CTNF 18/289,049 CTNF 101362 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. Priority This application claims priority to provisional applications 63/185,325, filed on 06 May 2021, and 63/222,748, filed on 16 July 2021, and is a 371 of PCT/US2022/028,139, filed on 06 May 2022. Receipt is acknowledged of certified copies of papers required by 37 CFR 1.55. The effective filing date is 06 May 2021. Information Disclosure Statement The information disclosure statement (IDS) filed on 24 November 2025 is being considered by the examiner. Status of Application, Amendments, and/or Claims Claims 1-44 are the original claims filed on 31 October 2023. In the preliminary amendment of 31 October 2023, claims 1-9, 13, 18, 22, 28, 32, 34, 36, 38, and 41-44 were cancelled, and claims 12, 14, 17, 19, and 20 were amended. Claims 10-12, 14-17, 19-21, 23-27, 29-31, 33, 35, 37, 39, and 40 are pending and the subject of this office action. Claim Rejections - 35 USC § 102 07-07-aia AIA 07-07 The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action: A person shall be entitled to a patent unless – 07-08-aia AIA (a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention. 07-12-aia AIA (a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention. 07-15 AIA Claim 21 is rejected under 35 U.S.C. 102( a)(1 ) as being anticipated by Lynn RC, et al. (2019) c-Jun overexpression in CAR T cells induces exhaustion resistance. Nature 576 , 293–300 (herein Lynn) . Lynn teaches a method for treating cancer comprising HA-28z CAR cell therapy, in which the CAR T cells have been engineered to overexpress the canonical AP-1 factor c-Jun (Abstract). It is shown that HA-28z cells, without the genetic modifications resulting in overexpressed c-Jun, rapidly induce T cell exhaustion, as a result of tonic signaling mediated via antigen-independent aggregation (Page 293 paragraph 3 and Figure 1). The authors determine that a factor leading to the rapid exhaustion of the HA-28z CAR cell is epigenetic and transcription dysregulation of AP-1, which leads to an increase in the AP-1-IRF:AP-1 Fos/Jun complex ratio (Figure 2, Epigenetic and transcriptional dysregulation of AP-1 section, and Discussion). An AP-1 Fos/Jun deficiency is taught to result in insufficient transcriptional activation of Il-2 and other genes necessary to prevent T cell exhaustion. The authors show that overexpression of c-Jun in HA-28z CAR T cells prevents T cell exhaustion and enhances T cell function in vivo (Figures 3 and 5, c-Jun overexpression prevents CAR T cell exhaustion section, and JUN CAR T cells enhance anti-tumour activity in vivo section) . 07-15 AIA Claim s 23 and 24 are rejected under 35 U.S.C. 102( a)(1) and (a)(2 ) as being anticipated by US 2019/0292539 A1 (herein Fulga) . Fulga teaches a method for treating cancer, which comprises the administration of an autologous T cells, engineered in such a way that a heterologous MRE is inserted into the 3’UTR of a gene encoding an immune checkpoint protein (Figure 4D and [0167-0168]). It is taught that the heterologous MRE is capable of binding specific complementary miRNA, which is upregulated in activated T cells ([0168]). Fulga teaches multiple potential embodiments comprising MRE that are complementary to miRNAs, such as let-7d, miR-155, miR-185, miR-34a, miR-15, miR-210, miR-142, miR-125a, miR-130 ([0037]). miR-155, in particular, is noted as a preferred miRNA (Table 2) . 07-15 AIA Claim s 27 is rejected under 35 U.S.C. 102( a)(1 ) as being anticipated by Zebley CC, et al, (2020) De novo DNA methylation programs regulate CAR T-cell exhaustion, The Journal of Immunology , Volume 204, Issue 1_Supplement, May 2020, Page 246.5 (herein Zebley) . Zebley teaches a methods of treating cancer involving the genetic deletion of de novo DNA methyltransferase 3a (Dnmt3a) in multiple human CAR T-cell systems (Abstract). The authors note that the deletion results in a striking preservation of CAR T cell proliferation and effector function during chronic antigen exposure. The authors go onto cross-reference the genome methylation profiles of the engineered CAR T cells to those from a previous murine Dnmt3a-KO model, and were able to identify a panel of epigenetically regulated exhaustion-associated genes. Claims 29 and 30 are rejected under 35 