CTNF 18/565,668 CTNF 101118 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 The instant application, filed on 30 November, 2023, is a 371 of PCT/US2022/032109 filed 03 June, 2022 and which claims domestic benefit to US provisional application no. 63/196,520, filed on 03 June, 2021. Information Disclosure Statement The information disclosure statement (IDS) submitted on 19, April, 2024 has been considered by the examiner. The information disclosure statement (IDS) submitted on 30, November, 2023 has been considered by the examiner. Status of Application, Amendments, and/or Claims The response filed on 26 June, 2024 has been entered in full. These are the amended claims of the original claim set received on 30 November, 2023. In the amendment, claims 1, 5, 9, 14, 19, 25, 26, 28, 29, 34, 41, 43, 44, and 46 are amended, claims 2-4, 6-8, 11-13, 16-18, 20-23, 27, 30-33, 35-40, 42, and 47 are cancelled, and claims 48-56 are new. Therefore, claims 1, 5, 9, 10, 14, 15, 19, 24-26, 28, 29, 34, 41, 43-46, and 48-56 are pending and are the subject of this Office Action. Claim Rejections - 35 USC § 112 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. Claims 24, 25, 44, 50, and 55 rejected under 35 U.S.C. 112(b) , as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor, regards as the invention. Claim 24 recites “one or more downstream targets of JUNB selected from Table 5 or Table 6.” Neither of tables 5 or 6 are present in claim 24 or any prior claims from which is depends. Claim 25 recites “one or more agent capable of inhibiting gene expression or activity of one or more targets selected from Table 1 or Table 3.” Neither of tables 1 or 3 are present in claim 25. Claim 44 recites “the expression or activity of one or more genes selected from candidate genes in Table 2.” Table 2 is not present in claim 44 or any prior claims from which is depends. Claim 50 recites “detecting in a tumor obtained from the subject the expression or activity of one or more genes selected from candidate genes in Table 2”. Table 2 is not present in claim 50 or any prior claims from which it depends. C laim 55 recites “detecting in a tumor obtained from the subject the expression or activity of one or more genes selected from candidate genes in Table 2”. Table 2 is not present in claim 55 or any prior claims from which is depends. Claims must be complete in themselves and incorporation by reference is “permitted only in exceptional circumstances where there is not practical way to define the invention in word” (See MPEP 2173.05(s)). Thus, these claims are not complete within themselves and are unclear. 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 1 is rejected under 35 U.S.C. 102( a)(1 ) as being anticipated by Togayachi et al. (2010, of record IDS 04/19/2024), as evidenced by Chen et al. (2017) Ovarian carcinoma glyco-antigen targeted by human IgM antibody PLoS One 12(12) e0187222 (hereafter Chen) . Togayachi anticipates knocking down B3GNT2 expression in mice using a random mutagenesis method with a retroviral vector (pg.197, lines 8-12). Further Togayachi anticipates the knockout of B3GNT2 decreases the expression of polylactosamine chains on N-glycan leading to enhanced initiation of immune response by T cells (enhanced anti-tumor immunity) (pg.196 line 9- pg.197 line 2). Further Togayachi anticipates including apoptosis by decreasing the expression of poly-n-acetyllactosamine as evidenced by Chen which demonstrates that inhibition of poly-n-acetyllactosamine initiates apoptosis (abstract/pg.9, lines 2-4) . 07-15 AIA Claim s 9, 10, 14, 15, and 25 are rejected under 35 U.S.C. 102( a)(1 ) as being anticipated by Hu et al. (2018) Sabutoclax, pan-active BCL-2 protein family antagonist, overcomes drug resistance and eliminates cancer stem cells in breast cancer Cancer Letters 423 47-59 (hereafter Hu) . In regards to claims 9, 14, and 25 Hu anticipates the administration of Sabutoclax to inhibit the activity of MCL-1 and BCL2A1 in chemoresistant breast cancer cells to make them more sensitive to chemotherapeutics (pg.48, col 1, lines 24-28). In regards to claim to claims 10 and 15 Hu anticipates the treatment of breast cancer cells with Sabutoclax further increases the expression of BIM, PUMA, and BAX (Figure 1F-G) . 07-15 AIA Claim 5 is rejected under 35 U.S.C. 102( a)(1 ) as being anticipated by Chen et al. (2017) Ovarian carcinoma glyco-antigen targeted by human IgM antibody PLoS One 12(12) e0187222 (hereafter Chen) . Chen anticipates an antibody Mab216 which binds to poly-N-acetyllactosamine on B cells and kills normal and malignant B cells in vitro and in vivo (abstract) and further enhances the anti-tumor effect against epithelial ovarian cancer cells in the absence or presence of cisplatin (Abstract/pg.8, lines 1-2) . 07-15 AIA Claim s 19 and 24 are rejected under 35 U.S.C. 102( a)(1 ) as being anticipated by Fan et al. (2017) The AP-1 transcription factor JunB is essential for multiple myeloma cell proliferation and drug resistance in the bone marrow microenvironment Leukemia 31, 1570-1581 (hereafter Fan) . In regards to claim 19 Fan anticipates knocking down JUNB gene expressions using lentiviral system to deliver shRNA (pg.1571, col 2, lines 7-21), and further anticipates the knockdown of JUNB results decreased cell proliferation (pg.1572, col 2, lines 50-55) and decrease tumor size in xenograft mice models (Figure 4) (enhanced anti-tumor immunity). In regards to claim 24 Fan anticipates the downstream effects of JUNB downregulation on a variety of genes including downregulating genes listed in tables 5 or 6 of the specification (Figure 5) . 