CTFR 18/339,230 CTFR 100669 DETAILED ACTION Notice of Pre-AIA or AIA Status 07-03-aia AIA 15-10-aia The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA. Objections/Rejections Withdrawn Rejections and/or objections not reiterated from previous Office Actions are hereby withdrawn. The following rejections and/or objections are either reiterated or newly applied, and constitute the complete set presently being applied to the instant application. Response to Arguments Applicant’s arguments filed 4/1/2026, with respect to the claim rejections under 35 U.S.C 102, have been fully considered and are persuasive. The rejections have been withdrawn. 07-37 AIA Applicant's arguments filed 4/1/2026, with regards to the claim rejections under 35 U.S.C. 103 , have been fully considered but they are not persuasive. Applicant’s position is that one skilled in the art would not have a reasonable expectation of success in combining the cited references, thereby rendering the instant claims obvious, because the references only teach administering an amphiphilic ligand conjugate to expand and activate endogenous CD8+ T cells rather than CAR-T cells, which are activated by different mechanisms . Applicant states that, per the teachings of Srivastava et al., CAR-T cells receive an activation signal when the CAR on the surface of the T cell binds to an antigen that is present on the surface of a cell (Remarks, Pg 13, second paragraph). Liu teaches amphiphilic ligand conjugates not only engage serum proteins and target/traffic to lymph nodes but also insert themselves into cell membranes via their diacyl tails (Pg 521, left column, first paragraph under Figure 2; Figure 3). In other words, Liu teaches that the amphiphilic ligand conjugates are “presented” on cell membranes in lymph nodes. Based on this knowledge, one skilled in the art would recognize that CAR-T cells need only recognize an antigen displayed on a cell membrane in order to be activated; thus, it would be obvious to administer the amphiphilic lipid conjugate to a subject either receiving or who had received CAR-T cell therapy in order to activate, expand, and increase proliferation of the CAR-T cells. Further, Applicant’s request that the double patenting rejections be held in abeyance is noted but they are maintained/modified herein. Claim Status Claims 77, 79-86, and 88-101 are pending under examination. Claims 99-101 have been withdrawn as non-elected inventions. Claims 1-76, 78, and 87 are cancelled. Claims 77, 80, and 86 are currently amended . Priority The instant application is a divisional of 16/644,893, filed 3/5/2020, which was the 371 national stage entry of PCT/US2018/051764, filed 9/19/2018, which claims priority to the provisional application 62/560,588, filed 9/19/2017. The priority date of 9/19/2017 is acknowledged. Information Disclosure Statement The IDS submitted on 4/10/2026 are under consideration. Claim Rejections - 35 USC § 112 07-36 AIA 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. 07-36-01 AIA Claim 96 is 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. Claim 96 recites the method of claim 77, further comprising administering to the subject the CAR-T cells. However, claim 77 has been amended to recite that the subject is receiving or has received CAR-T cell therapy comprising the CAR-T cells. Thus, claim 96 does not further limit its parent claim 77 . Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements. Claim Rejections - 35 USC § 103 07-20-aia AIA 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. 07-23-aia AIA 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. 07-20-02-aia AIA 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. 07-21-aia AIA Claim (s) 77, 79-85, 88, 89, 91, 92, and 96 are rejected under 35 U.S.C. 103 as being unpatentable over Liu et al. (Liu H, Moynihan KD, Zheng Y, Szeto GL, Li AV, Huang B, Van Egeren DS, Park C, Irvine DJ. Structure-based programming of lymph-node targeting in molecular vaccines. Nature. 2014 Mar 27;507(7493):519-22.) in view of Srivastava et al. (Engineering CAR-T cells: Design concepts. Trends Immunol. 