U.S.C. (a)(1) as being anticipated by WO 2019/178334 A1 (herein Blelloch). Blelloch teaches a method for treating cancer comprising the use of suppressive EV inhibitors to the enhance the efficacy of a co-administered immunotherapy treatment ([0044]). Blelloch teaches that the suppressive EV inhibitor may act to disrupt the production of EVs, and provides multiple embodiments using various small molecules such as GW4869 ([0054]). Blelloch also teaches that this method may be applied to a human cancer patient or non-human animals ([0034]) 07-15 AIA Claim 31 rejected under 35 U.S.C. 102( a)(1 ) as being anticipated by El Hage A, et al. (2021) Combining mTOR Inhibitors and T Cell-Based Immunotherapies in Cancer Treatment. Cancers (Basel). 2021 Mar 17;13(6):1359 (herein Hage) . Hage et al review the current state of cancer treatments comprising the combination of mTOR inhibitors and T cell-based immunotherapies. One of the many studies discussed involved the expansion of CAR T cells in the presences of IL-2 and rapamycin (Section 4.4). It was taught that cells cultured under these conditions exhibited a lower degree of T cell differentiation and superior anti-tumor activity, as compared to untreated CAR T cells. The authors go on to suggest that combination treatments comprising CAR T cell therapy with mTOR inhibitors possess therapeutic potential (Section 4.4) . 07-15 AIA Claim 33 rejected under 35 U.S.C. 102( a)(1 ) as being anticipated by Wang X, et al. (2020) HDAC inhibitors overcome immunotherapy resistance in B-cell lymphoma . Protein Cell . 2020 Jul;11(7):472-482 (herein Wang) . Wang et al provide a review of studies investigating the effect of combining HDAC inhibition with immunotherapy (Abstract). One of the methods discussed was from a study in which HDAC inhibitors were combined with anti-CD19 CAR T cells (Immune Modulation of B-cell lymphomas by HDAC Inhibitors section, paragraph 7). Wang teaches that adding HDAC inhibitors, vorinostat (a.k.a. SAHA) or Panobinostat to human NHL cell lines, that have become resistant to anti-CD19 CAR T cells, largely reversed their resistance to the anti-CD19 CAR T cells . 07-15 AIA Claim 35 rejected under 35 U.S.C. 102( a)(1 ) as being anticipated by Grosser R, et al. (2019) Combination Immunotherapy with CAR T Cells and Checkpoint Blockade for the Treatment of Solid Tumors. Cancer Cell . 2019 Nov 11;36(5):471-482 (herein Grosser) . Grosser et al provide a review of the state of combination checkpoint blockade and immunotherapy before the effective filing date of the instant application (Summary). This review makes it abundantly clear that invention described in instant claim 35 was anticipated by multiple groups, prior to the effective date of the current application (Combination Therapy section). An example of the methods, taught by Grosser, involved the administration of anti-GD2 CAR therapy in combination with pembrolizumab (an inhibitory anti-PD-1 antibody used for checkpoint blockade immunotherapy) (Combination Therapy section: paragraph 2). It was taught that this combination resulted in improved T-cell function and survival following repeated antigen stimulation against PD-L1-positive tumor cells . 07-15 AIA Claim 37 rejected under 35 U.S.C. 102( a)(1 ) as being anticipated by Weber EW, et al. (2019) Pharmacologic control of CAR-T cell function using dasatinib. Blood Adv . 2019 Mar 12;3(5):711-717 (herein Weber) . Weber et al teach a method for treating cancer comprising CAR T cell immunotherapy and administering dasatinib, a potent senolytic drug (Results and Discussion). Weber teaches that dasatinib may be used as a potent reversible CAR T cell proliferation suppressor, that may be used to temporarily mediate on-target toxicities associated with CAR T cell therapy. The authors suggest that this method could be refined to help treat CAR-associated neurotoxicity (Results and Discussion). Claims 39 and 40 are rejected under 35 U.S.C. (a)(1) and (a)(2) as being anticipated by US 2018/0154183 A1 (herein Sahadevan). Sahadevan teaches a method for radio-immunotherapy for treating cancer in a mammal (Abstract and Figure 22). This method comprises immunotherapy and apheresis of tumor-derived mutated subcellular micro and nanoparticles ([0314]). Sahadevan teaches that molecular apheresis, resulting in the dissemination of tumor-derived extracellular vesicles, leads to more curative cancer treatments ([0043]). In regard to claim 40, Sahadevan teaches that EVs may be disseminated through the use of an instrument diagramed in Figure 21, which incorporates drawings from U.S. Patent application 15/621,973. This apparatus uses pulse flow apheresis combined with affinity chromatography (a plasma adsorbent), and continuous flow ultracentrifugation plasmapheresis (plasma exchange) . 