: 48; Yellow box = deletion in reference application SEQ ID NO: 48.
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Regarding claim 3, the teachings of Izhar and Watanabe render obvious claim 1.
However, Izhar and Watanabe do not teach wherein the nucleotide sequence of the B2M gene encodes an amino acid sequence that is about, at least about, or at most about 5-100% identical to SEQ ID NO: 12.
Pulé teaches an amino acid sequence of SEQ ID NO: 3 identifying the B2M amino acid sequence. When comparing the amino acid of SEQ ID NO: 3 with the claimed amino acid of SEQ ID NO: 12 as recited in claim 3, the instant SEQ ID NO:12 is identical the amino acid of SEQ ID NO: 3.
See sequence alignment below Red box = SEQ ID NO:12; Green Box = reference application SEQ ID NO: 3.
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Regarding claim 4, the teachings of Izhar and Watanabe anticipate claim 1.
Moreover, Izhar teaches that, using FACS analysis, 80% of gene edited cells are negative for B2M (as shown in Figure 4; in para 0164), rendering obvious the population of iPSCs of claim 1, wherein about 80% of the iPSCs do not express a detectable level of B2M.
Regarding claim 5 and 6, the teachings of Izhar and Watanabe anticipate claim 1.
Moreover, Izhar teaches “wherein alleles of the B2M gene in the cell are subjected to an insertion or deletion mutation” (claim 6), rendering obvious wherein the disruption comprises a deletion (claim 5 of instant application) or insertion (claim 6 of instant application) of at least one nucleotide base pair.
Regarding claim 7 and 8, the teachings of Izhar and Watanabe anticipate claim 1.
Moreover, Izhar teaches using FACS analysis, 80% of gene edited cells (are negative for B2M and the expression is reduced compared to a negative control cell with no B2M disruption (as shown in Figure 4; in para 0164), rendering obvious wherein the disrupted B2M gene exhibits reduced B2M expression relative to an undisrupted B2M gene (claim 7 of instant application) and wherein the reduced expression of B2M is reduced by about or at least about 5-100% as compared to the expression of B2M in a reference iPSC (claim 8 of instant application).
Regarding claim 9, the teachings of Izhar and Watanabe render obvious claim 1.
However, Izhar and Watanabe do not teach wherein the iPSCs comprising a disrupted B2M gene exhibit reduced expression of HLA-A, HLA-B, and/or HLA-C as compared to the expression of HLA-A, HLA-B, and/or HLA-C in a reference iPSC.
Lee teaches “repressing a B2M gene to produce HLA class I null T cell or stem cell for example a cell that does not express one or more HLA receptors on its surface” (para 0017). Furthermore, Lee teaches “the cells with modulated B2M expression lack significant class I HLA on their cell surface” and “the B2M-gene modified cells are further modified at the HLA-A, -B, -C genes” (para 0019). Finally, Lee teaches that gene modified cells for B2M show 92% knockout of HLA signal and it is relative to no Zinc finger nuclease (ZFM) control cells (i.e reference cells) (as shown in Figure 4A-E.). The examiner notes that MHC class I molecules are heterodimers that consist of two polypeptide chains, α and β2-microglobulin (B2M) as evidenced by Wkipedia.
In light of the teachings of Lee, it is noted that the claim is directed to an inherent result based on reduction of B2M expression leading to reduction in HLA expression. It is noted that In re Best (195 USPQ 430) and In re Fitzgerald (205 USPQ 594) discuss the support of rejections wherein the prior art discloses subject matter which there is reason to believe inherently includes functions that are newly cited or is identical to a product instantly claimed. In such a situation the burden is shifted to the applicants to "prove that subject matter shown to be in the prior art does not possess characteristic relied on" (205 USPQ 594, second column, first full paragraph). It is noted that, if the prior art discloses identical chemical structure, the properties applicant discloses and/or claims are necessarily present, In re Spada, 911 F.2d 705, 709, 15 USPQ2d. As such the functional limitations would be present in the identical compounds taught by Lee would therefore exhibit the phenotype of reduced expression of HLA-A, HLA-B, and/or HLA-C.