2015 Aug;36(8):494-502.; cited on IDS filed 4/10/2026) . Liu teaches molecular vaccines that transport cargo to the lymphatic system via “albumin hitchhiking”, specifically through the synthesis of amphiphiles (amphiphilic ligand conjugate) comprising an antigen or adjuvant cargo (chimeric antigen receptor or CAR ligand) linked to a lipophilic albumin-binding tail (lipid) by a solubility-promoting polar polymer chain (linker) (Abstract, Extended Data Figure 2A). Liu further teaches administration of said amphiphilic ligand conjugate to mice, which results in marked increases in lymph node accumulation, decreased systemic dissemination, and increases in T-cell priming (activation, expansion, and proliferation) and anti-tumor efficacy (Abstract). This reads on administration of the amphiphilic ligand conjugate to a subject, as the instant specification defines a “subject” to include murines (Pg 24, line 4). Liu further teaches the amphiphilic ligand conjugates not only engage serum proteins and target/traffic to draining lymph nodes but also insert themselves into cell membranes via their diacyl tails (Pg 519, left column, second paragraph; Pg 521, left column, first paragraph under Figure 2; Figure 3). In other words, the amphiphilic ligand conjugates are expressed in the plasma membrane of cells within the lymph nodes. Liu does not teach that the subject is receiving or has received CAR-T cell therapy comprising CAR-T cells. Srivastava teaches that CAR-T cell therapy involves the design of synthetic tumor targeting receptors, termed CARs, that can be introduced into human T cells to redirect antigen specificity and enhance function in adoptive immunotherapy (Pg 494, “Introduction”). Srivastava further teaches CAR-T cells receive an activation signal when the CAR on the surface of the T cell binds to an antigen that is present on the surface of a cell (Abstract; Figure 1). In summary, Liu teaches administering an amphiphilic ligand conjugate to a subject, wherein the amphiphilic ligand conjugate inserts itself into the plasma membrane of cells in the lymph nodes; when administered to subjects, the amphiphilic ligand conjugate promotes endogenous T cell activation, expansion, and increased proliferation. Srivastava teaches CAR-T cells receive an activation signal when the CAR on the surface of the T cell binds to an antigen that is present on the surface of a cell. In light of these teachings, regarding claim 77, it would be obvious to activate, expand, or increase proliferation of CAR-T cells in a subject receiving or who has received CAR-T cell therapy by administering administer an amphiphilic ligand conjugate. One skilled in the art would be motivated to do so in order to take advantage of the ability of the amphiphilic lipid conjugate to incorporate into the plasma membrane of cells in the lymph nodes while said subject is receiving or has recently received CAR-T cell therapy as the amphiphilic ligand conjugate could be designed to comprise a CAR ligand recognizable by the CAR-T cells; said recognition of the CAR ligand by the CAR-T cells would then lead to their activation. One would have a reasonable expectation of success as Liu teaches amphiphilic lipid conjugates incorporate into the membrane of cells and Srivastava teaches CAR-T cells are activated upon recognition of a CAR ligand, leading to expansion and proliferation,. Moreover, based upon the above teachings, it would be obvious to try administering the claimed amphiphilic lipid conjugates either concurrently with or after CAR-T cell therapy to a subject in need thereof. As stated above, Liu teaches the administration of an amphiphilic ligand conjugate to a subject results in priming of endogenous T cells. Liu further teaches that administration of an amphiphilic ligand conjugate comprising a CAR ligand designed to target TC-1 tumors (expressing the E7 oncoportein from HPV) or B16F10 melanomas in mice; in both cases, the amphiphile ligand conjugate promoted tumor regression and/or slowed growth (Figure 4d and 4e). These results suggest that the amphiphilic lipid conjugate alone is capable of priming endogenous T cells to recognize the specified CAR ligand for