DETAILED ACTION
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 .
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 10/20/2025 has been entered.
Claims 44-49, 51-57, and 63-64, of record 6/23/2025, are pending and subject to prosecution. Claims 44, 47, and 57 are amended. Claims 50, 58, and 60-62 are cancelled.
Status of Prior Rejections/Response to Arguments
RE: Objection to claim 57:
The amendment to claim 57 is effective to obviate the objection. The objection is withdrawn.
RE: Rejection of claim 57 under 35 U.S.C. 112(b):
The amendment to claim 57 is effective to obviate the rejection. The rejection is withdrawn.
RE: Rejection of claims 44-50, 53, 57, and 64 under 35 U.S.C. 103 over Tanaka et al. (WO 2016127257 A1) in view of Stephan (WO 2014153114 A1) and Antov et al. (Journal of Immunology, 2003):
RE: Rejection of claims 44-51, 53, 57, and 64 under 35 U.S.C. 103 over Tanaka et al. (WO 2016127257 A1) in view of Stephan (WO 2014153114 A1) and Antov et al. (Journal of Immunology, 2003), further in view of Bradner et al. (US 11311609 B2):
RE: Rejection of claims 44-50, 52-54, 57, and 64 under 35 U.S.C. 103 over Tanaka et al. (WO 2016127257 A1) in view of Stephan (WO 2014153114 A1) and Antov et al. (Journal of Immunology, 2003), further in view of Riley et al. (US 11827705 B2):
RE: Rejection of claims 44-50, 52-54, 56-57, and 64 under 35 U.S.C. 103 over Tanaka et al. (WO 2016127257 A1) in view of Stephan (WO 2014153114 A1) and Antov et al. (Journal of Immunology, 2003), further in view of Riley et al. (US 11827705 B2), further in view of Chaudhary (WO 2017172981 A2):
RE: Rejection of claims 44-50, 53, 55, 57, and 64 under 35 U.S.C. 103 over Tanaka et al. (WO 2016127257 A1) in view of Stephan (WO 2014153114 A1) and Antov et al. (Journal of Immunology, 2003), further in view of Forman et al. (WO 2017079528 A1):
The cancellation of claim 50 renders the rejections thereto moot.
The applicant asserts that the prior art references do not teach Tregs comprising a CAR comprising a STAT5 association motif and a JAK1 or JAK2 binding motif, but not a JAK3 binding motif, wherein the CAR provides a STAT5-mediated pro-survival signal to the Treg upon CAR binding (Applicant Remarks, page 8-9, 13, and 17-18). The applicant asserts that Antov et al. teach away from the amended claims, which specifically exclude a JAK3 motif, in teaching that JAK3 signaling is required for regulatory T cell maintenance in vivo (Applicant Remarks, page 9). The applicant asserts that Tanaka et al. mention Tregs only in a long list of cell types and without specific teachings relevant to Treg function and do not teach a method of inducing tolerance to a transplant (Applicant Remarks, page 10). The applicant asserts that Tregs and effector T cells are fundamentally different and that there would be no reasonable expectation of success in using the CAR of Tanaka et al. in Tregs (Applicant Remarks, page 9-10 and 14-17). The applicant asserts unexpected results observed in the form of productive IL-2 signaling upon antigen binding, increased STAT5 signaling, and increased survival, all in the absence of a JAK3 binding motif CAR endodomain (Applicant Remarks, page 11-12 and 16-19).
These arguments are not found persuasive. One cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). Arguments pointing out the lack of a teaching of a specific limitation in a reference when the rejection is based on the combined teaching of references are not persuasive. The applicant is also reminded that the claims are not limited to a method of inducing tolerance to a transplant, therefore the prior art is not required to read on that particular limitation.
The applicant argues that Tanaka et al. is not enabling for the claimed subject matter (Applicant Remarks, page 9-10), even though Tanaka et al. teach that a CAR comprising a STAT5 association motif and a JAK1 binding motif can be expressed in Tregs (See Tanaka et al., ¶0003, 00068, and 000121). A reference is prior art for all that it teaches, including nonpreferred and alternative embodiments. See MPEP 2123(I)-(II). That the focus of Tanaka et al. is on effector T cells is immaterial, because regulatory T cells are also taught as a suitable alternative. Prior art that teaches or renders obvious all elements of a claimed invention is presumed to be enabling. See MPEP 2121(I). Further, one of ordinary skill in the art, able to construct a T cell comprising a CAR having the claimed limitations, would also be able to understand when the use of a effector T cell or a regulatory T cell would be appropriate and apply the teachings of Tanaka et al. accordingly. As the teachings of Stephan and Bradner et al. pertain the use of CAR-T cells, which can be Tregs, in treating inflammatory and autoimmune disorders, sufficient motivation exists for one of ordinary skill to combine their teachings with those of Tanaka et al. with a reasonable expectation of success.
