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 .
DETAILED ACTION
Applicant’s submission dated 05/08/2024 is duly acknowledged.
Claims 1-14 as currently presented are pending in this application, and have been examined on their merits in this action hereinafter.
Priority
This application is a CON of 18/341,692 (filed on 06/26/2023, now ABN), which is a CON of 16/533,109 (filed on 08/06/2019, now a US PAT 11723923), which is a CON of 15/299,394 (filed on 10/20/2016, now ABN), which claims domestic priority benefit from a US PRO 62/244,036 filed on 10/20/2015.
Claims
Instant claims 1-14 as currently presented have been interpreted and treated as Product-by-Process claims.
"[E]ven though product-by-process claims are limited by and defined by the process,
determination of patentability is based on the product itself. The patentability of a product
does not depend on its method of production. If the product in the product-by-process
claim is the same as or obvious from a product of the prior art, the claim is unpatentable
even though the prior product was made by a different process." In re Thorpe, 777
F.2d 695, 698, 227 USPQ 964, 966 (Fed. Cir. 1985).
NOTE: 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.
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.
1. Claims 1-11 (as presented) are rejected under 35 U.S.C. 103 as being unpatentable over Unutmaz (US 2013/0045491 A1; cited in applicant’s IDS dated 09/19/2024) taken with Van der Waart et al (2014, NPL cited in applicant’s IDS dated 09/19/2024).
Claim 1 is directed to “A population of T cells prepared by a method comprising culturing a lymphocyte sample in a culture medium comprising exogenous interleukin-7 (IL-7) and exogenous interleukin-15 (IL-15) for 1 to 10 days, wherein:
the culturing is in the absence of exogenous interleukin-2 (IL-2);
the lymphocyte sample comprises CD4+ T cells; and
at least 30% of the T cells in the population are immature or undifferentiated T cells.”
Claim 5 is directed to “The population of T cells of claim 1, wherein the culture medium further comprises an AKT inhibitor.”
See also limitations of claims 2, 3, 4, and 6-11 as currently presented.
Unutmaz (2013), while disclosing in vitro methods for activating T cells in order to prepare a population of activated T cells (see abstract, summary of the invention on pages 2-3), disclose the method for delaying or inhibiting T cell maturation or differentiation in vitro (the activated population of cells intended for use in T cell therapy by inhibiting IL-17/IL-22 in population of T cells that are useful for therapeutic purposes in patients in need thereof; see abstract, [0067], [0082]-[0084], [0158], for instance); wherein the method comprises contacting isolated CD4+ T cells (see Example 1, [0139], Fig. 1, for instance) from a subject in need with an AKT inhibitor (such as AKT-1/2 inhibitor, that acts directly on Akt by binding to it; see instant claim 5-6 for such inhibitors as recited by applicants; it is noted that instant claim 1 does not require presence of an AKT inhibitor, per se) and one or more of exogenous interleukins (IL) such as IL-7 or IL-15, in a serum-free culture medium (see abstract, [0067], Example 1 section “Human T Cell Purification and Activation”, for instance); wherein the resulting T cells exhibit delayed maturation or differentiation (see [0037], [0076], [0083]-[0084], [0158], for instance) and improved T cell function when compared to control cells that were cultured in absence of said AKT inhibitor; and wherein T cell function includes increased T cell activation and proliferation by repressing c-cytokine-driven IL-17/IL-22 expression (see abstract, [0010], in particular). Unutmaz discloses the method for preparing activated T cells, wherein the AKT-1/2 inhibitor is used in the culture medium at an amount of 1-10 g/ml for 2 days (see [0158]; at 10 g/ml, i.e. equivalent to about 18 M using the molecular weight of 552 Daltons for AKT-1/2 inhibitor); wherein the T cells are T helper cells isolated from peripheral blood lymphocytes of patients in need (see [0005], [0015], and Example 1, for instance); wherein the concentration of one or more exogenous cytokines in the serum-free medium is at least 0.1 ng/ml to 50 ng/ml, or more (i.e. IL-7, and/or IL-15; see [0015], Example 1 that uses 20 ng/ml of the cytokines, for instance; i.e. “at least 7 ng/ml IL-7” or IL-15); wherein the incubation (i.e. contacting with IL-2, IL-7 or IL-15 can be performed from at least 2 hours to ten (10) days or more; see [0016], claims 9, 19 disclose “at least 2 days”, also see [0156], [0158], for instances); and wherein Unutmaz discloses that IL-7 and IL-15 can act as substitute for IL-2 (see [0156], in particular), and that the resulting population of activated T cells (i.e. contacted with said AKT inhibitor) show repressed expression of IL-17/IL-22, however do not show altered expression of interferon-gamma (IFN-; see [0156]-[0158], for instance). Unutmaz discloses that the such in vitro activated T cell population can be used as therapeutic modalities for various diseases where TGF signaling is involved in promoting tumors such as breast and lung cancer (see [0033], also see [0101], for instance), and where TH17 or Th22 related genes play a role such as in prostate and breast cancers.
