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 .
Claim status
In the reply filed 26 March 2026, Applicant has amended claims 1, 2, 17, and 233, and claim 3 has been cancelled. Claims 4-16, 18-39, 41-46, 48-59, and 61-222 were previously cancelled. Upon entry of these amendments, claims 1-2, 17, 40, 47, 60, and 223-239 are herein pending.
Election/Restrictions
Applicants previously without traverse of Group 1, claims 1-3, 17, 40, 47, and 60 and 223-239, drawn to a cell expressing a chimeric antigen receptor (CAR), wherein the cell has reduced expression and/or a reduced biological activity of ZBTB32 in the reply filed on 26 November 2025.
Claims 76-77,87,89,97,100,116,118,122,126,129,131,136,207,211,215 and 217 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. However, applicant has cancelled the withdrawn claims in the reply filed on 26 November 2025.
Claims 1-2, 17, 40, 47, 60, and 223-239 are under current examination.
Priority
This application was filed 12/09/2022 and is a 371 application of PCT/US2021/037048 filed on 06/11/2021, which claims benefit to the Provisional Application 63037826 filed on 06/11/2020. Thus, the earliest possible priority for the instant application is 06/11/2020.
Withdrawn Objections
Applicant has submitted amended tile to “CAR-EXPRESSING CELLS AND ZBTB32 INHIBITORS AND USES THEREOF" on 26 March 2026 and compliant with MPEP 606.01. Examiner has updated the bib data (see the attached BibData sheet), therefore, the objection to the tile has been withdrawn.
Withdrawn of rejections
Applicant amends claim 1 to recite " wherein the cell comprises a ZBTB32 inhibitor, or the cell has been contacted with, or is being contacted with a ZBTB32 inhibitor," therefore, breadth of a claim 1 renders the indefiniteness. Accordingly, the prior rejection of claims 1, 3, 17, 40, 47, 60, and 223-239 under 35 U.S.C. 112(b) is withdrawn.
The Applicant has amended the claim 1 and exclusively included the limitation, “wherein the cell comprises a ZBTB32 inhibitor, or the cell has been contacted with, or is being contacted with a ZBTB32 inhibitor.” In the prior art Busser et al., (WO2019076486A1) discloses CAR expressing T cells further comprising an exogenous sequence encoding an NK inhibitor integrated at the ZBTB32 locus (p. 29, lines 16 to 31 of Busser) via, the TALEN system or CRISPR-Cas9 (p. 17, Ins 4-19 of Busser). However, Busser did not to teach or reasonably suggest that the cell comprises a ZBTB32 inhibitor. Therefore, the prior rejection of claims 1-3, 40, 47, 60, 223-226, 229 and 235-239 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Busser et al (WO2019076486A1; cited in IDS filed 06/30/2023; hereinafter “Busser”) is hereby withdrawn.
Accordingly, the prior rejection of claims 1-3, 17, 40, 47, 60, 223-226, 229, 232 and 235-239 under 35 U.S.C. 103 as being unpatentable over Busser et al (WO2019076486A1; cited in IDS filed 06/30/2023; hereinafter “Busser”), in view of Shahi et al. (Proceedings of the National Academy of Sciences, 114(12), pp.3169-3174; cited in IDS filed 06/30/2023; hereinafter “Shahi”).
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 set forth in Graham v. John Deere Co., 383 U.S. 1, 148 USPQ 459 (1966), that are applied 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 1-3, 17, 40, 47, 60, 223-226, 229, 232 and 235-239 are newly rejected under 35 U.S.C. 103 as being unpatentable over Busser et al (WO2019076486A1; cited in IDS filed 06/30/2023; hereinafter “Busser”), in view of Shahi et al. (Proceedings of the National Academy of Sciences, 114(12), pp.3169-3174; cited in IDS filed 06/30/2023; hereinafter “Shahi”). The new rejection is necessitated by applicant’s claim amendments.