Regarding claim 10, the teachings of Izhar, Watanabe, and Lee render obvious claim 1 and 9. Moreover, Lee teaches that gene modified cells for B2M show 92% knockout of HLA signal and it is relative to no Zinc finger nuclease (ZFM) control cells (i.e reference cells) (as shown in Figure 4A-E), rendering obvious wherein the reduced expression of HLA- A, HLA-B, and/or HLA-C is reduced by about or at least about 5-100% as compared to the expression of HLA-A, HLA-B, and/or HLA-C in a reference iPSC.
Regarding claim 11, the teachings of Izhar and Watanabe render obvious claim 1, 7, and 8. Moreover, Izhar teaches a reference population of cells that are negative control cells with no nuclease and no guide sequence for B2M disruption (Table 7, Example 5), rendering obvious wherein the reference iPSC is a population of iPSCs in which B2M gene is not disrupted.
Regarding claim 12, the teachings of Izhar and Watanabe render obvious claim 1. Moreover, Izhar teaches a guide RNA (gRNA), used for targeting and knocking-out of the B2M gene by electroporating into primary T cells (para 0145) and Cpf1 which is an RNA-guided endonuclease (para 0128), rendering obvious wherein the disrupted B2M gene is generated by contacting the population of iPSCs with an RNA-guided endonuclease or a nucleic acid encoding the RNA-guided endonuclease and a guide RNA (gRNA), and wherein the gRNA binds to a target motif of a B2M gene.
Regarding claim 13 and 16, the teachings of Izhar and Watanabe render obvious claim 1 and 12.
However, Izhar and Watanabe do not teach wherein the RNA-guided endonuclease is MAD7.
Fry teaches inserting transgenes into endogenous gene loci such as B2M (abstract) of cells that can be iPSCs (page 2, para 0005) and the transgene insertion is carried out using a site-direct nuclease (i.e. RNA-guided endonuclease) such as MAD7 (page 5, para 0013).
It would have been prima facie obvious to one of ordinary skill, in the art at the time of the effective filing date, to modify the teachings of disrupting a B2M gene in iPSCs using a gRNA that targets a B2M gene from Izhar and Watanabe with the teachings of using MAD7 as the RNA-guided endonuclease for B2M gene disruption from Fry to generate a functional gene-editing system for disrupting the B2M gene. One would be motivated to do so to have multiple options of RNA-guided endonucleases when performing gene editing in cells. Since MAD7 can be used as an RNA guided endonuclease for B2M gene editing, as shown in Fry, one would have a reasonable expectation of success.
Regarding claim 17, the teachings of Izhar and Watanabe render obvious claim 1 and 12.
However, Izhar and Watanabe do not teach wherein the gRNA binds to at least a portion of a complement sequence of SEQ ID NO: 1.
Ando teaches gRNAs comprising a targeting sequence against the B2M gene (para 0468). More specifically, Ando teaches a targeting sequence of SEQ ID NO: 8661. When comparing the nucleotide sequence of SEQ ID: 8661 with the claimed nucleotide of SEQ ID NO: 1 as recited in claim 17, the instant SEQ ID NO: 1 is 100% identical to the nucleotide sequence of SEQ ID NO: 8661.
See sequence alignment below. NOTE: a nucleic acid sequence that binds to the complement of a template sequence, as recited in claim 17, would be identical to the template sequence, hence the sequence alignment below. Red box = SEQ ID NO:1; Green Box = reference application SEQ ID NO: 8661)
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It would have been prima facie obvious to one of ordinary skill, in the art at the time of the effective filing date, to modify the teachings of disrupting a B2M gene in iPSCs using a gRNA that targets a B2M gene from Izhar and use the gRNA sequence set forth in SEQ ID NO: 8661 from Ando to properly target and edit the B2M gene in iPSCs. One would be motivated to do so to generate cells with edited B2M genes, which is a known technique in the art, and therefore one would have reasonable expectation of success.