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. 07-21-aia AIA Claim s 10-12 and 15-17 are rejected under 35 U.S.C. 103 as being unpatentable over WO 2019/094727 A1 (herein Cumba-Garcia) in view of Ayala-Mar S, et al. (2021) Clinical Implications of Exosomal PD-L1 in Cancer Immunotherapy. J Immunol Res . 2021 Feb 8;2021:8839978 (herein Ayala-Mar) . In regard to claims 10-12 and 15-17 , Cumba-Garcia teaches a method for treating cancer comprising analyzing the composition of a mammalian subject’s extracellular vesicles, in order to ascertain whether the level(s) of one or more immunomodulatory polypeptide is reduced, and if the level is reduced, then the patient is administered a cancer treatment (Abstract and Claim 1). PD-L1 is taught to be one of the immunomodulatory polypeptides, whose levels are measured (Claim 13). In regard to the cancer treatment administered, it is taught that various treatments may be employed, including various immunotherapies, such as checkpoint blockade, tumor vaccination, or targeted therapy (Page 3 lines 16-19). It is also taught that the method may be applied to human subjects, who have cancer, wherein said cancer is selected from the group consisting of glioblastoma, breast cancer , prostate cancer , ovarian cancer, bladder cancer, head and neck cancer , melanoma , lung cancer , renal cell carcinoma, colon cancer, pancreatic cancer, leukemia, lymphoma, thyroid cancer, and osteosarcoma , which is relevant to instant claims 11, 12, 16, and 17 (Reference claims 2 and 3). Cumba-Garcia does suggest that the level of PD-L1, within extracellular vesicles taken from the subject, may be used as a diagnostic marker, indicating whether or not a cancer therapy should be administered, they do not provide motivation to use this marker over the others suggested. Ayala-Mar teaches this deficiency. Ayala-Mar et al provide a detailed review of the clinical implications of exosomal PD-L1 in cancer immunotherapy, and suggest that exosomal PD-L1 levels may be a useful biomarker to predict immunotherapy response and to assess therapeutic efficacy (Abstract). It is taught that exosomal PD-L1 contributes to an immunosuppressive tumor microenvironment by inhibiting T cell receptor-mediated T cell activation, utilizing the same mechanism of its cellular counterpart (Section 2.3). The authors state that there is evidence that suggests that higher exosomal PD-L1 levels, prior to immunotherapy, were associated with a worse clinical outcome (Section 3.2 paragraph 5). It is also noted that higher levels of exosomal PD-L1 is associated with a more advanced disease state, and the authors hypothesize that in this scenario immunotherapy may fail, because the immune response has reached a level of suppression that is beyond reinvigoration. It is also taught that measuring the level of exosomal PD-L1 could be an effective diagnostic assay to define which patients may benefit from immunotherapy and to assess therapeutic efficacy (Section 4: Concluding Remarks and Future Directions). It would have been obvious to combine the teachings of Cumba-Garcia (determining that a patient has low exosomal levels of immunomodulatory polypeptides before administering the patient cancer therapy) and Ayala-Mar (the use of exosomal PD-L1 as a potential biomarker for the prediction of immunotherapy efficacy). One skilled in the art would have recognized that the teachings of Ayala-Mar provide clear motivation for assaying the levels of exosomal PD-L1 levels prior to the administration of a cancer therapy, as suggested by Cumba-Garcia. The method of confirming that a subject has low exosomal levels of PD-L1, prior to administering an immunotherapy, ensures that the recipient actually has a reasonable chance to benefit from the treatment. Reciprocally, if the subject has high levels of exosomal PD-L1, then the administration of the immunotherapy has a lower likelihood of efficacy, as taught by Ayala-Mar . 