cancer treatment. Because the ultimate goal of CAR-T therapy is to reinfuse T cells that already recognize a specific tumor antigen for cancer cell destruction, thus circumventing the steps involved in T cell recognition, it would further be obvious to try combining CAR-T cell therapy and administration of the amphiphilic ligand conjugate as claimed. See MPEP 2143(I)(E). Regarding claim 79, Liu further teaches that diacyl lipids of diacyl lipid conjugates interact with albumin (Pg 519, right column, first paragraph; Figure 1). Regarding claim 80, Liu teaches that amphiphiles with long diacyl tails (greater than or equal to 16 carbons) exhibit a high affinity for albumin (Pg 521, right column, first paragraph; Figures 1 and 3). Regarding claims 81-83, Liu teaches linking peptide antigens to a diacyl lipid tail via a PEG block to promote conjugate solubility. Further, increasing the polar block to 48 ethylene glycol units yielded amphiphiles that partitioned preferentially into solution while retaining albumin binding (Pg 521, left column, first paragraph; Figure 3a). Regarding claim 84, as stated above, Liu teaches amphiphiles with long diacyl tails great than or equal to 16 carbons as well as linking peptide antigens to said diacyl tail via a PEG block, which can comprise 48 ethylene glycol units (Pg 521, right column, first paragraph; Figures 1 and 3; Pg 521, left column, first paragraph; Figure 3a). Regarding claims 85 and 88, Liu teaches the species 1,2-distearoyl-sn-glycero-3-phosphoethanolamine-N-PEG(DSPE-PEG 2kDa) conjugated to peptide antigens, such as HIV antigen (AL11 epitope from SIV Gag; viral antigen) (Pg 521, right column, first and second paragraph). Regarding claim 89, Srivastava teaches that second and third generation CARs include costimulatory signals (co-stimulation domain) to augment cytokine production and proliferation of CAR-T cells in vitro (Pg 494, “Introduction”; Figure 1). Regarding claims 91 and 92, as stated above, Liu teaches amphiphilic lipid conjugates comprising an antigen or adjuvant cargo (chimeric antigen receptor or CAR ligand) linked to a lipophilic albumin-binding tail (lipid) by a solubility-promoting polar polymer chain (linker), which are targeted to lymphatics and draining lymph nodes where they accumulate in antigen presenting cells (Abstract, Extended Data Figure 2A; Pg 519, left column, second paragraph). Regarding claim 96, as described above, Srivastava teaches that CAR-T cell therapy involves the design of synthetic tumor targeting receptors, termed CARs, that can be introduced into human T cells to redirect antigen specificity and enhance function in adoptive immunotherapy (Pg 494, “Introduction”) . 07-21-aia AIA Claim (s) 77, 79-85, 88, 89, 91, 92, and 96 are rejected under 35 U.S.C. 103 as being unpatentable over Liu et al. (Liu H, Moynihan KD, Zheng Y, Szeto GL, Li AV, Huang B, Van Egeren DS, Park C, Irvine DJ. Structure-based programming of lymph-node targeting in molecular vaccines. Nature. 2014 Mar 27;507(7493):519-22.) and Srivastava et al. (Engineering CAR-T cells: Design concepts. Trends Immunol. 2015 Aug;36(8):494-502.; cited on IDS filed 4/10/2026), as applied to claims 77, 79-85, 88, 89, 91, 92, and 96, and in further view of Johnson et al. (Johnson et al., Rational development and characterization of humanized anti-EGFR variant III chimeric antigen receptor T cells for glioblastoma. Sci Transl Med. 2015 Feb 18;7(275):275ra22.) . The teachings of Liu and Srivastava have been set forth above. Liu and Srivastava do not teach a method wherein the CAR ligand is a tumor-associated antigen, specifically the elected species EGFRvIII. Johnson teaches the development and characterization of CAR-T cells that can target EGFRvIII, mutations of which often contribute to glioblastoma (Title, Abstract). Although peptide vaccines that treat EGFRvIII mutant glioblastoma exist and are effective, direct transfer of EGFRvIII-directed T cells is potentially more effective and may have more favorable kinetics compared to peptide- or cell-based vaccine (Pg 2, left column, first full paragraph). Thus, regarding claim 88, Liu and Srivastava teach