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 .
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 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.
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 06/25/2026 has been entered.
Claim 1 is amended and claims 4, 7-8, 10-11, 13, 15, 17, 21, 23, 25-26, 28-32, 34-35, and 45 are cancelled. Claims 1-3, 5-6, 9, 12, 14, 16, 18-20, 22, 24, 27, 33, and 36-44 are currently pending and are examined on the merits herein.
Priority
The instant application, filed 01/24/2023, is a 371 filing of PCT/US2021/070943, filed 07/23/2021, and claims domestic benefit to US provisional application 63/056,467, filed 07/24/2020.
The following rejections have been modified.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 1-3, 5-6, 9, 12, 14, 16, 18-20, 22, 24, 27, 33, and 36-44 are rejected under 35 U.S.C. 103 as being unpatentable over WO 2018/007263 A1 (Cabaniols, J.P., et al) 11 Jan 2018.
WO’263 teaches that the potential of gene editing in various therapies has long been envisioned, particularly in the field of cell therapy, where immune cells can be genetically modified ex-vivo and then reintroduced into patients (page 1, lines 13-16). The disclosed methods pertain to the field of adaptive cell immunotherapy and aims at reducing the occurrence of translocations and cell deaths when several specific endonuclease reagents are used together to genetically modify primary immune cells at different loci. The method allows for the production of safer immune primary cells harboring several genetic modifications, such as triple or quadruple gene inactivated cells, from populations or sub-populations of cells originating from a single donor or patient, and their subsequent use in therapeutic treatments (abstract).
WO’263 teaches that the gene editing steps presented aim to disrupt the expression of a protein involved in immune cells inhibitory pathways, in particular, those referred to in the literature as “immune checkpoint”. WO’263 further teaches that “immune cells inhibitory pathways” means any gene expression in immune cells that leads to a reduction of the cytotoxic activity of the lymphocytes towards malignant or infected cells (page 24, lines 25-34). WO’263 teaches that, for instance, one of the sequence-specific reagents used in the method can reduce or prevent the expression by the immune cell of at least one protein selected from a list which includes PD1 and SIT1 (page 25, line 25 – page 26, line 7; page 25). WO’263 further discloses that PD1 is a co-inhibitory receptor and SIT1 acts in prevention of TCR signaling (page 26, Table 1). WO’263 teaches that these genes could be reduced or suppressed to turn up activation in the engineered immune cells (page 25, 22-24). WO’263 further teaches disruption of CTLA4 (page 26, line 8; table 1, row 1), TIM3 (page 26, table 1, row 4), and/or LAG3 (page 26, Table 1, row 4).
WO’263 further teaches that Table 4 provides a selection of antigen markers of various cancers found to be expressed on the surface of T cells. The inactivation of the genes encoding these antigen markers is proposed as part of one of the gene editing steps according to the disclosure (page 11, lines 28-32). Table 4 of WO’263 discloses cluster of differentiation (CD) antigen markers including CD317, also known as BST2 or HM1.24 (page 59, Table 4, row 10). WO’263 further teaches that table 4 provides a selection of antigen markers of various cancers found to be expressed on the surface of T cells. The inactivation of the genes encoding these antigen markers is proposed as part of one of the gene editing steps according to the invention, especially when the engineered immune cells are endowed with chimeric antigen receptors targeting these very antigens (page 11, line 28-32).
WO’263 further teaches that the immune cell is a T cell and that the T cells are from peripheral blood mononuclear cells (PBMC) (page 7, claim 18; page 1, lines 23-24). Alternatively, WO’263 teaches that the T cells are tumor infiltrating lymphocytes collected from a patient, engineered, and re-infused into said patient (page 10, lines 11-13). WO’263 teaches that the tumor infiltrating lymphocytes are from tumors (page 13, line 34). WO’263 further teaches that the immune cell is derived from a healthy donor, a patient diagnosed with cancer, or a patient diagnosed with an infection and that the cell is part of a mix population of immune cells which comprise CD4, CD8, and CD56 positive cells (page 13, line 34 - page 14, line 4)
WO’263 teaches that gene editing can also be performed on a receptor or surface protein, such as TCR. The sequence specific reagent can permanently reduce or prevent expression of TCR by the primary T-cell (page 5, lines 17-23; page 7, claim 20). WO’263 further teaches that recently, engineered T cells disrupted in their TCR using TALE-nucleases, endowed with CARs targeting CD19, had shown therapeutic potential in at least two infants who had refractory leukemia (page 3, lines 6-13).