Examiner’s claim interpretation:
MPEP 2111.01 (i) states that Under a broadest reasonable interpretation (BRI), words of the claim must be given their plain meaning, unless such meaning is inconsistent with the specification. The plain meaning of a term means the ordinary and customary meaning given to the term by those of ordinary skill in the art at the relevant time. The ordinary and customary meaning of a term may be evidenced by a variety of sources, including the words of the claims themselves, the specification, drawings, and prior art. However, the best source for determining the meaning of a claim term is the specification - the greatest clarity is obtained when the specification serves as a glossary for the claim terms. Phillips v. AWH Corp., 415 F.3d 1303, 1315, 75 USPQ2d 1321, 1327 (Fed. Cir. 2005) (en banc) ("[T]he specification ‘is always highly relevant to the claim construction analysis. Usually, it is dispositive; it is the single best guide to the meaning of a disputed term.’" (quoting Vitronics Corp. v. Conceptronic Inc., 90 F.3d 1576, 1582 (Fed. Cir. 1996)).
The amended claim 1 has drawn to a product “A cell” that comprises a CAR and a ZBTB32 inhibitor. Therefore, the cell is comprising two distinct molecules i) a CAR; and ii) a ZBTB32 inhibitor. For the sole purpose of expediting prosecution and for clarifying the record (MPEP 2106.07(c)), examiner construes the cell does not comprise a vector that contains both a nucleotide sequence encoding a CAR and a nucleotide sequence encoding a ZBTB32 inhibitor (see [0040] ¶ of US20230332104A1).
With respect to claims 1-2, 223-226, and 229, Busser discloses CAR expressing T cells further comprising an exogenous sequence encoding an NK inhibitor integrated at the ZBTB32 locus (p. 29, lines 16 to 31 of Busser) via, the TALEN system or CRISPR-Cas9 (p. 17, lns 4-19 of Busser), and the medical use thereof for the treatment of cancer (claim 27 on p. 148 of Busser).
Although regarding claim 1, Busser does not specifically teach the cell comprises a ZBTB32 inhibitor and also Busser is silent to the ZBTB32 inhibitor comprises a small interfering RNA (siRNA) or a small hairpin RNA (shRNA) targeting the ZBTB32 gene, however, such was known in the prior art. However, such was known in the prior art.
With respect to claims 1-2, 17, 223-226, 229, and 232, Shahi discloses that the ZBTB32 comprises with siRNAs is essential for downregulation of GATA3 (associates with breast cancer development) in the immune cell (i.e., CD4+ T cell) and promote cellular invasion via binding partner Zinc-finger elbow-related praline domain protein 2 (Zpo2) (abstract, p. 3171 right col. 1st ¶ and Fig. 3 on page 3172). Furthermore, Shahi teaches that Intriguingly, the inhibitory effect of Zpo2 on GATA3 is ZBTB32-dependent. Knockdown of Zbtb32 restored GATA3 levels in cells overexpressing Zpo2 (p. 3172 right col. 2nd ¶). Therefore, a person of ordinary skill in the art reading Shahi would understand that the cell comprises a ZBTB32 inhibitor have a reduced expression of ZBTB32.
MPEP 2143 (A) states that combining prior art elements according to known methods to yield predictable results. The rationale to support a conclusion that the claim would have been obvious is that all the claimed elements were known in the prior art and one skilled in the art could have combined the elements as claimed by known methods with no change in their respective functions, and the combination yielded nothing more than predictable results to one of ordinary skill in the art. KSR, 550 U.S. at 416, 82 USPQ2d at 1395. Accordingly, it would have been obvious to practice the CAR T cell of Busser and include ZBTB32 comprises siRNAs with Zpo2 as taught by Shahi with a reasonable expectation of success. The POSITA would have been motivated at the time of filing to do so as taught by Shahi because it is essential for downregulation of GATA3 and promote cellular invasion (abstract, p. 3171 right col. 1st ¶ and Fig. 3 on page 3172 of Shahi). The POSITA would have had a reasonable expectation of success in combining the teachings of Busser and Shahi because each of these teachings both successfully generated T cell with CAR and ZBTB32 inhibitor respectively. Therefore, the products and method as taught by Busser et al. in view of Shahi et al. would have been prima facie obvious over the products of the instant application. In regard to the reasonable expectation of success in doing so, include ZBTB32 comprises siRNAs with Zpo2 of Shahi had a reasonable expectation of success since the steps thereof required no more than recombinant DNA technology and pipetting the appropriate Zpo2 concentration.