However, Unutmaz does not explicitly disclose and/or exemplify the population of T cells using a method wherein: 1) the CD4+ T cells are cultured in the presence of both IL-7 and IL-15 (and in the absence of IL-2; see instant claim 1); and wherein specific AKT inhibitor is as recited in instant claim 7 (i.e. an AKT inhibitor VIII).
Van der Waart et al (2014) disclose that inhibition of Akt signaling promotes the generation of superior tumor reactive T cells that can be used for adoptive cancer immunotherapy (see title, abstract, in particular), wherein they disclose the art-known fact that “effective T-cell therapy against cancer is dependent on the formation of long-lived, stem cell-like T cells with the ability to self-renew and differentiate into potent effector cells” (see Abstract), and wherein they experimentally demonstrate that by inhibiting the Akt pathway, one can generate highly potent MiHA-specific CD8+ T cells ex vivo, wherein the Akt-inhibited CD8+ T cells showed superior expansion potential upon removal of the Akt inhibitor, which results in a superior antitumor effect in mice, thus providing a strategy that is expected to be safe and potent as additive T-cell therapy after allogeneic stem cell transplantation (see entire section “Introduction”). They further disclose the method for isolating/obtaining patient’s naïve T cells from blood samples (see section “Materials and methods” and subsection “In vitro Akt inhibitor VIII treatment and priming of MiHA-specific T cells”, in particular), which were treated in vitro in culture with 8 M of Akt inhibitor VIII (reads on instant claim 7; 50% inhibitory concentration, 58 nM, 210 nM, and 2.12 M for Akt1, Akt2, and Akt3, respectively) in combination with cytokines (such as 50 U/ml IL-2, 5 ng/ml each of the IL-7 and IL-15) and MiHA peptide loaded dendritic cells in order to prime said naive T cells from patients in a co-culture conditions (see subsection “In vitro Akt inhibitor VIII treatment and priming of MiHA-specific T cells”, in particular), wherein the resulting MiHA-specific CD8+ T cell population contained a high number of stem cell-like T cells compared with terminal differentiated effector T cells in control cultures (i.e. that were not treated with Akt inhibitor), and showed superior anti-tumor effect in intrafemural multiple myeloma-bearing mice (see abstract, in particular), wherein the resulting T cells showed increased mRNA expression of the effector molecules IFN and PRF1 (see Figure 2H, and entire section “Generation of stem cell-like MiHA-specific CD8+ T cells by inhibiting Akt signaling”, in particular 3rd paragraph) compared with controls. In addition, they showed that CD62L, CCR7 and CD28, surface markers expressed by less differentiated T cells, were expressed on Akt-inhibited MiHA-specific CD8+ T cells to a higher level compared with controls (see Figure 2F, for instance). They also disclose art-known fact that certain subset of memory cells including stem cell memory T cells (Tscm) and central memory T cells (Tcm) are more favorable activated T cell populations for MiHA-based adoptive immunotherapy, as the Tscm and Tcm cells are known for their property of enhanced proliferation, self-renewal and multipotency, and they also provide better chance to generate long-term antitumor T-cell responses and ultimately eliminate all residual malignant cells (see Introduction, entire 2nd paragraph, for instance; and Fig. 1). More importantly, they demonstrated that Akt-inhibited CD8+ T cells were superior in proliferation capability, which resulted in highly functional effector T cells (see section “Discussion”, 4th paragraph, for instance) that showed less replicative senescence characteristics, greater expression of co-stimulatory molecules such as CD28, and increased expression of cytokine receptors such as IL-7R and markers such as CXCR4 that may help such T cells home more effectively to the bone marrow for their in vivo antitumor effects shown in experimental model using mice. Thus, Van der Waart et al conclude that “inhibiting Akt signaling during the ex vivo priming, expansion, and culture of MiHA-specific CD8+ T cells gives rise to potent tumor-reactive T cells” (see “Discussion”, last paragraph).