WO’263 also teaches embodiments in which the TCR is edited in combination with two of the disclosed genes involved in immune cell inhibitory pathways (page 27, lines 1-15).
WO’263 further teaches that the methods disclosed, which use sequence specific endonuclease reagents, can be combined with other types of cell transformation not involving sequence specific endonuclease reagents, such as retroviral transduction. This is of particular interest, for instance, for the production of primary immune cells expressing a recombinant receptor, such as a chimeric antigen receptor (CAR) or a recombinant TCR. Such chimeric receptors are generally encoded by exogenous sequences which are introduced into the cells by means of viral vectors, in particular lentiviral vectors. It is therefore advantageous to combine the sequential gene editing steps of the present invention with viral transduction steps, such as illustrated in figures 3, 5, 6, and 7 (page 16, lines 17-25).
WO’263 further teaches therapeutic compositions comprising populations of engineered cells and teaches that such compositions or populations of cells can be used as a medicament, especially for treating cancer (page 33, lines 19-28; page 34, lines 5-6). The cells or population of cells can be administered in one or more doses, for instance, the effective amount of cells are administered as a single dose or as more than one dose over a period of time. While individual needs vary, determination of optimal ranges of effective amounts of a given cell type for a particular disease or conditions are within the skill of the art. An effective amount means an amount which provides a therapeutic or prophylactic benefit (page 35, lines 25-35). WO’263 further teaches that the treatment with the engineered immune cells may be in combination with one or more therapies against cancer selected from the group of antibodies, chemotherapy, cytokines therapy, DC therapy, gene therapy, hormone therapy, laser light therapy, and radiation therapy (page 35, lines 2-5).
WO’263 further teaches that the gene editing is to improve the efficiency of the engineered immune cells. Any gene inactivation listed under each function in Figure 1 can be combined with another to obtain a synergistic effect on the overall therapeutic potency of the immune cells (page 24, lines 1-4). WO’263 further teaches that the efficiency of the engineered cells are improved (page 26, lines 9-10). WO’263 teaches sequential gene editing to obtain immune cells with higher recovery, better activation, persistence or therapeutic efficacy (page 5, lines 12-16).
WO’263 teaches that the genes are reduced or suppressed and also teaches knockout of the gene expression (page 25, lines 22-24; page 42, lines 8-13). WO’263 further teaches that the reagents permanently reduce or prevent expression of the genes (page 8, claim 21), indicating knockout of the genes.
It would have been prima facie obvious to one of ordinary skill in the art prior to the effective filing date of the claimed invention to produce a BST2 targeting CAR T cell that has disrupted BST2 gene expression and to further disrupt expression of at least one endogenous gene that is involved in an immune cell inhibitory pathway, including PD-1 and SIT1, based on the teachings of WO’263.
It would have been obvious to produce a BST2 targeting CAR T cell that has disrupted BST2 gene expression as WO’263 teaches that BST2 is an antigen that is present in cancers and is also expressed on the surface of T cells and proposes gene editing of the antigen markers especially when the engineered immune cells are endowed with CARs targeting the antigen. Therefore, one of ordinary skill in the art would have had a reasonable expectation of success.
An ordinarily skilled artisan would have been motivated to further disrupt at least one endogenous gene that is involved in an immune cell inhibitory pathway in order to turn-up activation in the engineered immune cells and improve efficacy (page 25, lines 22-24; page 26, lines 9-12). It would have also been obvious to have these genes include both PD-1 and SIT1 as WO’263 teaches the genes as being involved in immune cell inhibitory pathways. WO’263 also suggests that combining gene disruptions can provide synergistic effect on the overall therapeutic potency of the immune cells and provides examples with at least two targeted immune inhibitory genes. An ordinarily skilled artisan would have had a reasonable expectation of success as WO’263 teaches methods for double, triple, or quadruple gene edited T cells for therapeutic use. WO’263 also discusses the function of each of PD-1, SIT1, and BST2 for the proposed modifications demonstrating that the disruption would lead to predictable results including enhancing efficacy and activity.
The selection of PD-1 and SIT1 gene disruption in BST2 depleted T cells with CARs targeting BST2 is further supported by KSR(E) and KSR(B).