07-21-aia AIA Claim 14 is rejected under 35 U.S.C. 103 as being unpatentable over WO 2019/094727 A1 (herein Cumba-Garcia) in view of Ayala-Mar S, et al. (2021) Clinical Implications of Exosomal PD-L1 in Cancer Immunotherapy. J Immunol Res . 2021 Feb 8;2021:8839978 (herein Ayala-Mar) and Cox, MJ, et al. (2020) Circulating Extracellular Vesicles Induce Chimeric Antigen Receptor T Cell Dysfunction in Chronic Lymphocytic Leukemia (CLL) Biol Blood Marrow Transplant. Volume 26, Issue 3, Supplement, 2020, Pages S2-S3 (herein Cox), published in March of 2020 . As discussed for the 35 U.S.C. 103 rejections of claims 10-12 and 15-17, Cumba-Garcia and Ayala-Mar teach a method of treating cancer comprising measuring exosomal PD-L1 levels in a subject prior to administering a treatment comprising either immunotherapy (low PD-L1 EV levels) or a therapy that is not immunotherapy (high PD-L1 EV levels). Cumba-Garcia and Ayala-Mar do not teach that the immunotherapy is a CAR T cell therapy. This deficiency is taught by Cox. Cox teaches that EVs containing high levels of PD-L1 impair CAR T antigen-specific proliferation (Results and Figure 1). The authors show that the presence of the EVs led to the upregulation of inhibitory receptors, reduction of effector cytokines levels, upregulation of exhaustion pathways, and ultimately a reduction of the anti-tumor response. They conclude their report stating that cancer-derived EVs can lead to CAR T cell disfunction. It would have been obvious to combine the method taught by Cumba-Garcia and Ayala-Mar (measuring PD-L1 EV levels prior to administering a cancer treatment) with the teachings of Cox (high levels of exosomal PD-L1 cause CAR T cell disfunction). As discussed above for the 35 U.S.C. 103 rejections of claims 10-12 and 15-17, Ayala-Mar teaches that exosomal PD-L1 functions much like its cellular counterpart and inhibits T cell receptor-mediated T cell activation. This teaching coupled with Cox’s observation that this mechanism is maintained in the context of CAR T cells, provides clear motivation for applying the method of using PD-L1 as a biomarker for the prognostic evaluation prior to the administration of CAR T cell therapy . 07-21-aia AIA Claim s 19 and 20 are rejected under 35 U.S.C. 103 as being unpatentable over WO 2019/094727 A1 (herein Cumba-Garcia) in view of Ayala-Mar S, et al. (2021) Clinical Implications of Exosomal PD-L1 in Cancer Immunotherapy. J Immunol Res . 2021 Feb 8;2021:8839978 (herein Ayala-Mar) Arina A, et al. (2016) Enhancing T cell therapy by overcoming the immunosuppressive tumor microenvironment. Semin Immunol. 2016 Feb;28(1):54-63 (herein Arina) . As discussed for the 35 U.S.C. 103 rejections of claims 10-12 and 15-17, Cumba-Garcia and Ayala-Mar teach a method of treating cancer comprising measuring exosomal PD-L1 levels in a subject prior to administering a treatment comprising either immunotherapy (low PD-L1 EV levels) or a therapy that is not immunotherapy (high PD-L1 EV levels). Cumba-Garcia and Ayala-Mar do not teach that when immunotherapy is not administered, due to high PD-L1 EV levels, radiation therapy or chemotherapeutic agents should be administered. This deficiency is taught by Arina. Arina et al present a review of methods used to overcome immunosuppressive tumor microenvironment and enhance T cell therapy (Abstract). It is taught that conventional therapies (i.e. radiation therapy or chemotherapy) may be used as immunostimulants, in order to enable the elimination of suppressive mechanisms preventing the efficacy of immunotherapy (Section 4). It is taught that both of these traditional cancer therapies may be used either as preconditioning treatments for immunotherapy or in combination with immunotherapies. In regard to radiotherapy, it is taught that systemic ionizing radiation treatments, sometimes in conjunction with chemotherapy, may be used as a preconditioning regime in patients resistant to immune therapy, after which subsequent immunotherapy may be applied (Section 4.1 paragraph 5). In regard to chemotherapy, a cisplatin preconditioning treatment is taught, in which cisplatin is administered to a patient increasing