Regarding the teachings of Antov et al., JAK3 signaling was indeed demonstrated to be indispensable for regulatory T cell development and maintenance through the use of JAK3 knockout mice (See Antov et al., fig. 1). Antov et al. do not teach away from the exclusion of a JAK3 binding motif in a CAR, Further, there is no requirement by Tanaka et al., Stephan, Bradner et al., Riley et al., or Forman et al. that the CAR comprise a JAK3 binding motif. Indeed, Tanaka et al. teach an embodiment wherein the cytoplasmic domain of the CAR comprises at least a STAT5 association motif, optionally a STAT5 association motif and a JAK binding motif (See 00066-00067), which indicates that the CAR as well as the immune cell function in the absence of a CAR JAK binding motif, which also encompasses the absence of a JAK3 binding motif.
Regarding the assertion of unexpected results in the form of antigen-specific IL-2 signaling, improved STAT5 signaling, and improved cell survival, the scope of the claims and the experimental conditions used to achieve any unexpected results must be commensurate in order for a showing of unexpected results to support an argument of nonobviousness. See MPEP 716.02(d). The applicant points to examples in the instant specification, however, only two or three constructs featuring the claimed limitations are tested in the experiments. The claimed method encompass a much broader scope than these constructs. Further, two or three constructs do not provide a sufficient basis for one of ordinary skill in the art to be able to extrapolate such results for every cell that can be generated by the claimed method. Thus, the assertion of unexpected results does not overcome the rejections of record.
The rejections are maintained in modified form to address amended limitations.
RE: Rejection of claims 58 and 60-61 under 35 U.S.C. 103 over Tanaka et al. (WO 2016127257 A1) in view of in view of Chaudhary (WO 2017172981 A2):
RE: Rejection of claims 58 and 60-62 under 35 U.S.C. 103 over Tanaka et al. (WO 2016127257 A1) in view of in view of Chaudhary (WO 2017172981 A2), further in view of Bradner et al. (US 11311609 B2):
The cancellation of claims 58 and 60-62 renders the rejections thereto moot.
RE: Rejection of claims 44-54, 57, and 63-64 are provisionally rejected on the ground of nonstatutory double patenting over claims 1-3, 7, 10, 16, 24, 26-28, 33-34, 38, 40, and 43 of co-pending Application No. 17/802018 in view of Antov et al. (Journal of Immunology, 2003):
RE: Provisional rejection of claims 44-55, 57, and 64 are provisionally rejected on the ground of nonstatutory double patenting over claims 1-3, 7, 10, 16, 24, 26-28, 33-34, 38, 40, and 43 of co-pending Application No. 17/802018 (reference application) in view of Antov et al. (Journal of Immunology, 2003), further in view of Forman et al. (WO 2017079528 A1):
The amendment of claim 44 to exclude a JAK3 binding motif is effective to obviate the provisional rejections. The provisional rejections are withdrawn.
Maintained Rejections
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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.
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 44-49, 53, 57, and 64 remain rejected under 35 U.S.C. 103 as being unpatentable over Tanaka et al. (WO 2016127257 A1), of record, in view of Stephan (WO 2014153114 A1), of record, and Antov et al. (Journal of Immunology, 2003), of record.
Regarding claims 44-45, 57, and 64: Tanaka et al. teach CARs that can comprise an intracellular STAT5 association motif and a JAK1-binding motif (See ¶0003 and 00068). In an embodiment, the cytoplasmic domain of the CAR comprises at least a STAT5 association motif, optionally a STAT5 association motif and a JAK binding motif (which reads on “the CAR endodomain does not comprise a JAK3 binding motif”) (See 00066-00067). Tanaka et al. teach that the claimed CAR can be expressed in Tregs (See ¶000121). Tanaka et al. teach administering the CAR-T cells to a subject for treating inflammatory or autoimmune diseases such as asthma or eczema (which reads on “treating an autoimmune or allergic disease”) (See ¶000117). Tanaka et al. teach that the CAR-expressing T cell may have an increased proliferation rate and/or increased survivability (See 00040) but do not expressly teach that the CAR provides a STAT5-mediated pro-survival signal to the cell upon antigen binding. Tanaka et al. also do not teach an embodiment wherein a Treg expresses the CAR for the treatment of atopic dermatitis, inflammatory bowel disease, systemic lupus erythematosus, or diabetes mellitus.