With respect to claim 40, Busser teaches that the T cell is a human cell (p. 30 ln 8; p. 47 ln 15).
With respect to claims 47, and 236-237, Busser teaches that the cell is an immune effector CD4+ and CD8+ T cell or a population of immune effector CD4+ and CD8+ T cells (p. 5 ln 10; p. 56 lns 15-20).
With respect to claim 60, Busser teaches that the antigen-binding domain binds to a tumor antigen selected from a group consisting of CD19, CD22, CD123, CS1, CL1, HSP70, GD3, and ROR1.
With respect to claims 230-231, Shahi discloses that the Zpo2 translocate to the nucleus and functions as a transcriptional repressor, suggesting that Zpo2 can interact and form complexes with other proteins. Furthermore, Zpo2 contains one zinc finger protein domain, it may lack DNA-binding ability (p. 3172 right-col 2nd ¶).
MPEP 2112.01 state that “Where the claimed and prior art products are identical or substantially identical in structure or composition, or are produced by identical or substantially identical processes, a prima facie case of either anticipation or obviousness has been established,” 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). In the instant case Shahi discloses the cell with ZBTB32 inhibitor comprises a small interfering RNA (siRNA) and binding partners Zpo2, therefor, POSITA would have expected that the transcription repressor function of ZBTB32 is reduced and interaction between ZBTB32 and binding partners (Zpo2) is reduced.
With respect to claim 235, Busser teaches that the antibody molecule comprises a single-domain antibody (sdAb) or nanobody that binds directed to against inhibitory peptides or proteins (i.e., a protein encoded by the ZBTB32 gene) (p. 28 lns 8-14).
With respect to claims 238-239, Busser teaches that the intracellular signaling domain comprises a primary signaling domain CD3 zeta or the Fc receptor gamma chains and costimulatory signaling domain selected from the group consisting of CD28, OX-40 (CD134), ICOS and 4-1BB (CD137) have (p. 3 lns 18-25).
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary.
Claims 1-3, 17, 40, 47, 60, 223-226, 227-228, 229 and 232, 233-234, 235-239 are rejected under 35 U.S.C. 103 as being unpatentable over Busser et al (WO2019076486A1; cited in IDS filed 06/30/2023; hereinafter “Busser”), and Shahi et al. (Proceedings of the National Academy of Sciences, 114(12), pp.3169-3174; cited in IDS filed 06/30/2023; hereinafter “Shahi”) as applied to claims 1-2, 17, 40, 47, 60, 223-226, 229, 232 and 235-239 above, and further in view of Coley et al., (F1000Research (2018) 7: 318; cited in IDS filed 06/30/2023; hereinafter “Coley”).
As stated above, Busser in view of Shahi discloses CAR expressing T cells further comprising a ZBTB32 inhibitor and the medical use thereof for the treatment of cancer.
Regarding claim 227, Busser is silent to the ZBTB32 genomic locus is altered, however, such was known in the prior art.
With respect to claims 227-228, 233-234, Coley discloses CRISPR gene editing systems targeting the ZBTB32 gene (Figure 1 on page 4 of Coley). Furthermore, ZBTB32 gene is preferentially induced in autoreactive CD4 T cells stimulated by these tolerogenic DCIR2+ DCs, and overexpression of ZBTB32 in islet-specific T cells inhibited the diabetes development by limiting T cell (abstract of Coley). The CRISPR/Cas9 technique was used to target exon 2 of the ZBTB32 gene directly in NOD mice, therefore, the loss of the ZBTB32 protein after CRISPR-mediated deletion was confirmed by Western blotting extracts from stimulated CD4+ splenocytes (Fig. 1 of Coley). Therefore, POSITA would have expected that the ZBTB32 genomic locus is altered.