Thus, given the detailed benefits and motivation for using Akt signaling inhibition of T cells (performed in culture in vitro in the presence of one or more cytokines; for example, combinations of IL-7 and IL-15; see teachings from Van der Waart et al, as discussed above), a person of ordinary skill in the art would have modified the method disclosed by Unutmaz in order to employ combination of IL-7 and IL-15 (and remove IL-2, as it was known that IL-7 and IL-15 can be substituted for IL-2; see Unutmaz, above) for preparation of activated T cell population in culture, and can further include CD8+ T cells obtained from patients undergoing T cell therapy of cancer in order to achieve a superior T cell functionality, especially in terms of obtaining potent tumor-reactive T cells (having desired markers; see discussion from Van der Waart et al, above) expressing higher amounts of effector molecules such as IFN, and that could be broadly exploited for the adoptive immunotherapy of cancer and viral infections (as disclosed by Van der Waart et al, discussed above). Since, generation of such stem cell-like CD8+ T cells having highly potent tumor-reactive functionality have been experimentally demonstrated (in vitro as well as in mouse model of cancer) by Van der Waart et al, it would have been obvious to an artisan of ordinary skill in the art before the effective filing date of this invention, to incorporate steps suitable to obtain inhibition of Akt signaling in T cells in order to potentiate and transform T cells into effective treatment modality for cancer immunotherapy, as already shown by Van der Waart et al. Since, the same amounts of combination cytokines (i.e. IL-7 and IL-15, without the need for employing IL-2, as specifically suggested by Unutmaz discussed above), duration of activation, and the same Akt inhibitor have been shown to be effective in the method for activating population of T cells (both CD4+ and CD8+ cells) in culture by the cited references as discussed above, such modification in the method for preparing activated T cell population (and thus the resulting population of activated T cells comprising CD4+ T cells) would have been obvious and/or fully contemplated by an artisan of ordinary skill in the art of T cell therapy of cancer, unless evidence provided on record to the contrary (which is currently lacking on record; see parent disclosure in 15/299394, Examples 1-6). In addition, the limitations of specific markers for the resulting naïve and undifferentiated population of T cells would be intrinsic to the activated T cells (as already disclosed by Van der Waart et al, above), the percentage of which can be optimized by an artisan in the art given the detailed procedural disclosure from the cited prior art references of record, as discussed above.
Thus, the population of activated lymphocyte sample comprising CD4+ T cells prepared by the method as currently claimed (i.e. in the presence of suitable amounts of cytokines such as IL-7 and IL-15, without the need of exogenous IL-2 in culture), and further in the presence of an AKT inhibitor as claimed, fails to distinguish itself over the combined teachings and/or suggestions from the cited prior art as discussed above.
2. Claims 12-14 (as presented) are rejected under 35 U.S.C. 103 as being unpatentable over Unutmaz (US 2013/0045491 A1; cited in applicant’s IDS dated 09/19/2024) taken with Van der Waart et al (2014, NPL cited in applicant’s IDS dated 09/19/2024) as applied to claims 1-11 above, and further in view of Sadelain et al (US 7,446,190 B2, USPAT cited in applicant’s IDS dated 09/19/2024).
Claims 12-14 are directed to the population of T cells of claim 1, wherein the T cells are transduced with a retrovirus (claim 12); wherein the retrovirus comprises a heterologous gene encoding a T cell receptor (TCR) or a chimeric antigen receptor (CAR) (claim 13); which is capable of binding an antigen, from the list as specifically recited in instant claim 14.