administering an amphiphilic ligand conjugate designed activate, expand, and increase proliferation of CAR-T cells in a subject who is receiving or has received CAR-T cell therapy. Johnson teaches CAR-T cells that can target EGFRvIII useful in the treatment of glioblastoma. Therefore, it would be prima facie obvious to use an EGFRvIII CAR ligand, as taught by Johnson, in the method of activating and expanding CAR-T cells taught by Liu and Srivastava, in order to effectively target glioblastoma or other EGFRvIII mutant-expressing cells. One skilled in the art would have a reasonable expectation of success as Johnson established that treating glioblastoma through EGFRvIII-directed T cells is more effective than other types of available therapeutics . 07-21-aia AIA Claim (s) 77, 79-85, 88, 89 and 91-98 are rejected under 35 U.S.C. 103 as being unpatentable over Liu et al. (Liu H, Moynihan KD, Zheng Y, Szeto GL, Li AV, Huang B, Van Egeren DS, Park C, Irvine DJ. Structure-based programming of lymph-node targeting in molecular vaccines. Nature. 2014 Mar 27;507(7493):519-22.) and Srivastava et al. (Engineering CAR-T cells: Design concepts. Trends Immunol. 2015 Aug;36(8):494-502.; cited on IDS filed 4/10/2026), as applied to claims 77, 79-85, 88, 89, 91, 92, and 96, and in further view of Irvine et al. (WO 2013/151771 A1, published 10/10/2013; cited on IDS filed 11/21/2023) . The teachings of Liu and Srivastava have been set forth above. Liu and Srivastava do not teach a method further comprising administering an adjuvant. Irvine teaches lipid conjugates for enhanced delivery of cargo to the lymph nodes, wherein lipid conjugates typically include a lipophilic domain that binds to albumin, a polar block domain, and a cargo such as a molecular adjuvant or immunostimulatory compound or antigenic peptide (Abstract). Irvine teaches pharmaceutical compositions of the invention that can be immunogenic in that they comprise the invention in addition to adjuvants, antigens, or a combination thereof (Pg 31, “B. Immunogenic Compositions”). Irvine teaches that administration of multiple adjuvants is sometimes necessary to invoke an effective immune response (Pg 1, “Background of the Invention”, first paragraph). Thus, regarding claim 93, Liu and Srivastava teach administering an amphiphilic ligand conjugate designed activate, expand, and increase proliferation of CAR-T cells in a subject who is receiving or has received CAR-T cell therapy. Irvine teaches similar methods that can be further improved through administration of an additional adjuvant. Therefore, it would be prima facie obvious to incorporate an additional adjuvant, as taught by Irvine, in the method of activating and expanding CAR-T cells taught by Liu and Srivastava, in order to improve more effectively stimulate the immune system and, by extension, improve treatment efficacy. One skilled in the art would have a reasonable expectation of success as it was already established that such adjuvants could be added to pharmaceutical compositions sand administered to patients in order to generate a greater immune response. Regarding claims 94 and 95, Irvine teaches that adjuvants can be a lipid conjugate (Pg 31, lines 11-13). Some adjuvants act through TLR9 including synthetic oligodeoxynucleotides (ODN) such as CpG ODN (Pg 36, lines 7-9). Irvine further indicates that immunostimulatory oligonucleotides, such as those containing unmethylated cytosine-phosphate-guanine (“CpG”) motifs, can be used as an adjuvant to stimulate both cellular and humoral immune responses (Pg 1, lines 19-21). Regarding claims 97 and 98, Irvine teaches that the conjugates can be administered to a subject, such as a subject with cancer (Abstract). The subject can be a human (Pg 10, lines 28-31) . 07-21-aia AIA Claim (s) 77, 79-85, 88-92, and 96 are rejected under 35 U.S.C. 103 as being unpatentable over Liu et al. (Liu H, Moynihan KD, Zheng Y, Szeto GL, Li AV, Huang B, Van Egeren DS, Park C, Irvine DJ. Structure-based programming of lymph-node targeting in molecular vaccines. Nature. 2014 Mar 27;507(7493):519-22.) and Srivastava et al. (Engineering CAR-T cells: Design concepts. Trends Immunol. 