Stephan teaches the use of CAR-T cells for targeting autoimmune markers expressed by on the surface of cells in autoimmune or allergic conditions (See ¶0008, 0081, 0083, and 0086-0087). The T cells can be Tregs (See ¶0006). The conditions include atopic dermatitis, Crohn’s disease, and cutaneous lupus erythematosus (See ¶0081).
Antov et al. teach that STAT5 signaling is associated with homeostasis and cell survival in Tregs and that it is essential for maintaining peripheral Treg populations (See Abstract; page 3436, col. 1, full ¶1; page 3439, col. 2, full ¶1 and 3; and page 3440, col. 1, full ¶1).
It would have been obvious to one having ordinary skill in the art prior to the effective filing date of the claimed invention to modify the method of Tanaka et al. to comprise use of the CAR-T reg cells for treating the conditions named by Stephan. One would be motivated to make this modification because Stephan teaches that CAR-T cells, such as CAR-expressing Tregs, can be used to protect cells from autoimmune attack or reduce immune system activity in an area (See ¶0006 and 0083). Naturally occurring regulatory T cells constitutively express FoxP3, thereby reading on “FoxP3+”. There would be a reasonable expectation of success in making this modification because Tanaka et al. teach that the claimed CAR can be expressed in Tregs (See ¶000121).
It also would have been obvious to one having ordinary skill in the art that the CAR of Tanaka et al., if expressed in Tregs, would be reasonably expected to provide a STAT-5 mediated pro-survival signal, as Antov et al. demonstrate that STAT5 is associated with Treg homeostasis and survival (See Abstract; page 3436, col. 1, full ¶1; page 3439, col. 2, full ¶1 and 3; and page 3440, col. 1, full ¶1).
Regarding claim 46: Following the discussion of claims 44-45 and 57, Tanaka et al. teach that the CAR endodomain can comprise but do not require a STAT3 association motif (See Abstract and ¶00068). The CAR of Tanaka et al. therefore reads on “does not comprise a STAT3 association motif”.
Regarding claim 47: Following the discussion of claims 44-45 and 57, Tanaka et al. teach that the CAR intracellular domain can have multiple STAT5 association motifs (which reads on “two or more STAT5 association motifs”) (See ¶00076). The STAT5 association motif can be derived from the cytoplasmic portion of an interleukin receptor such as IL2Rβ (which reads on “is from an interleukin receptor… endodomain” and “is from IL2Rβ”) (See ¶0006 and 00016). The STAT5 association motif can comprise sequence YXXL, YLSL, YCTF, YFFF, and/or YLSLQ (which reads on “comprises the amino acid motif YXXF/L (SEQ ID NO: 8)”, “comprises one or more of the amino acid motifs YCTF (SEQ ID NO: 9), YFFF (SEQ ID NO: 10), YLSL (SEQ ID NO: 11), and/or YLSLQ (SEQ ID NO: 12)”, “comprises the amino acid motif YLSLQ (SEQ ID NO: 12”, “comprises a first STAT5 association motif comprising the amino acid motif YLSLQ (SEQ ID NO: 12) and a second STAT5 association motif comprising the amino acid motif YCTF (SEQ ID NO: 9) or YFFF (SEQ ID NO: 10)”, and “comprises the following STAT5 association motifs: YLSLQ (SEQ ID NO: 12), YCTF (SEQ ID NO: 9), and YFFF (SEQ ID NO: 10)”) (See ¶00070 and 00097).
Regarding claim 48: Following the discussion of claim 44-45 and 57, Tanaka et al. teach a truncated portion of the IL-2RB chain that comprises instant SEQ ID NO 13 (which reads on “the JAK-binding motif is a JAK-1 binding motif”, “the JAK-binding motif is a JAK1-binding motif from an interleukin receptor… endodomain”, “the JAK-binding domain is a JAK1-binding motif comprising an amino acid motif as shown in any one of SEQ ID NO: 13-19 or a variant which has at least 80% identity to SEQ ID NO: 13-19”, and “the JAK-binding domain is a JAK1-binding motif being the amino acid motif shown as SEQ ID NO: 13; or a variant which has at least 80% identity to SEQ ID NO: 13”) (See ¶00079, SEQ ID NO 5 and alignment below).
