DETAILED ACTION
Notice of Pre-AIA or AIA Status
1. The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
2. Applicant’s reply filed on 6/26/2026 is acknowledged. Claims 1-14, 16 and 23-26 are pending. Claims 15, 17-22 and 27-56 are canceled.
3. Claims 1-14, 16 and 23-26 are under examination.
Information Disclosure Statement
4. The information disclosure statement (IDS) submitted on 4/20/2026 has been considered by the examiner.
Objections and Rejections withdrawn
5. All objections and rejections in the office action mailed on 3/26/26 except those maintained below are withdrawn in view of applicant’s amendments.
Objections Maintained
6. The objection to claim 12 because the last step of the claim does not correlate with the preamble is maintained as applicant failed to respond to the objection.
Rejections Maintained
Claim Rejections - 35 USC § 112
7. The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
8. Claim 23 remain rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Applicant’s Arguments
The response states that claim 23 recites that "the CIML-like properties enhance anti-tumor activity, persistence, and memory recall of the administered cells in vivo." This is an additional functional limitation that is not recited in claim 1. Claim 1, as amended, recites that progeny cells retain cytokine-induced memory-like IFN[Symbol font/0x67] recall activity after cytokine removal, but does not recite the in vivo effects of the CIML properties. Claim 23 further specifies that the CIML-like properties enhance anti-tumor activity, persistence, and memory recall of the administered cells in vivo, which is a further limitation on the functional characteristics of the administered cells. Accordingly, claim 23 properly further limits claim 1.
Response to Arguments
Applicant’s arguments have been carefully considered but are not persuasive. Claim 23 recites “administering an effective amount of cytokine induced memory-like (CIML) NK-92 cells according claim 1”. Claim 23 depends from claim 1. However, claim 1 is not drawn to a product of cytokine induced memory-like (CIML) NK-92 cells. A proper dependent claim of claim 1 should recite “The method of claim 1, …”. Furthermore, claim 1 recites “administering a therapeutically effective amount of the NK-92 cells to the patient” and “wherein at least some of the progeny cells retain cytokine-induced memory-like IFN[Symbol font/0x67] recall activity”. However, claim 23 recites “administering an effective amount of CIML NK-92 cells”. CIML NK-92 cells are a subpopulation of the NK-92 cells administered in claim 1. Therefore, claim 23 does not include all the limitations of claim 1 (administering NK-92 cells), and is not in a proper dependent claim form.
Claim Rejections - 35 USC § 103
9. 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.
10. Claims 1-2, 4, 9, 11-13, 23 and 25-26 remain rejected under 35 U.S.C. 102(a)(1) as being anticipated by Duggal et al. (WO 2021/006876A1, pub. date: 1/14/2021), in view of Copik et al. (WO 2018/067825A1, pub. date: 4/12/2018).
Regarding claims 1, 9, 11 and 12, Duggal et al. teaches a method of producing cytokine induced memory like (CIML) NK cells with enhanced cytotoxicity, the method comprising exposing NK cells to a stimulatory cytokine composition comprising IL-12, IL-15 and IL-18, or to IL-12, N-803 and IL-18 or to IL-18/IL-12-TxM fusion protein complex ([0012]). Duggal et al teaches that exposure to the stimulatory cytokine composition can be terminated by replacement of the medium with fresh medium ([0064]). Duggal et al. teaches a method of treating an individual having a cancer comprising administering to the individual a therapeutically effective amount of the CIML NK cells ([0021], [0065]).
Regarding claims 2 and 13, Duggal et al. teaches that cytokine stimulation will typically performed for a period of between 4-24 hours, more typically 12-16 hour ([0042])
Regarding claim 4, Duggal teaches that the generated CIML NK cells can be subjected to a resting period prior to subsequent use that can last that between 4-12 hours, 12-24 hours or 1-4 days, and even longer ([0064]).
Duggal does not teach the NK cells are NK-92 cells.