With regards to KSR(E), WO’263 teaches a finite number of genes involved in immune cell inhibitory pathways as well as their function in Table 1. WO’263 also suggests double, triple, or quadruple gene editing of the T cells and provides examples in which two immune cell inhibitory pathways are edited. For instance, TCR, PD1 and LAG3; TCR, PD1 and FOXP3; TCR, CTLA4 and LAG3; or TCR, CTLA4 and FOXP3. As such, it would have bene obvious to one of ordinary skill in the art to pursue combinations of the immune cell inhibitory pathways in Table 1 in the BST2 depleted T cells with CARs targeting BST2 with a reasonable expectation that the disruption of the immune cell inhibitory genes would provide enhanced activity and efficacy of the engineered T cells.
With regards to KSR(B), WO’263 provides preferred embodiments in which the TCR and two immune cell inhibitory pathways are disrupted. For instance, TCR, PD1 and LAG3; and TCR, PD1 and FOXP3. It would have been obvious to make these modifications in the BST2 depleted T cells with CARs targeting BST2 and to have further substituted the LAG3 or FOXP3 with SIT1 based on the teachings of WO’263. Specifically, WO’263 teaches that LAG3 and FOXP3 are immune cell inhibitory pathways and also teaches that SIT1 is an alternative immune cell inhibitory pathway. Therefore, one of ordinary skill in the art would have been able to substitute LAG3 or FOXP3 with SIT1 with a reasonable expectation that the disruption of the immune cell inhibitory genes would provide enhanced activity and efficacy of the engineered T cells.
Regarding claim 14, as discussed above, WO’263 teaches reagents that permanently reduce or prevent expression of the disclosed genes, indicating knockout of the genes. WO’263 also teaches methods of making triple or quadruple gene inactivated cells. It would have been prima facie obvious to one of ordinary skill in the art prior to the effective filing date of the claimed invention to use the methods disclosed by WO’263 to knockout the disclosed genes, which include PD-1, SIT1, and BST2 with a reasonable expectation of success. The triple knockout of all three genes meets the instant claim limitation of knockout of one or more of STI1, BST2, and PD-L1. While WO’263 does not explicitly disclose knockdown, in the broadest reasonable interpretation of the claim, the claim does not require knockdown when all three genes are disrupted via knockout. That said, WO’263 also teaches that the expression could be reduced, which is suggestive of knockdown of gene expression.
Regarding claim 37, based on the teachings of WO’263, an ordinarily skilled artisan would reasonably expect that the engineered cells would overcome immunosuppression in the tumor microenvironment. WO’263 teaches gene editing steps aimed to disrupt the expression of a protein involved in immune cell inhibitory pathways, such as immune checkpoints. Such immune cell inhibitory pathways are taught to mean any gene expression in immune cells that leads to a reduction in the cytotoxic activity of the lymphocytes towards malignant or infected cells (page 24, lines 25-34). As WO’263 teaches disruptions that will overcome such inhibitory pathways and administration of the cells to treat cancers, an ordinarily skilled artisan would reasonably expect that the inhibitory pathways, such as the immune checkpoints, in the tumor microenvironment would be overcome.
Response to Arguments
Applicant’s arguments in the response filed 06/25/2026 have been fully considered but are not persuasive.
In the response, applicant argues that BST2 is disclosed in a different functional context in WO’263. Applicant argues that WO’263 teaches BST2 disruption especially when the engineered immune cells have a CAR targeting the antigen and that WO’263 does not teach disrupting BST2 as a general immunological enhancement strategy. Rather, BST2 disruption is taught for a different purpose: to prevent CAR T cells from killing each other (fratricide). Applicant argues that WO’263 specifically addresses anti-fratricide. Applicant argues that this has nothing to do with immune checkpoint inhibition and that BST2 is not listed anywhere in Table 1.
This argument is not persuasive.
Even if WO’263 teaches disrupting BST2 when the T cell also expresses a CAR targeting BST2 for the purposes of preventing fratricide, such disruption still meets the limitations of the instantly claimed invention which encompasses any immune cell comprising engineered disruption in SIT1, BST2, and PD-1. Furthermore, the reason or motivation to make the modification in the reference does not need to be for the same purpose that applicant is making the modification. See MPEP 2144 IV., which states “[t]he reason or motivation to modify the reference may often suggest what the inventor has done, but for a different purpose or to solve a different problem. It is not necessary that the prior art suggest the combination to achieve the same advantage or result discovered by applicant.”