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Regarding claim 49: Following the discussion of claims 44-45 and 57, Tanaka et al. teach a human IL-2RB fragment having a sequence identical to that of instant SEQ ID NO 1 (which reads on “the CAR endodomain comprises an IL2Rβ endodomain shown as SEQ ID NO: 1; or a variant which has at least 80% sequence identity to SEQ ID NO: 1”) (See ¶00064, SEQ ID NO 11 and alignment below (first 120 bp displayed)).
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Regarding claim 53: Following the discussion of claims 44-45 and 57, Tanaka et al. teach that the CAR can bind the surface molecule of an inflammatory cell that appears in an autoimmune disease (which reads on “an antigen whose expression is upregulated during… tissue inflammation”) (See ¶00046).
Claims 44-49, 51, 53, 57, and 64 remain rejected under 35 U.S.C. 103 as being unpatentable over Tanaka et al. (WO 2016127257 A1), of record, in view of Stephan (WO 2014153114 A1), of record, and Antov et al. (Journal of Immunology, 2003), of record, further in view of Bradner et al. (US 11311609 B2), of record.
The teachings of Tanaka et al., Stephan et al., and Antov et al. are set forth in the rejections above and are incorporated herein in their entirety.
Regarding claim 51: Following the discussion of claims 44-45, 57, and 64, Tanaka et al., modified by Stephan and Antov et al., teach the generation of Tregs expressing a CAR and their administration to a subject (See ¶00030 and 00036) but do not expressly teach the generation of CAR-T cells from a regulatory T cell-enriched sample.
Bradner et al. teach the generation of CAR-T cells from cells, such as regulatory T cells, and their use in treating autoimmune conditions (See Abstract; col. 42, line 60-64; and col. 81, line 56-60). The starting population of T cells can be enriched for or positively selected for regulatory T cells on the basis of CD4, CD25, CD62, GITR, and FoxP3 expression (See col. 83, line 25-28).
It would have been obvious to one having ordinary skill in the art prior to the effective filing date of the claimed invention to modify the method of Tanaka et al., modified by Stephan and Antov et al., to comprise an enrichment step, such as that taught by Bradner et al., prior to transfection or transduction. One would be motivated to make this modification in order to obtain a desired cell population for therapeutic use. There would be a reasonable expectation of success in doing so because the cells of Tanaka et al., modified by Stephan and Antov et al., could be readily subjected to enrichment by immunosorting before deliver of a CAR-encoding polynucleotide.
Claims 44-49, 52-54, 57, and 64 remain rejected under 35 U.S.C. 103 as being unpatentable over Tanaka et al. (WO 2016127257 A1), of record, in view of Stephan (WO 2014153114 A1), of record, and Antov et al. (Journal of Immunology, 2003), of record, further in view of Riley et al. (US 11827705 B2), of record.
The teachings of Tanaka et al., Stephan, and Antov et al. are set forth in the rejections above and are incorporated herein in their entirety.
Regarding claims 52 and 54: Following the discussion of claims 44-45, 57, and 64, Tanaka et al., modified by Stephan and Antov et al., teach the CAR-T cells can be used to treat to a subject receiving a transplant but do not expressly teach the subject as undergoing immunosuppressive therapy or the CAR as specific for an HLA antigen present in the graft donor but not the recipient.
Riley et al. teach regulatory T cells expressing a CAR specific for HLA-A2 (which reads on “capable of specifically binding to a HLA antigen” and “capable of specifically binding to the HLA antigen HLA-A2”) (See Abstract). Riley et al. teach that the CAR suppresses alloresponses provoked by donor-MHC class molecules expressed by allografts (which reads on “antigen that is present in the graft donor but not the graft recipient”) (See col. 16, line 4-11). The subject can be administered immunosuppressive drugs in addition to the CAR-T cells (which reads on “undergoing immunosuppression therapy”) (See col. 59, line 28-30). The transplanted tissue can be liver, kidney, heart, lung, pancreas, intestine, or skin (See col. 59, line 19-25).