Copik teaches a method of treating a cancer in a subject comprising administering to the subject NK cells and an anti-PD-L1 antibody (page 1, lines 28-30), wherein the NK cells may be NK92 (NK-92) cell line (last line of page 1), and wherein prior to administration, the NK cells including NK-92 cells are contacted with IL-12, IL-15 and IL-18 (page 2, lines 1-4, page 10, lines 3-7, and page 12, line 5).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method of Duggal to use NK-92 cells in view of Copik. One of ordinary skill in the art would have been motivated to do so with a reasonable expectation of success because Copik teaches a method of treating a cancer in a subject comprising administering to the subject NK cells and an anti-PD-L1 antibody (page 1, lines 28-30), wherein the NK cells are NK92 (NK-92) cell line (last line), and wherein prior to administration, the NK cells including NK-92 cells are contacted with IL-12, IL-15 and IL-18 (page 2, lines 1-4, page 10, lines 3-7, and page 12, line 5).
Regarding claims 1 and 23, NK-92 cells expanded in the presence of same cytokines (i.e. IL-12, IL-15 and IL-18) for the same amount of time (e.g. 12-16, or 24 hours) as suggested by the cited references would necessarily comprise progeny cells having CIML-like properties (i.e. IFN[Symbol font/0x67] recall activity, enhanced anti-tumor activity, persistence, and memory recall of the administered cells in vivo).
Regarding claim 25, the culture supernatants from cultures of NK-92 cells would be capable of increasing PD-L1 expression on target cells. The increased PD-L1 expression would make the target cells more sensitive to killing by CAR engineered NK-92 cells.
Regarding claim 26, NK-92 cells expanded in the presence of same cytokines (i.e.. IL-12, IL-15 and IL-18) for the same amount of time (e.g. 12-16, or 24 hours) as suggested by the cited references would necessarily have CIML properties persist for at least 14 days post-cytokine stimulation.
11. Claims 1-4, 9, 11-14 and 23-26 remain rejected under 35 U.S.C. 102(a)(1) as being anticipated by Duggal et al. (WO 2021/006876A1, pub. date: 1/14/2021), in view of Copik et al. (WO 2018/067825A1, pub. date: 4/12/2018), further in view of Marcus et al. (WO 2018/165208A1, pub. date: 9/13/2018).
The teachings of Duggal and Copik have been set forth above as they apply to claims 1-2, 4, 9, 11-13, 23 and 25-26.
Regarding claims 3, 14 and 24, Duggal and Copik do not teach NK-92 cells are cryopreserved after removing the cytokines and provided as an off-the-shelf composition.
Marcus teaches a method of treating cancer comprising: a) contacting NK cells with hIL18/IL12/TxM, a combination of recombinant IL-12, IL-18, and ALT-803 (also known as N-803) for 18 hours, washing the cells, and adoptively transferring to a subject (page 79, Example 4). Marcus teaches that cells can be administered after ex vivo activation or cryogenically preserved and administered after thawing (and washing as needed) (page 8, para 3). Marcus teaches immortalized immune cells such as NK-92 may be used (page 6, last line and page 7 1st line).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have cryopreserved NK-92 cells after removing the cytokines and provided as an off-the-shelf composition in view of Marcus. One of ordinary skill in the art would have been motivated to do so with a reasonable expectation of success because Marcus teaches that activated NK cells including NK-92 cells can be administered after ex vivo activation or cryogenically preserved and administered after thawing (and washing as needed) (page 8, para 3).
12. Claims 1-2, 4, 6-9, 11-13, 16, 23 and 25-26 remain rejected under 35 U.S.C. 102(a)(1) as being anticipated by Duggal et al. (WO 2021/006876A1, pub. date: 1/14/2021), in view of Copik et al. (WO 2018/067825A1, pub. date: 4/12/2018), further in view of Emtage et al. (WO 2022/036041A1, pub. date: 2/17/2022).
The teachings of Duggal and Copik have been set forth above as they apply to claims 1-2, 4, 9, 11-13, 23 and 25-26.
Regarding claims 6-8 and 16, Duggal and Copik do not teach engineering the NK-92 cells to express a CAR, wherein the CAR binds a tumor antigen such as CD19.
Emtage et al. studied the effect of IL-18, IL-15 and IL-12 for augmenting NK cell-based immunotherapy using CD19 CAR NK cells derived from the NK-92 cell line ([0347]). Emtage teaches transducing NK-92 cell line with a lentiviral construct expressing CD19 CAR. The CD19 CAR NK-92 cells were exposed to IL-2+IL12+IL15+IL18 for 24 hours ([0350]). Emtage teaches a method of treating cancer expressing a tumor antigen in a subject comprising administering to the subject an effective amount of CAR NK cells (claims).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method of Duggal and Copik to use CIML-like CD19 CAR NK-92 cells to treat cancer in view of Emtage. One of ordinary skill in the art would have been motivated to do so with a reasonable expectation of success because Emtage teaches a method of making CD19 CAR NK-92 cells and further activating the CD19 CAR NK-92 with cytokines comprising IL12+IL15+IL18 and a method of treating cancer using CAR NK-92 cells.