It is also noted that the rejection of the instant office action has been amended to be clear that it would have been obvious to disrupt at least one immune inhibitory gene, including both PD-1 and SIT1, as well as BST2, particularly in CAR T cells in which the CAR targets BST2. An embodiment which still meets the instant claim limitations which only require a composition comprising at least one immune cell is engineered to comprise disruption in expression of SIT1, BST2, and PD-1. As discussed above, the reason for the modification to arrive at the instantly claimed product does not need to be the same as applicant’s.
Applicant further argues that WO’263 does not disclose the specific combination of SIT1, BST2, and PD-1. Applicant argues that WO’263 states preference for the production of immune cells combining gene editing for different combinations. Applicant argues that one of ordinary skill in the art would be directed towards these combinations, not toward the combination of SIT1, BST2, and PD-1. Applicant references WO’263 as stating that preference is given to inactivation of PD1, CTLA4, in combination with TCR. Applicant argues that SIT1 and BST2 are not mentioned as preferred targets in any combination.
This argument is not persuasive.
WO’263 is not required to explicitly disclose a specific combination of SIT1, BST2, and PD-1 as the rejection is not an anticipation rejection under 35 USC 102, but rather an obviousness rejection under 35 USC 103. As discussed in the rejection, and in applicant’s response, WO’263 teaches immune inhibitory genes for disruption including PD-1 and SIT1. WO’263 also teaches embodiments in which two immune inhibitory genes are disrupted. For instance, as recited in the response, TCR, PD1, and LAG3; TCR, PD1, and FOX3; TCR, CTLA4, and LAG3; etc. As such, it would have been obvious to interrupt two inhibitory genes, including PD-1 and SIT1, in T cells including those that have BST2 targeting CARs and BST2 gene knockouts.
Although WO’263 provides alternative embodiments, the teaching of alternative, even preferred, embodiments is not sufficient in itself to overcome a prima facie case of obviousness.
MPEP 2143.01 states “The disclosure of desirable alternatives does not necessarily negate a suggestion for modifying the prior art to arrive at the claimed invention. In In re Fulton, 391 F.3d 1195, 73 USPQ2d 1141 (Fed. Cir. 2004)”.
MPEP 2123 states “"[t]he 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).”
Applicant further argues that an ordinarily skilled artisan would not have “envisage” the specifically claimed combination and references page 11 of the office action of 04/10/2026 as stating that one would have “envisaged” the claimed combination. Applicant argues that WO’263’s claim 22 discloses a list of immune checkpoint genes that can be inactivated that includes approximately 50 distinct genes and that table 4 discloses approximately 100+ cancer antigen markers. Applicant argues that to say that one would envisage each member of possible combinations defies the legal standard.
Applicant’s reference to page 11 of the office action of 04/10/2026 is specifically to the statement “Because WO’263 discusses the benefits of triple and quadruple gene inactivation, one of ordinary skill in the art would have also envisaged triple or quadruple combinations of the genes disclosed for disruption.” The statement is not made with regards to the specifically claimed combination, nor does the obviousness rely exclusively on one of ordinary skill in the art being able to envisage the exact combination all at once from the disclosure of WO’263. Rather, the rejection relies on teachings from WO’263 in which at least one immune cell inhibitory pathway is disrupted in a T cell that comprises a BST2 targeting CAR with the BST2 gene disrupted. As discussed by applicant, WO’263 teaches approximately 50 distinct immune checkpoint genes, which includes PD-1 and SIT1. In table 1, WO’263 also provides the pathway and function that each of these genes has in immune inhibition. For instance, PD-1 is taught to be a co-inhibitory receptor and SIT1 is taught to prevent TCR signaling. As WO’263 teaches double, triple, and quadruple gene targeting, one of ordinary skill in the art would have reasonably arrived at the instantly claimed invention for the reasons discussed in detail in the rejections of the instant office action.
Applicant further argues that there is no teaching of functional synergy for the specifically claimed combination. Applicant argues that WO’263 teaches synergy in the context of specific, functionally related combinations. Applicant argues that WO’263 does not teach or predict synergy when combining genes from entirely different functional categories.
The rejection references synergy teachings of WO’263 not to suggest that WO’263 teaches that the instantly claimed triple combination would result in synergistic results, but rather to demonstrate that WO’263 considered advantages in combining gene disruption of multiple immune inhibitory pathways. Additionally, while applicant interprets the statement to indicate synergy among genes within the same functional categories, e.g., combining multiple immune checkpoint knockouts, such as PD-1 and CTLA-4; the statement could also be interpreted as being a combination of one of the functional categories with another. For instance, in addition to combinations of PD-1 and CTLA-4, WO’263 also teaches combinations that include PD-1 and FOXP3 or CTLA4 and FOXP3. In these cases, PD-1 and CTLA4 are both co-inhibitory receptors but FOXP3 is identified as inducing Tregs (table 1). Based on this, it is not apparent that WO’263 only considered combinations comprising two genes from the same functional pathway.