2015 Aug;36(8):494-502.; cited on IDS filed 4/10/2026), as applied to claims 77, 79-85, 88, 89, 91, 92, and 96, and in further view of Zah et al. (Zah E, Lin MY, Silva-Benedict A, Jensen MC, Chen YY. T Cells Expressing CD19/CD20 Bispecific Chimeric Antigen Receptors Prevent Antigen Escape by Malignant B Cells. Cancer Immunol Res. 2016 Jun;4(6):498-508.) . The teachings of Liu and Srivastava have been set forth above. Liu and Srivastava do not teach a method wherein the CAR comprises a bispecific binding domain. Zah teach bispecific CARs that trigger robust cytotoxicity against target cells expressing either CD19 or CD20, two clinically validated targets for B-cell malignancies (Abstract). The instant specification teaches that CD19 and CD20 are examples of tumor-associated antigens (Pg 4, second full paragraph). Zah further teaches that the probably of an antigen escape by spontaneous mutations and selective expansion of antigen-negative tumor cells decreases with each additional antigen that can be recognized by the CAR-T cells, thereby making it beneficial to generate T cells capable of recognizing multiple antigens (Pg 2, paragraph 2). Thus, regarding claim 90, Liu and Srivastava teach administering an amphiphilic ligand conjugate designed activate, expand, and increase proliferation of CAR-T cells in a subject who is receiving or has received CAR-T cell therapy. Zah teaches that it is beneficial to design CAR-T cells that can recognize multiple antigens in order to limit the likelihood of antigen escape and selective expansion of antigen-negative tumor cells. Therefore, it would be prima facie obvious to use a bispecific CAR, as taught by Zah, in the method of activating and expanding CAR-T cells taught by Liu and Srivastava, in order to improve the therapeutic outcomes of cancer patients. One skilled in the art would have a reasonable expectation of success as Zah previously established methods of making bispecific CAR-T cells compatible with existing T-cell manufacturing processes and implementable by current clinical protocols (Abstract) . 07-21-aia AIA Claim (s) 77, 79-88, 89, 91, 92, and 96 are rejected under 35 U.S.C. 103 as being unpatentable over Liu et al. (Liu H, Moynihan KD, Zheng Y, Szeto GL, Li AV, Huang B, Van Egeren DS, Park C, Irvine DJ. Structure-based programming of lymph-node targeting in molecular vaccines. Nature. 2014 Mar 27;507(7493):519-22.) and Srivastava et al. (Engineering CAR-T cells: Design concepts. Trends Immunol. 2015 Aug;36(8):494-502.; cited on IDS filed 4/10/2026), as applied to claims 77, 79-85, 88, 89, 91, 92, and 96, and in further view of Tamada et al. (Tamada K, Geng D, Sakoda Y, Bansal N, Srivastava R, Li Z, Davila E. Redirecting gene-modified T cells toward various cancer types using tagged antibodies. Clin Cancer Res. 2012 Dec 1;18(23):6436-45.) . The teachings of Liu and Srivastava have been set forth above. Liu and Srivastava do not teach a method wherein the CAR ligand is a tag. Tamada teaches the creation of human and mouse T cells genetically engineered to express CARs that recognize fluorescein isothiocyanate (FITC; CAR ligand), or anti-FITC CAR-T cells (Abstract). Tamada teaches that anti-FITC CAR-T cells overcome several limitations associated with T-cells, such as the lack of a universal CAR ligand expressed in all cancer cells as well as costs associated with generating CAR-T cells. The creation of anti-FITC CAR-T cells overcomes these issues, as FITC is a readily available and inexpensive fluorochrome dye that can be conjugated to a variety of clinically-approved antibodies that target different types of cancer cells (Pg 6436, right column, second paragraph – Pg 6436, left column, first full paragraph; also see Abstract and Translational Relevance). Thus, regarding claim 86, Liu and Srivastava teach administering an amphiphilic ligand conjugate designed activate, expand, and increase proliferation of CAR-T cells in a subject who is receiving or has received CAR-T cell therapy. Tamada teaches the need for a universally applicable CAR ligand, such as FITC, which can be conjugated to various antibodies and targeted to cancer cells. Therefore, it would be prima facie obvious to incorporate a common and readily available biological tag, such as FITC, taught by Tamada, in the method of activating and expanding CAR-T cells taught by Liu and Srivastasva, in order to overcome the aforementioned challenges. One skilled in the art would have a reasonable expectation of success as Tamada previously established methods of making anti-FITC CAR-T cells and targeting various types of cancer cells with them . Double Patenting 08-33 AIA 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. 