The teachings and/or suggestions of Unutmaz taken with Van der Waart et al for the population of activated T cells prepared by the method of culturing lymphocytes (comprising CD4+ T cells) in vitro in the presence of a combination of cytokines, and with treatment of suitable Akt signaling inhibitor, have been discussed above in details, and are further relied upon in the same manner hereinafter.
However, the population of T cells, wherein the T cells are transduced with a retrovirus” (comprising a heterologous gene encoding a TCR, or a CAR, that are capable of binding CD19 (one of the antigens as listed in instant claim 14) has not been explicitly disclosed by the cited references of Unutmaz taken with Van der Waart et al, as discussed above.
Sadelain et al (2008), while disclosing nucleic acids encoding chimeric T cell receptors (see title and abstract, summary of the invention, and claims), disclose T cells transduced with retroviral constructs having suitable genes encoding a chimeric T cell receptors (i.e. CAR T cells) comprising intracellular domain of human CD3 chain, a costimulatory signaling region, and a binding element that specifically interacts with a selected target such as CD19 (see Sadelain et al, claims 1 and 5, for instance), wherein the CAR T cells can be used for induction of potent tumor immunity, a major challenge for cancer immunotherapy (see abstract, column 1, lines 13-28, and summary of the invention on column 2) in order to facilitate T cell response to a specific target. Sadelain et al disclose the fact that T-lymphocytes from the individual to be treated, for example a human individual, are transduced with the chimeric TCR, which may be done ex vivo, after which the cells are re-introduced into the individual (i.e. autologous T cell therapy of cancer, for instance; see Summary, on column 2, lines 31-36) in order to enhance and/or stimulate the T cell immune response in the treated individual at the selected target cells (such as tumors; see column 4, 4th paragraph, in particular). Thus, Sadelain et al disclose the motivation for transducing T cells (comprising both CD4+ and CD8+ T cells; using heterologous retroviral gene constructs; see column 2, lines 45-56, Fig. 5 A-F, and Examples 1-3, for instance) with suitable TCR or chimeric constructs that can bind and selectively target tumor cell antigens (such as CD19; see Examples 7-8 on column 11), and therefore activate immune response against such tumor targets in vivo (see column 7, lines 4-40, for instance).
Thus, given the explicit disclosure and motivation provided by Sadelain et al that relates to cancer immunotherapy using in vitro activated population of T cells (that can comprise both CD4+ and CD8+ T cells) that can be further engineered using retroviral gene constructs in order to target selected tumor cells in vivo (such as using CAR T cells that can specifically bind CD19 expressed on tumor cells, for instance), it would have been obvious to an artisan of ordinary skill in the art (before the effective filing date of this invention, as claimed) to further include steps that can provide selectivity and/or targeting capability of such T cells that can be re-introduced into an individual in need thereof during activated T cell-based cancer immunotherapy, as already disclosed by the cited references of Unutmaz taken with Van der Waart et al, as discussed above. Since, such constructs can be designed as per need based on the selected target tumor(s) and their specific antigen profile(s), incorporation of such a step in the T cell activation method would be readily envisioned by an artisan in the art involved in T cell therapy (i.e. for preparing an activated population of T cells), unless evidence/data provided by applicants to the contrary (which is currently lacking on record; see for instance, the variety of target antigens listed by the applicants in instant claim 14).
Thus, the invention as a whole would have been prima facie obvious to a person of ordinary skill in the art, before the effective filing date of the invention as currently claimed.
As per MPEP 2111.01, during examination, the claims must be interpreted as broadly as their terms reasonably allow. In re American Academy of Science Tech Center, F.3d, 2004 WL 1067528 (Fed. Cir. May 13, 2004)(The USPTO uses a different standard for construing claims than that used by district courts; during examination the USPTO must give claims their broadest reasonable interpretation.). This means that the words of the claim must be given their plain meaning unless applicant has provided a clear definition in the specification. In re Zletz, 893 F.2d 319, 321, 13 USPQ2d 1320, 1322 (Fed. Cir. 1989).