13. Claims 1-2, 4-9, 11-13, 16, 23 and 25-26 remain rejected under 35 U.S.C. 102(a)(1) as being anticipated by Duggal et al. (WO 2021/006876A1, pub. date: 1/14/2021), in view of Copik et al. (WO 2018/067825A1, pub. date: 4/12/2018), Emtage et al. (WO 2022/036041A1, pub. date: 2/17/2022) and further in view of Klingemann et al. (US 10,765,701B2, date of patent: 9/8/2020).
The teachings of Duggal, Copik and Emtage have been set forth above as they apply to claims 1-2, 4, 6-9, 11-13, 16, 23 and 25-26.
Regarding claim 5, Duggal teaches that the CIML NK cells expresses CD16 and IL-2 (claim 34).
Duggal, Copik and Emtage do not teach that the CAR NK-92 cells are engineered to express CD16 and erIL-2.
Klingemann teaches a method of treating cancer using NK-92 cells expressing CD19 CAR, CD16 and erIL-2 (claims and column 2). Klingemann teaches that the integration the CAR enables effector cells to specifically engage and kill target cells that express a target recognized by the CAR; the integration of CD16 enables ADCC when combined with a therapeutic monoclonal antibody; and erIL2, which allows cell expansion in absence of exogenous IL-2 and maintains selective pressure for transgene expression (column 18, lines 46-52).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method of Duggal, Copik and Emtage to use CIML-like CD19 CAR NK-92 cells expressing CD16 and erIL-2 to treat cancer in view of Klingemann. One of ordinary skill in the art would have been motivated to do so because Klingemann teaches that the integration the CAR enables effector cells to specifically engage and kill target cells that express a target recognized by the CAR; the integration of CD16 enables ADCC when combined with a therapeutic monoclonal antibody; and erIL2, which allows cell expansion in absence of exogenous IL-2 and maintains selective pressure for transgene expression (column 18, lines 46-52). One would have had a reasonable expectation of success because Klingemann teaches a method of treating cancer using NK-92 cells expressing CD19 CAR, CD16 and erIL-2 (claims and column 2).
14. Claims 1-2, 4, 9-13, 23 and 25-26 remain rejected under 35 U.S.C. 102(a)(1) as being anticipated by Duggal et al. (WO 2021/006876A1, pub. date: 1/14/2021), in view of Copik et al. (WO 2018/067825A1, pub. date: 4/12/2018), further in view of Becker-Hapak et al. (Cancer Immunol Res, 2021, 9(9): 1071-1087).
The teachings of Duggal and Copik have been set forth above as they apply to claims 1-2, 4, 9, 11-13, 23 and 25-26.
Regarding claim 10, Duggal and Copik do not teach exposing NK-cells including NK-92 cells to cytokines comprising HCW-9201.
Becker-Hapak teaches that priming blood NK cells with recombinant human (rh)IL12, rhIL15, and rhIL18 (12/15/18) results in memory-like NK cell differentiation and enhanced responses against cancer, however, the lack of available, scalable good manufacturing process (GMP)-grade reagents required to advance this approach beyond early phase clinical trials is limiting (abstract). To address this challenge, they developed a novel platform centered upon an inert tissue factor scaffold for production of heteromeric fusion protein complexes (HFPCs) which combined IL12, IL15 and IL18 receptor engagement (HCW9201) (abstract). HCW9201 stimulated activation and proliferation signal in NK cells (page 2, para 1). Becker-Hapak teaches that HCW9201-primed NK cells can be advanced as an ideal approach for clinical GMP-grade memory-like NK cell production for cancer therapy.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have used HCW-9201 to make CIML-like NK-92 cells in view of Becker-Hapak. One of ordinary skill in the art would have been motivated to do so with a reasonable expectation of success because Becker-Hapak teaches that heteromeric fusion protein complexes (HFPCs) HCW9201 which combined IL12, IL15 and IL18 receptor engagement (HCW9201) stimulated activation and proliferation signal in NK cells (page 2, para 1) and HCW9201-primed NK cells can be advanced as an ideal approach for clinical GMP-grade memory-like NK cell production for cancer therapy.