DC, eliminating MDSC, and enhancing cytokine-induced killer cell response (Section 4.2 paragraph 7). It would have been obvious to one skilled in the art to combine the teachings of Cumba-Garcia and Ayala-Mar (a method of assessing PD-L1 EV levels in a subject prior to determining the nature of cancer treatment) with the teachings of Arina (chemotherapy/radiation preconditioning treatment of immunotherapy resistant cancer). As taught by Ayala-Mar, high levels of exosomal PD-L1, indicate that immunotherapy would have a lower likelihood of success. In this scenario, the administration of radiation therapy and/or chemotherapy would have been obvious to one skilled in the art, when considering the teachings of Arina, as it is taught that the treatments stimulate the immune system. The stimulating effect of the treatments, taught by Arina, provide clear motivation for their use in patients with high PD-L1 EV levels, as they provide a means for reversing the immunosuppression, which would have previously resulted in the exclusion of immunotherapy . By administering either radiation and/or chemotherapy to a subject, with the subject’s immune system, following treatment, may be in such a state that would allow for subsequent immunotherapy . 07-21-aia AIA Claim s 25 and 26 are rejected under 35 U.S.C. 103 as being unpatentable over Michaels YS, et al. (2019) Precise tuning of gene expression levels in mammalian cells. Nat Commun . 2019 Feb 18;10(1):818 (herein Michaels) in view of US 2019/0292539 A1 (herein Fulga), Wells AC, et al. (2017) Modulation of let-7 miRNAs controls the differentiation of effector CD8 T cells. Elife. 2017 Jul 24;6:e26398 (herein Wells), and Hilly O, et al. (2016) Distinctive pattern of let-7 family microRNAs in aggressive carcinoma of the oral tongue in young patients. Oncol Lett. 2016 Sep;12(3):1729-1736 (herein Hilly) . Michaels teaches a method for tuning gene expression levels in mammalian cells using engineered miRNA response elements (MREs) (Abstract). In brief the authors designed a 23nt degenerate oligonucleotide pool with 91% complementarity to miR-17, and assayed the resulting pool of synthetic MREs for their relative regulatory strength (Figure 1 and Results: The regulatory landscape of a synthetic miRNA response element). After ranking the relative strength of the MREs within the library, the authors created a “dictionary” of microRNA silencing-mediated fine-tuners (miSFITs) (Results: Fine-tuning gene expression levels in human cells). The tunability of gene expression utilizing these miSFITS was validated in multiple cellular systems, culminating with the step-wise tuning of endogenous BRCA1 expression in HEK293T cells (Figure 5 and Results: Tuning endogenous BRCA1 expression with miSFITs). The authors used a “scrambled” MRE as a negative control for this experiment (i.e. this MRE did not bind miR-17 and the target gene expression was not inhibited), relevant to instant claim 25. The author’s note that the MRE-tunability of gene-expression has the potential to influence the efficacy of cancer immunotherapy (Discussion paragraph 6). Tuning the expression of endogenous PD-1 in autologous CAR T cells is noted as a potential implementation of this technology, as the fine-tuning of this immunomodulating protein could optimize the balance of T cell exhaustion and autoimmunity, associated with either increased or decreased levels of PD-1, respectively. In summary, Michaels et al teach that modifying MREs of endogenous genes has the potential to influence the efficacy of the immunotherapy. Michaels does suggest the use of autologous CAR T cells in which the MRE of an endogenous gene is modified, but does not explicitly teach that the MRE is modified to abolish binding to a specific miRNA (i.e Let-7d). This deficiency is taught by Fulga, Wells, and Hilly. Fulga teaches a method for treating cancer, which comprises the administration of an autologous T cell, engineered in such a way that a heterologous MRE is inserted into the 3’UTR of a gene (Figure 4D and [0167-0168]). Much like Michaels, Fulga teaches a “scrambled” MRE, that is used as a control, and is not bound by the miRNA of interest (Figure 5 and [0191]). Fulga teaches multiple potential embodiments comprising MRE that are complementary to miRNAs, such as