08-34 AIA Claim s 77, 88, 93, and 97-98 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim s 1-23 of U.S. Patent No. 12,433,954 (US ‘954) . Although the claims at issue are not identical, they are not patentably distinct from each other because they contain overlapping subject matter . The claims of US ‘954 are drawn to a method of activating anti-CD19 CAR T cells or increasing proliferation of anti-CD19 CAR T cells in a subject, or a method of stimulating an immune response to a target cell population or a target tissue expressing CD19 in a subject, or a method of inducing an anti-tumor response in a subject with cancer where the subject is receiving or has received anti-CD19 CAR T cells, comprising administering an amphiphilic ligand conjugate, wherein the amphiphilic ligand conjugate comprises an anti-CD19 CAR ligand or a multimer thereof and a lipid operably linked to the ligand or the multimer. The claims of US ‘954 anticipate the instant claims . 08-35 AIA Claim s 77, 79-87, 89, and 96-97 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim s 1-4, 9, and 11 of copending Application No. 18/123,112 (‘112, reference application, claim set filed 4/13/2026) . Although the claims at issue are not identical, they are not patentably distinct from each other because they contain overlapping subject matter. The claims of copending Application No. ‘112 are drawn to a method of treating a tumor comprising intratumorally administering a membrane-inserting amphiphilic ligand into a tumor of a subject in need of treatment followed by intravenously administering an engineered immune cell expressing a chimeric antigen receptor (CAR) that specifically binds to the amphiphilic ligand . This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented. Conclusion No claim is allowed. 07-40 AIA 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. Any inquiry concerning this communication or earlier communications from the examiner should be directed to Sara Konopelski Snavely whose telephone number is (571)272-1841. The examiner can normally be reached Monday - Friday 9-6pm EST. Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Melissa L Fisher can be reached at 571-270-7430. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300. Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. 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If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000. /SARA E KONOPELSKI SNAVELY/Examiner, Art Unit 1658 /Melissa L Fisher/ Supervisory Patent Examiner, Art Unit 1658 Application/Control Number: 18/339,230 Page 2 Art Unit: 1658 Application/Control Number: 18/339,230 Page 3 Art Unit: 1658 Application/Control Number: 18/339,230 Page 4 Art Unit: 1658 Application/Control Number: 18/339,230 Page 5 Art Unit: 1658 Application/Control Number: 18/339,230 Page 6 Art Unit: 1658 Application/Control Number: 18/339,230 Page 7 Art Unit: 1658 Application/Control Number: 18/339,230 Page 8 Art Unit: 1658 Application/Control Number: 18/339,230 Page 9 Art Unit: 1658 Application/Control Number: 18/339,230 Page 10 Art Unit: 1658 Application/Control Number: 18/339,230 Page 11 Art Unit: 1658 Application/Control Number: 18/339,230 Page 12 Art Unit: 1658 Application/Control Number: 18/339,230 Page 13 Art Unit: 1658 Application/Control Number: 18/339,230 Page 14 Art Unit: 1658 Application/Control Number: 18/339,230 Page 15 Art Unit: 1658 Application/Control Number: 18/339,230 Page 16 Art Unit: 1658 Application/Control Number: 18/339,230 Page 17 Art Unit: 1658
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