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
1. Claims 1-14 (as presented) are rejected on the ground of nonstatutory double patenting as being unpatentable over at least claim 1 of U.S. Patent No. 11,723,923 B2 (issued to common inventors and assignee; on August 15, 2023, from the parent US application 16/533,109 filed on August 6th, 2019). Although the claims at issue are not identical, they are not patentably distinct from each other because issued claim 1 of US’923, while drawn to a method of culturing T cells, recites the same method that is currently being used for making the “population of T cells” in the instant application under examination. Issued claim 1 of US’923 recites the following:
“A method for culturing T cells for a T cell therapy while delaying or inhibiting maturation or differentiation of the T cells, comprising:
contacting, in a culture medium, one or more T cells with exogenous Interleukin-7 (IL-7) and exogenous Interleukin-15 (IL-15) in the absence of exogenous Interleukin-2 (IL-2),
wherein the one or more T cells comprise CD4+ T cells, and the contacting is for 1 day to 10 days such that the CD4+ T cells, following such contacting, comprise a higher percentage of naive T cells and central memory T (Tcm) cells as compared to when the CD4+ T cells are contacted with exogenous IL-2 in the absence of exogenous IL-7 and exogenous IL-15.”
Thus, it is clear that the issued claim 1 in US’923 represents essentially the same preparation method that results in the same population of cells as currently claimed (in the form of product-by-process claims) in instant CON application under examination. Therefore, an ODP rejection is still deemed proper.
Conclusion
NO claims are currently allowed.
Pertinent Prior Art:
1. GEGINAT J. et al. (2001; NPL cited in applicant’s IDS dated 09/19/2024)- “Cytokine-driven Proliferation and Differentiation of Human Naïve, Central Memory, and Effector Memory CD4+ T Cells”, J. Exp. Med., 2001, vol. 194 (12), pages 1711-1719 (disclose human CD4+ naïve T, TCM, and TEM cells for their capacity to proliferate in response to cytokines that have been implicated in T cell homeostasis including IL-7 and IL-15, that expanded with very high efficiency TEM, while TCM were less responsive and naïve T cells failed to respond. They also disclose that “while IL-7 acts synergistically with IL-15 on all CD4+ T cell subsets, only TEM can directly proliferate in response to these cytokines, as naïve and TCM require DCs or DC-derived cytokines to upregulate the relevant receptors”. They also disclose the art-known fact that both memory CD4+ and CD8+ T cell comprise at least two functionally distinct subsets- one including nonpolarized “central memory” T cells (Tcm) which express the chemokine receptor CCR7 and CD62L, and home to the T cell areas of secondary lymphoid organs.. (see Abstract, entire Introduction, and Results, Fig. 2A; and page 1717, right column, 1st paragraph, in particular).
2. BONINI et al (US 8,999,715 B2; cited as ref. [A] on PTO 892 form) – “Use of common g chain cytokines for the visualization, isolation and genetic modification of memory T lymphocytes” (described in vitro methods for expanding, detecting or isolating rare populations of antigen specific memory T cell population that is CD4+ or CD8+, prepared by treating, for 3-4 days, activated lymphocytes in vitro in a cell-free medium with effective amounts of IL-7 and IL-15 at 5-50 ng/ml concentrations, in order to selectively expand/enrich populations of memory T cells, up to 80% of which are central memory T lymphocytes and comprise undifferentiated T cell marker expression including CD62L, CCR7, CD127; see Abstract; column 1, ll. 46-57; column 3, ll. 48-67 and column 4, ll. 1-7; column 5, ll. 38-47; column 29, section “Generation of Gene-Modified Central Memory Human T-Cells” and Fig. 27C; Figs. 6 and 31; and claim 1, for instances).
Any inquiry concerning this communication or earlier communications from the examiner should be directed to SATYENDRA K. SINGH whose telephone number is (571)272-8790. The examiner can normally be reached M-F 8:00- 5:00.
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SATYENDRA K. SINGH
Primary Examiner
Art Unit 1657
/SATYENDRA K SINGH/Primary Examiner, Art Unit 1657