It is noted that the examples of the instant disclosure have been considered for the presentation of synergistic results when the combination of claimed genes are disrupted. Figure 9 is replicated below for convenience.
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In figure 9, SIT[1] + BST2 + PD1 modified T cells are shown to have higher MC38 tumor killing compared to controls, single gene modifications, as well as double combinations including SIT1 + BST2 and BST2 + PD-1 at the T cell : tumor ratio of 10:1. The example; however, does not provide a comparison to the double combination of SIT1 + PD-1, or any of the combinations suggested by WO’263, in order to demonstrate that the increased killing is a result of the triple combination as opposed to the combination of SIT1 and PD-1, or the disruption of two alternative immune inhibitory domains. If applicant has additional data to support synergistic results of the claimed combination compared to the closest prior art, such data could be presented, including in the form of a declaration, for consideration.
Applicant further argues that the response to hindsight reasoning arguments is insufficient. Applicant argues that the only “knowledge” that would lead to the selection of SIT1 + BST2 + PD-1 from among hundreds of thousands of possible combinations is applicant’s own disclosure.
The rejections of the instant office action have been modified to demonstrate that the production of BST2 targeting CAR T cells with BST2 gene disruption would have been obvious and that it would have further been obvious to disrupt immune inhibitory genes as disclosed by WO’263, which include both PD-1 and SIT1. The rejection does not rely on applicant’s disclosure for the selection of the genes; but rather on the teachings of the prior art which directly suggests the disruption of BST2 when the T cell comprises a CAR that targets BST2 as well as the disruption of inhibitory genes which include PD-1 and SIT1. The rejection relies on the teachings of the cited prior art reference and only takes into account knowledge within the level of an ordinarily skilled artisan at the time of the claimed invention.
Additionally, WO’623 does not have to expressly disclose that SIT1 is “preferred” as suggested by applicant. WO’623 teaches a finite number of immune inhibitory signaling pathways and it would reasonably be expected that any of these could be selected resulting in enhanced efficacy and activation of the T cells. Furthermore, as discussed in MPEP 2143.01 I, even the disclosure of desirable alternatives does not necessarily negate a suggestion for modifying the prior art to arrive at the claimed invention. In In re Fulton, 391 F.3d 1195, 73 USPQ2d 1141 (Fed. Cir. 2004),
Applicant also argues that there is no teaching to combine BST2 with immune checkpoint genes outside of the anti-BST2 CAR context. This context; however, still meets the limitations of the instantly claimed invention and the rejection has been modified to reflect such context disclosed by WO’623.
It is also noted that explicit motivation in the prior art is not required in order establish a prima facie case of obviousness. MPEP 2143 provides 7 exemplary rationales that may be used to support a conclusion of obviousness, KSR (A)-(G), only one of which requires that there be some teaching, suggestion, or motivation in the prior art. The modified rejections of the instant office action rely on motivation to include gene disruption of inhibitory pathways and KSR(A) for the selection of SIT1 and PD-1 specifically. The selection of the inhibitory pathway genes is further supported by KSR(E) and KSR(B). None of KSR(A), KSR(E), or KSR(B) require explicit motivation in the art in order to arrive at the instantly claimed invention.
Applicant further argues that the significance of the open ended “comprising” language is misread. Applicant argues that the claim defines a composition requiring disruption of the three specifically recited genes at a minimum. Applicant argues that a reason to select these three genes together, regardless of how many additional genes may also be disrupted, has not been identified.
The rejections in the instant office action have been modified to further detail the obviousness of including disruption of the three claimed genes in the T cells of WO’263.
In the office action of 04/10/2026, the scope of the instantly claimed invention, and the use of “comprising” language was discussed in order to demonstrate that any number of genes disclosed in WO’263 could be disrupted and meet the instant claim limitations so long as they include SIT1, BST2, and PD-1, an interpretation which is consistent with the interpretation offered by applicant in the response.
Conclusion
No claims are allowed.
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/AUDREY L BUTTICE/Examiner, Art Unit 1647
/SCARLETT Y GOON/Supervisory Patent Examiner
Art Unit 1693
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