Regarding claim 18, the teachings of Izhar and Watanabe render obvious claim 1 and 12.
However, Izhar and Watanabe do not teach wherein the gRNA binds to a complement sequence of any one of SEQ ID NO: 17.
Barghetti teaches a spacer sequence (“The spacer sequence is designed to hybridize with the target nucleotide sequence” (i.e. gRNA) (para 0107)) and “wherein the spacer sequence is capable of hybridizing with the human B2M gene” (para 0111).
More specifically, Barghetti teaches a spacer sequence of SEQ ID NO: 625. When comparing the nucleotide sequence of SEQ ID NO: 625 with the claimed nucleotide sequence of SEQ ID: NO 17 as recited in claim 18, the instant SEQ ID NO: 17 is 100% identical to the nucleotide sequence of SEQ ID NO: 625
See sequence alignment below. NOTE: a nucleic acid sequence that binds to the complement of a template sequence, as recited in claim 18, would be identical to the template sequence, hence the sequence alignment below. Red box = SEQ ID NO:17; Green Box = reference application SEQ ID NO: 625).
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It would have been prima facie obvious to one of ordinary skill, in the art at the time of the effective filing date, to modify the teachings of disrupting a B2M gene in iPSCs using a gRNA that targets a B2M gene from Izhar and use the gRNA (spacer sequence) set forth in SEQ ID NO: 625 from Barghetti to properly target and edit the B2M gene in iPSCs. One would be motivated to do so to generate cells with edited B2M genes, which is a known technique in the art, and therefore one would have reasonable expectation of success.
Regarding claim 19-22, the teachings of Izhar and Watanabe render obvious claim 1 and 12.
However, Izhar and Watanabe do not teach wherein the gRNA comprises or consists of a sequence of SEQ ID NOs: 18.
Donohoue teaches a CRISPR guide RNA that comprises and consists of a sequence of SEQ ID: 416 (para 0149) that targets the B2M gene. When comparing the nucleotide sequence of SEQ ID NO: 416 with the claimed nucleotide of SEQ ID NO: 18 as recited in claim 19-22, the instant SEQ ID NO: 18 is 100% identical to the nucleotide sequence of SEQ ID NO: 416. See sequence alignment below. Red box = SEQ ID NO:18 ; Green Box = reference application SEQ ID NO: 416.)
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It would have been prima facie obvious to one of ordinary skill, in the art at the time of the effective filing date, to modify the teachings of disrupting a B2M gene in iPSCs using a gRNA that targets a B2M gene from Izhar and use CRISPR guide RNA set forth in SEQ ID NO: 416 from Donohoue to properly target and edit the B2M gene in iPSCs. One would be motivated to do so to generate cells with edited B2M genes, which is a known technique in the art, and therefore one would have reasonable expectation of success.
Regarding claim 77, the teachings of Izhar and Watanabe render obvious claim 1.
However, Izhar and Watanabe do not teach wherein the disruption further comprises a knock-in of a polynucleotide encoding a transgene, wherein the polynucleotide is inserted within the B2M gene.
Lee teaches “cells in which the expression of a B2M gene is modulated” and that an exogenous transgene may be integrated into a B2M gene as the modulation (para 0019).
It would have been prima facie obvious to one of ordinary skill, in the art at the time of the effective filing date, to modify the teachings of disrupting a B2M gene in iPSCs using a gRNA that targets a B2M gene from Izhar and Watanabe with the teachings of disrupting the B2M gene by inserting a transgene within the B2M gene from Lee to generate an B2M gene with a transgene insertion within the genome of an iPSC. One would be motivated to do so to disrupt the B2M gene via an insertion that could cause alternative controlling of gene expression, such as inserting an exogenous transgene that is a stop codon, or express a chimeric antigen receptor for cell therapy purposes. As insertion of exogenous transgenes into known gene loci is known in the art, one would have a reasonable expectation of success.