Applicant’s Arguments
The response states that the cited references, whether considered alone or in combination, fail to teach or suggest the claimed method, particularly the limitation that at least some progeny cells originating from the NK-92 cells retain cytokine-induced memory-like IFN[Symbol font/0x67] recall activity after cytokine removal. Duggal is directed to CIML NK cells derived from primary peripheral blood or cord blood mononuclear cells, not NK-92 cells. See Duggal, paragraphs [0002], [0012]. Duggal does not teach or suggest that immortalized NK cell lines such as NK-92 could acquire memory-like properties. Copik does not teach or suggest that NK-92 cells contacted with these cytokines would exhibit durable memory-like properties. Critically, Copik does not teach or suggest that NK-92 cells can acquire memory-like properties at all, let alone that such properties would be inherited by progeny cells and persist after cytokine removal. Copik's disclosure of contacting NK-92 cells with IL-12, IL-15, and IL-18 is directed to activation, not to inducing durable memory-like reprogramming that extends to progeny cells. The specification discloses that the claimed result is unexpected. As explained in the specification, cytokine-induced memory-like features "had been documented only in primary NK cells from donors, not in immortalized NK-92-derived cell lines." As-Filed Specification, paragraph [0046]. The specification further explains that "NK-92 cells are highly engineered and continuously cultured, and therefore they were believed to lack the epigenetic flexibility required for 'training' or memory formation." Id. The present inventors surprisingly discovered that a short stimulation with IL-12, IL-18, and IL-15 (or N-803) reprogrammed NK-92 cells to exhibit long-lasting IFN[Symbol font/0x67] induction and memory recall upon rechallenge, behaviors previously thought unique to primary NK cells. Id.
Moreover, the specification discloses that the durable IFN[Symbol font/0x67] expression without continuous cytokine support is unexpected because typical NK-92 lines require constant exogenous IL-2 or IL-15 for IFN[Symbol font/0x67] secretion, and removal of cytokines usually causes rapid decline in function within 24-48 hours. As-Filed Specification, paragraph [0048]. The inventors demonstrated that following just 16 hours of cytokine induction, NK-92 cells maintained 6- to 8- fold higher IFN[Symbol font/0x67] secretion for at least seven days, even under normal IL-2 culture conditions. Id. Most notably, the specification discloses that "the memory recall also extended to progeny cells of the stimulated cells, and was even observed with progeny cells (e.g., up to 3rd, 4th, or 5th generation)." As-Filed Specification, paragraph [0044]. The specification further explains that "the enhanced memory recall function in the progeny cells is 'inherited' from the stimulated parental cells." As-Filed Specification, paragraph [0056]. Neither Duggal nor Copik teaches or suggests this unexpected result. Neither Marcus, Emtage, nor Klingemann cures these deficiencies. Marcus teaches cryopreservation of activated NK cells and that immortalized immune cells such as NK-92 may be used, but does not teach or suggest that NK-92 cells can acquire durable memory-like properties that persist to progeny cells. See Marcus, page 6, last line through page 7, first line; page 8, paragraph 3. Emtage teaches CD19 CAR NK-92 cells exposed to IL-12, IL-15, and IL-8, but does not teach or suggest that such exposure would result in memory-like reprogramming with IFN[Symbol font/0x67] recall activity that extends to progeny cells. See Emtage, paragraphs [0347], [0350]. Klingemann teaches NK-92 cells expressing CD 19 CAR, CD 16, and erIL-2, but similarly does not teach or suggest that NK-92 cells can acquire memory-like properties that are inherited by progeny cells. See Klingemann, column 2; column 18, lines 46-52.