let-7d, miR-155, miR-185, miR-34a, miR-15, miR-210, miR-142, miR-125a, miR-130 ([0037] and Table 2). The teachings of Hilly involves the analysis of miRNA expression levels in carcinoma of the oral tongue in young patients (Abstract). The authors identify a distinct pattern of let-7 family miRNA levels associated with aggressive forms of the cancer. It was found that patients with aggressive tumors had increased levels of let-7c and let-7d compared those with non-aggressive tumors (Table 1 and Discussion paragraph 13). Wells teaches that let-7 miRNAs play a dual role in the regulation of CD8 T cell response (Abstract). It is taught that in order to maintain naïve phenotypical CD8 T cells, high levels of let-7 miRNAs are required, but upon activation let-7 miRNA levels are decreased, leading to enhanced clonal expansion and acquisition of effector function. The authors further teach that the expression of let-7 miRNAs in activated CD8 T cells inhibits proliferation and prevents the metabolic transition from oxidative phosphorylation (resting) to glycolysis (activated) (Results: Expression of let-7 miRNAs in activated CD8 T cells inhibits proliferation and the gene expression program responsible for the metabolic switch). It is shown that the forced expression of let-7 miRNAs in mouse models severely impacted the clonal expansion and differentiation of CTLs in response to viral infection, and in a related experiment led to an impaired antitumor response (Figure 2 and Results: let-7 miRNA expression in CTLs affects both the antiviral and antitumor immune responses). The authors attribute the effects of let-7 miRNA overexpression to the suppressed expression of specific let-7 targets, Myc and Eomesodermin, responsible for the metabolic reprogramming and acquisition of effector function, respectively. It would have been obvious to combine the teachings of Michaels (CAR T cells with MRE-tuned endogenous protein expression) with those of Fulga, Wells, and Hilly. Both Fulga and Michaels teach a method for treating cancer comprising autologous CAR T cells modified to have the MRE of an endogenous gene replaced with a heterologous MRE. Fulga and Michaels also both teach a “scrambled” MRE that is incapable of binding miRNA. Fulga suggests let-7d- targetted MRE as a target for heterologous replacement. Hilly and Wells provide motivation for targeting let-7d, as Hilly teaches that let-7d is upregulated in aggressive forms of carcinoma of the oral tongue, and Wells teaches that let-7 family miRNAs prevent CD8 T cells from the metabolic transition to glycolysis and prevents the proliferation of activated CD8 T cells. Both Fulga and Michaels demonstrate that the “scambled” MRE is effective at preventing miRNA binding, and demonstrate that its use has a high likelihood of success. Conclusion No claims allowed. Any inquiry concerning this communication or earlier communications from the examiner should be directed to MATTHEW CURRAN METCALF whose telephone number is (571)272-5520. The examiner can normally be reached 7:30AM-5:00PM. 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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. /MATTHEW CURRAN METCALF/Examiner, Art Unit 1647 /JOANNE HAMA/Supervisory Patent Examiner, Art Unit 1647 Application/Control Number: 18/289,049 Page 2 Art Unit: 1647 Application/Control Number: 18/289,049 Page 3 Art Unit: 1647 Application/Control Number: 18/289,049 Page 4 Art Unit: 1647 Application/Control Number: 18/289,049 Page 5 Art Unit: 1647 Application/Control Number: 18/289,049 Page 6 Art Unit: 1647 Application/Control Number: 18/289,049 Page 7 Art Unit: 1647 Application/Control Number: 18/289,049 Page 8 Art Unit: 1647 Application/Control Number: 18/289,049 Page 9 Art Unit: 1647 Application/Control Number: 18/289,049 Page 10 Art Unit: 1647 Application/Control Number: 18/289,049 Page 11 Art Unit: 1647 Application/Control Number: 18/289,049 Page 12 Art Unit: 1647 Application/Control Number: 18/289,049 Page 13 Art Unit: 1647 Application/Control Number: 18/289,049 Page 14 Art Unit: 1647 Application/Control Number: 18/289,049 Page 15 Art Unit: 1647 Application/Control Number: 18/289,049 Page 16 Art Unit: 1647 Application/Control Number: 18/289,049 Page 17 Art Unit: 1647
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