Regarding claim 78, the teachings of Izhar, Watanabe, and Lee render obvious claim 1 and 77. Moreover, Lee teaches that the exogenous transgene encodes an engineered TCR (para 0019), rendering obvious wherein the transgene encodes a chimeric antigen receptor, a TCR, a therapeutic payload or a therapeutic protein.
Regarding claim 79, the teachings of Izhar, Watanabe, and Lee render obvious claim 1 and 77. Moreover, Lee teaches that the exogenous transgene may be integrated into a B2M gene, rendering obvious wherein the polynucleotide is inserted within SEQ ID NO: 1 (i.e. the B2M gene).
Response to Applicant’s arguments as they apply to rejection of claims 1-13, 16-22, and 77-79 under 35 USC § 103
Applicant’s arguments filed 06/18/2026 have been fully considered but are not persuasive.
On page 13 of the Remark filed 06/18/2026, Applicant asserts that 1) none of the cited references teaches, discloses, or suggests the claimed invention as none of the references provide any guidance or motivation to expect that knocking out B2M in iPSCs generated by reprogramming γδ T cells would be successful. Applicant asserts although Izhar may disclose knocking out B2M in any cell type capable of being reprogrammed by an iPSC, the reference is silent on γδ T cells, and thus necessarily cannot provide any guidance or motivation to look to any other reference discussing γδ T cells and 2) reprogramming them to generate iPSCs would be impermissible hindsight.
In response to applicant’s argument 1 that there is no teaching, suggestion, or motivation to combine the references, the examiner recognizes that obviousness may be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so found either in the references themselves or in the knowledge generally available to one of ordinary skill in the art. See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007). With regard to Applicant’s argument that Izhar does not teach the entire claimed subject matter, the Examiner agrees. However, Izhar is not applied alone, but in combination with Watanabe and the cited references, and the claimed invention becomes obvious when the references are considered together as a whole rather than each alone. In this case, Izhar teaches knocking out (i.e. disrupting) the B2M gene in cells to minimize the immunogenicity of CAR-T cells such that an allogeneic adoptive transfer strategy can be implemented in which universal CAR cells derived from cells from healthy donors can be applied to treat multiple patients (para 005). Izhar teaches that the cells with disrupted B2M genes can be a lymphocyte, a T cell, a T regulatory cell, a B cell, a natural killer (NK) cell, a macrophage, a stem cell, or a fibroblast, blood cell, hepatocyte, keratinocyte, or any other cell type capable of being reprogrammed to an induced pluripotent stem cell (iPSC) and can be an iPSC. While Izhar does not teach that the cells are iPSCs which have been generated by reprogramming γδ T cells, the prior art of Watanabe teaches a method of generating iPSCs from γδ T cells and that they provide a therapeutic cell source for novel adoptive cell therapies as they exhibit anti-tumor activity. Hence, the motivation to combine Izhar and Watanabe would be to generate a disrupted B2M cell that is derived from a γδ T cell as they are a cell source with anti-tumor activities and can ultimately generate universal CAR cells derived from cells from healthy donors and can be applied to treat multiple patients.
In response to applicant's argument 2 that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971). In this case, as stated above, Izhar teaches knocking out (i.e. disrupting) the B2M gene in cells to minimize the immunogenicity of CAR-T cells such that an allogeneic adoptive transfer strategy can be implemented in which universal CAR cells derived from cells from healthy donors can be applied to treat multiple patients (para 005), therefore Izhar teaches the need to disrupt the B2M gene, thus there is teaching, suggestion, and motivation to use the Izhar teaching for such application.
Conclusion
Claims 1-13, 16-22, and 77-79 are rejected.
THIS ACTION IS MADE FINAL. 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.
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/JULIANA IRENE CANDELARIA/ Examiner, Art Unit 1634
/MARIA G LEAVITT/ Supervisory Patent Examiner, Art Unit 1634
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