MPEP 2143 (A) states that combining prior art elements according to known methods to yield predictable results. The rationale to support a conclusion that the claim would have been obvious is that all the claimed elements were known in the prior art and one skilled in the art could have combined the elements as claimed by known methods with no change in their respective functions, and the combination yielded nothing more than predictable results to one of ordinary skill in the art. KSR, 550 U.S. at 416, 82 USPQ2d at 1395. Accordingly, it would have been obvious to practice the CAR T cell of Busser and include CRISPR gene editing systems targeting the ZBTB32 gene as taught by Coley with a reasonable expectation of success. The POSITA would have been motivated at the time of filing to do so as taught by Coley because CRISPR can cause a frameshift mutation in the Zbtb32 gene, and validated the loss of the Zbtb32 protein therefore, the transcription repressor Zbtb32 reduced to play a critical role in the inhibition of T-cell mediated autoimmune T1D (p. 3 right-col 1st ¶). The POSITA would have had a reasonable expectation of success in combining the teachings of Busser and Coley because each of these teachings both successfully generated CAR T cell with ZBTB32 inhibitor. Therefore, the products and method as taught by Busser et al. in view of Coley et al. would have been prima facie obvious over the products and method of the instant application. In regard to the reasonable expectation of success in doing so, include CRISPR gene editing systems targeting the ZBTB32 gene of Coley had a reasonable expectation of success since the steps thereof required no more than recombinant DNA technology and cell culture technology.
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary.
RESPONSE TO ARGUMENTS
Applicant's arguments filed on 26 March 2026 are acknowledged.
Regarding rejection under 35 U.S.C. §102, applicant argues that claim 1 has been amended to recite, inter alia, "[a] cell expressing a chimeric antigen receptor (CAR) ... wherein the cell comprises a ZBTB32 inhibitor, or the cell has been contacted with, or is being contacted with, a ZBTB32 inhibitor." and in the cited prior art Busser et al. discloses CAR expressing T cells further comprising an exogenous sequence encoding an NK inhibitor integrated at the ZBTB32 locus that the NK inhibitor allegedly integrated at the ZBTB32 locus, however, Busser does not teach a CAR-expressing cell with ZBTB32 inhibition. See remark p. 11 1st ¶.
The rejection under 35 U.S.C. §102 over Busser has been withdrawn in view of the amendments to the claims. Accordingly, applicant’s arguments are moot. In the new rejection, Busser et al. in view of Shahi et al. addressed the cell comprising CAR and ZBTB32 inhibitor.
Regarding rejection under 35 U.S.C. §103, applicant argues that claim 1 has been amended to recite “wherein the cell comprises a ZBTB32 inhibitor” and Applicant discovered that ZBTB32 inhibition in CAR-expressing cells resulted in not only enhanced CAR cell expansion and cytokine production, but also enhanced T cell-mediated anti-tumor response in vivo, improved persistence of immune protection, and resistance to exhaustion. See remark p. 12 last ¶.
Applicant also argues that amended claim 1 showed unexpected result (see remark p. 14).
With respect to claim 1, MPEP 2112.01 states that “Where the claimed and prior art products are identical or substantially identical in structure or composition, or are produced by identical or substantially identical processes, a prima facie case of either anticipation or obviousness has been established,” 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 the claimed wherein clauses do not recite any additional active method steps, but simply state a function, characterization or measurement of the results of product positively recited (e.g., yield of recombinant POIs). In here, Busser et al. in view of Shahi et al. suggest to producing the instant cell with CAR and ZBTB32 inhibitor, so the function of the product would have been obvious. Accordingly, at the time of the invention POSITA would have obvious expectation that the cell with a CAR and a ZBTB32 inhibition will enhance CAR cell expansion and cytokine production, with improved persistence of immune protection, and resistance to exhaustion. Therefore, it would be obvious that unexpected result would be expected as disclosed by the product of Busser et al. in view of Shahi et al.
Applicant argues that Shahi does not remedy the deficiencies of Busser. Shahi focuses on Zpo's role in mammary epithelial cells in driving aggressive breast cancer progression. Shahi does not provide any teaching of a CAR-expressing cell, and Shahi does not demonstrate contacting a CAR-expressing cell with a ZBTB32 inhibitor. Furthermore, Shahi does not provide any indication or prediction of how ZBTB32 inhibition may affect the efficacy of a CAR-expressing cell. Therefore, contrary to the Office's assertions, a skilled artisan would not have been motivated to apply the teachings of Shahi to the cells of Busser, nor would the skilled artisan have had a reasonable expectation of success. See remark p. 13 last ¶.