It would have been obvious to one having ordinary skill in the art prior to the effective filing date of the claimed invention to modify the method of Tanaka et al., modified by Stephan and Antov et al., to use a host antigen-specific CAR, such as that taught by Riley et al., for administration to a transplant recipient. It also would have been obvious to use immunosuppressive drugs, as taught by Riley et al., in conjunction with CAR-T cell therapy. One would be motivated to make these modifications in order to reduce adverse immune responses following transplantation. There would be a reasonable expectation of success in doing so because the CAR construct of Tanaka et al. could be readily modified to comprise an HLA-A2-specific binding moiety and because immunosuppressive drugs could be readily administered to the subject.
Claims 44-49, 52-54, 56-57, and 64 remain rejected under 35 U.S.C. 103 as being unpatentable over Tanaka et al. (WO 2016127257 A1), of record, in view of Stephan (WO 2014153114 A1), of record, and Antov et al. (Journal of Immunology, 2003), of record, further in view of Riley et al. (US 11827705 B2), of record, further in view of Chaudhary (WO 2017172981 A2), of record.
The teachings of Tanaka et al., Stephan, Antov et al., and Riley et al. are set forth in the rejections above and are incorporated herein in their entirety.
Regarding claim 56: Following the discussion of claims 44-45, 52-54, 57, and 64, Tanaka et al., modified by Stephan, Antov et al., and Riley et al., render obvious the use of CAR-T cells for targeting an HLA-A2 moiety but do not expressly teach the sequences of instant SEQ ID NOs 93-95 and 105-107.
Chaudhary teaches SEQ ID NO 1932 and SEQ ID NO 2173 as VL and VH fragments for binding HLA-A2 (See tables 4 and 6). SEQ ID NO 2173 comprises instant SEQ ID NOs 93-95 (which reads on “an antigen binding domain comprising SEQ ID NOs: 93-95”) (See alignments below).
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SEQ ID NO 1932 comprises instant SEQ ID NOs 105-107 (which reads on “an antigen binding domain comprising… SEQ ID NOs: 105-107”) (See alignments below).
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It would have been obvious to one having ordinary skill in the art prior to the effective filing date of the claimed invention to modify the method of Tanaka et al., modified by Stephan, Antov et al., and Riley et al., to comprise the heavy and light chains taught by Chaudhary. One would be motivated to make this modification because Chaudhary teaches SEQ ID NOs 1932 and 2173 as exemplary sequences for targeting HLA-A2. There would be a reasonable expectation of success in doing so because Chaudhary teaches that these sequences can be used in a CAR (See ¶0021).
Claims 44-49, 53, 55, 57, and 64 remain rejected under 35 U.S.C. 103 as being unpatentable over Tanaka et al. (WO 2016127257 A1), of record, in view of Stephan (WO 2014153114 A1), of record, and Antov et al. (Journal of Immunology, 2003), of record, further in view of Forman et al. (WO 2017079528 A1), of record.
The teachings of Tanaka et al., Stephan, and Antov et al. are set forth in the rejections above and are incorporated herein in their entirety.
Regarding claim 55: Following the discussion of claims 44-45, 57, and 64, Tanaka et al., modified by Stephan and Antov et al., teach a CAR comprising a CD8 transmembrane domain but do not expressly teach a CD8α transmembrane domain.
Forman et al. teach CAR-T cells wherein the CAR comprises a CD8α transmembrane domain (See ¶007 and table 2, SEQ ID NO 17). The CD8α transmembrane domain is identical to the sequence of instant SEQ ID NO 87 (which reads on “the CAR comprises a CD8α transmembrane domain” and “comprising the amino acid sequence of SEQ ID NO: 87, or a variant which is at least 80% identical to SEQ ID NO: 87”) (See table 2, SEQ ID NO 17 and alignment below).
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It would have been obvious to one having ordinary skill in the art prior to the effective filing date of the claimed invention to modify the CAR of Tanaka et al., modified by Stephan and Antov et al., to substitute the transmembrane domain taught by Forman et al. Substitution of one known element for another known element is considered to be prima facie obvious, absent a showing that the result of the substitution yields more than predictable results.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to JENNIFER S SPENCE, whose telephone number is 571-272-8590. The examiner can normally be reached M-F 8:30-5:30.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Christopher M Babic, can be reached at 571-272-8507. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/J.S.S./Examiner, Art Unit 1633
/CHRISTOPHER M BABIC/Supervisory Patent Examiner, Art Unit 1633