Response to Arguments
Applicant’s arguments have been carefully considered but are not persuasive. NK-92 cells cultured/expanded in the presence of same cytokines (i.e. IL-12, IL-15 and IL-18) for the same amount of time (e.g. 12-16, or 24 hours) as suggested by Duggal and Copik would necessarily comprise progeny cells having CIML-like properties, including IFN[Symbol font/0x67] recall activity, enhanced anti-tumor activity, persistence, and memory recall of the administered cells in vivo. Furthermore, Emtage et al. teaches exposing the CD19 CAR NK-92 cells to IL-2+IL12+IL15+IL18 for 24 hours ([0350]). After 24 hours, the CD19 CAR NK-92 cells (which are encompassed by instant claims as evidenced by claims 6-8) would inherently comprise some progeny cells having CIM-like properties, including IFN[Symbol font/0x67] recall activity, enhanced anti-tumor activity, persistence, and memory recall of the administered cells in vivo.
Applicant’s arguments of unexpected results are not persuasive because the prior art has recognized that NK-92 cells can acquire durable memory-like properties. Klingemann (Cytotherapy, 2023, 25, 451-457) teaches “intra-tumor injection of CD19 CAR-modified NK-92 cells can induce regression of subcutaneous lymphoma. Remarkably, upon re-challenge of the mice with the same lymphoma cell line, no tumor re-growth occurred. This strongly suggest that intra-tumor injection of NK-92 cells can induce a systemic memory-like immune response. In a murine glioblastoma model, intra-tumor injection of ErbB2 CAR-NK-92 cells the Frankfurt group confirmed that specific IgG antibodies against the tumor had developed in treated mice that together with T cells provided long-term protection against rechallenge with the same tumor” (page 455, column 2, para 1). Preechanukul et al. (iScience, 2023, 26, 10724) teaches assay to generate memory-like NK-92 MI cells (NK-92-derived IL-2 independent cell line) in vitro and show that NK-92 MI cells acquire cell intrinsic memory-like properties through priming with BP-primed THP-1 cells. These memory like NK-92 MI cells upregulate IFN-[Symbol font/0x67] production in response to IL-12 and IL-18 stimulation, display bacteria-specific polyfunctional cytokine responses, and increased killing of intracellular BP upon re-challenge, the presence of both IL-12 and IL-18 either with or without IL-15 resulted in dramatic increase in IFN[Symbol font/0x67] secretion (page 4, Fig. 1). Preechanukul et al. shows that THP-1+iBP-primed NK-92 MI cells exhibit memory-like responses by enhancing polyfunctionality and killing of intracellular BP upon restimulation (Fig. 2). Therefore, the prior art has recognized that NK-92 cells can acquire memory-like properties.
For the foregoing reasons, the rejections are deemed proper and are therefore maintained.
New Grounds of Objection and Rejection
Claim Objections
15. Claim 1 is objected to for reciting “after cytokine removal” because more than one cytokine is used. It is suggested to recite “after removing the cytokine cocktail” as in claim 3.
Claim Rejections - 35 USC § 112
16. The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
17. Claims 9 and 10 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 9 is indefinite for the following reasons:
A broad range or limitation together with a narrow range or limitation that falls within the broad range or limitation (in the same claim) may be considered indefinite if the resulting claim does not clearly set forth the metes and bounds of the patent protection desired. See MPEP § 2173.05(c). In the present instance, claim 9 recites a broad range or limitation “comprising an IL-15 variant, and an IL-15 receptor α sushi domain/IgG1 Fc fusion protein”, together with a narrow range or limitation “N-803” which consists of a specific IL-15 variant, i.e. IL-15 N72D, and an IL-15 receptor α sushi domain/IgG1 Fc fusion protein (emphasis added). The claim(s) are considered indefinite because there is a question or doubt as to whether the feature introduced by such narrower language is (a) merely exemplary of the remainder of the claim, and therefore not required, or (b) a required feature of the claims.
Claim 10 is indefinite for reciting” a heteromeric fusion protein complex combining IL-12, IL-15, and IL-18 receptor engagement (HCW-9201)”. The claim can be interpretated as a fusion protein complex of IL-12 (cytokine), IL-15 (cytokine), and IL-18 (cytokine) which are capable of receptor engagement. However, HCW-9201 is known in the art to consist of IL-12R, IL15Rα and IL18R1. Therefore, the metes and bounds of the claimed invention cannot be determined and the claim is indefinite.
Conclusion
18. No claims are allowed.
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 nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
19. Any inquiry concerning this communication or earlier communications from the examiner should be directed to HONG SANG whose telephone number is (571)272-8145. The examiner can normally be reached Monday-Friday 8am-5pm.
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/HONG SANG/Primary Examiner, Art Unit 1646
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