In response to applicant’s argument 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). In this case, Busser teaches a T cell with CAR, and the adoptive transfer of CART-cells represents a highly promising strategy to fight against multiple cancers. The clinical outcome of such therapies is intimately linked to the ability of effector cells to engraft, proliferate and specifically kill tumor cells within patients (see p. 5 lns 8-10 of Busser). Additionally, Shahi teaches that ZBTB32 facilitates Zpo2 targeting to the GATA3 promoter, leading to down-regulation of GATA3 expression and activity. Modulation of GATA3 by Zpo2 in turn results in the development of aggressive breast cancers. Shahi also teaches that ZBTB32 plays a crucial role during Th1 and Th2 specification by negatively regulating GATA3 activity (see p. 3172 right col. 2nd ¶ of Shahi) ZBTB32 directly binds to the GATA3 promoter sequence and inhibits the activation of GATA3 target genes. Therefore, POSITA would have recognized that the ZBTB32 inhibitor reduce the aggressiveness of breast cancer.
The instant amended claim 1, the cell is comprising two distinct molecules i) a CAR; and ii) a ZBTB32 inhibitor. The POSITA would have had a reasonable expectation of success in combining the teachings of Busser and Shahi because each of these teachings both successfully generated T cell with CAR and ZBTB32 inhibitor respectively. Accordingly, at the time of the invention POSITA would have obvious expectation that the cell with a CAR and a ZBTB32 inhibition will enhance CAR cell expansion and cytokine production, with improved persistence of immune protection, and resistance to exhaustion. See MPEP 2145 (III).
Applicant argues that, Coley does not provide any teaching or suggestion of a CAR-expressing cell, let alone a CAR-expressing cell comprising a ZBTB32 inhibitor, or has been contacted with, or is being contacted with, a ZBTB32 inhibitor. Furthermore, a skilled artisan reading Coley may be led away from the presently claimed subject matter. Coley discloses that deletion of ZBTB32 in a mouse model did not result in increased T cell activation, but rather "no significant alteration in lymphocyte number or function was observed. Therefore, a skilled artisan reading Coley, alone or in combination with Busser and Shahi, would not be motivated to use an immune cell with decreased ZBTB32 expression in treating a disease. See remark p. 14-15 last and 1st ¶ respectively.
Applicant's arguments have been fully considered but they are not persuasive because the new ground of rejection relies on amendment claims and references applied in the prior rejection of record for any teaching or matter specifically challenged in the argument. In the new rejection, Busser et al. in view of Shahi et al. addressed the cell comprising CAR and ZBTB32 inhibitor. Second, applicants argue that Coley teaches away because deletion of ZBTB32 in a mouse model did not result in increased T cell activation. Applicant's arguments have been fully considered but they are not persuasive. In response to applicant's argument, MPEP 2145X(D1) states that "the prior art’s mere disclosure of more than one alternative does not constitute a teaching away from any of these alternatives because such disclosure does not criticize, discredit, or otherwise discourage the solution claimed…." In re Fulton, 391 F.3d 1195, 1201, 73 USPQ2d 1141, 1146 (Fed. Cir. 2004). Clearly Coley teaches CRISPR gene editing systems targeting the ZBTB32 gene (Figure 1 on page 4 of Coley). Furthermore, ZBTB32 gene is preferentially induced in autoreactive CD4 T cells stimulated by these tolerogenic DCIR2+ DCs, and overexpression of ZBTB32 in islet-specific T cells inhibited the diabetes development by limiting T cell (abstract of Coley) as an alternative.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any extension fee 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 date of this final action.
No claims are allowed.
Examiner Contact Information
Any inquiry concerning this communication or earlier communications from the examiner should be directed to MASUDUR RAHMAN whose telephone number is (571)272-0196. The examiner can normally be reached M-F 8-5 (EST).
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Christopher Babic can be reached on (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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/MASUDUR RAHMAN/ Patent Examiner, Art Unit 1633
/CHRISTOPHER M BABIC/Supervisory Patent Examiner, Art Unit 1633
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