07-15 AIA Claim s 26, 28, 29, and 34 are rejected under 35 U.S.C. 102( a)(1) and 102(a)(2 ) as being anticipated by Alkhateeb et al. WO 2020/142727 (hereafter Alkhateeb) . In regards to claim 26 and 28 Alkhateeb anticipates the development of a T cell engineered to express sialidase (pg.82, lines 10-12, 27-31) to treat cancer by reducing immune inhibition mediated by the salic acid and/or salic acid containing molecules (pg.2 lines 15-16). In regards to claim 29 Alkhateeb anticipates also delivering a CAR T cells to treat cancer (pg.82, lines 27-31). In regards to claim 34 Alkhateeb anticipates treating tumor baring mice with transduced T cells followed by T cells engineered to express sialidase every 5 days after (pg.82, lines 22-26) . 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. 07-22-aia AIA Claim s 43 and 49-53 are rejected under 35 U.S.C. 103 as being unpatentable over Hu as applied to claim s 9 and 14 above, and further in view of Lickliter et al. (2007) Small molecule Bcl-2 inhibitors sensitise tumor cells to immune-mediated destruction British Journal of Cancer 96, 600-608 (hereafter Lickliter) , Garcia-Aranda et al. (2018) Bcl-2 Inhibition to Overcome Resistance to Chemo- and Immunotherapy Int. J. Mol. Sci. 19, 3950 (hereafter Garcia-Aranda) , and Hoos (2012) Evolution of end point for cancer immunotherapy trials Annals of Oncology 23(Supplemental 8) viii47-viii52 (hereafter Hoos) . Hu teaches the delivery of Sabutoclax to chemoresistant breast cancer cells to enhance their antitumor immunity as outlined above. Hu fails to teach the further administering an immunotherapy such as a CAR, TCR, TIL, or checkpoint inhibitor of claims 49 and 51. Hu also fails to teach the method of treating cancer comprising determining if the subject is an immunotherapy responder or non-responder by determining the activity of a gene candidate and further if they are a responder treating them with an immunotherapy and if a non-responder treating them with the method of claims 9 or 14, of claims 50 and 52. Further, Hu fails to teach the method of monitoring the efficacy of an immunotherapy comprising detecting the expression of one or more genes selected from MCL1, BCL2A1, JUNB, and B3GNT2 in a subject at two or more timepoints and further if increase is observed it dictates a poor outcome and the methods of claims 9 or 14 are administered of claims 43 and 53. Lickliter, however, in regards to claims 49 and 51 teaches the Bcl-2 family of proteins are potent inhibitors of cell death, and have high expression in many cancers (pg.600, col 1, lines 9-13). Lickliter also teaches inhibition of Bcl-2 with the small molecule inhibitor HA14-1 in combination with the immunotherapy Vα24+ Vβ11+ T CR expressing NK cells to treat lymphoma cells or ABT-737 in combination with Melan-A/MART-1 specific cytotoxic T-lymphocytes to treat melanoma cells (pg.601, col 1, lines 12-29), and found that these combination significantly reduced cell viability and increased apoptosis (pg.603, col 2, lines 1-2 & 16-19/ pg.603, col 2, lines 48-58). Lickliter fails to teach the method of treating cancer comprising determining if the subject is an immunotherapy responder or non-responder by determining the activity of a gene candidate and further if they are a responder treating them with an immunotherapy and if a non-responder treating them with the method of claims 9 or 14, of claims 50 and 52. Lickliter also fails to teach the method of monitoring the efficacy of an immunotherapy comprising detecting the expression of one or more genes selected from MCL1, BCL2A1, JUNB, and B3GNT2 in a subject at two or more timepoints and further if increase is observed it dictates a poor outcome and the methods of claims 9 or 14 are administered of claims 43 and 53. However, in regards to claims 43, 50, 52, and 53 Garcia-Aranda teaches immunotherapies directly and indirectly activate cellular apoptosis, and that tumor sensitivity to these immunotherapies depends on the level of expression of anti-apoptotic proteins as well as on their ability to activate apoptotic pathways (pg.7, lines 5-8). Further Garcia-Aranda teaches the Bcl-2 family is an attractive target in cancer treatment, and as a means to overcome immunotherapy resistant (non-responder) which is caused by the over expression of anti-apoptotic genes and the silencing of pro-apoptotic genes (pg.12, lines 8-11), and that BH3-domian mimicking proteins are a promising method to treating apoptosis resistant cancer (pg.12, lines 23-27). Garcia-Aranda fails to teach the monitoring of immunotherapy by measurement of gene expression at two or more timepoint of claims 43 and 53, however, Hoos teaches that monitoring or immunotherapy response in cancer needs to be monitored over time because immunotherapies can cause an initial tumor burden increase caused by a surge of infiltrating immune cells which might not be indicative of inefficiency and more information is needed (pg.viii47, col 2, lines 12-18/ pg.viii49, col 1, line 16- col 2, line 3), further Hoos teaches that efficacy can be measured by biomarker development (pg.viii48, col 1, lines 1-3). Thus, Hu discloses the delivery of Sabutoclax to chemoresistant breast cancer cells to enhance their antitumor immunity. Lickliter teaches using Bcl-2 inhibitors in combination with adoptive cell therapy improves their efficacy. Garcia-Aranda teaches that the Bcl-2 protein family which includes BCL2A1 and MCL1 is an indicator of a subject response to immunotherapies, and measuring these apoptotic factors can determine the efficacy of an immunotherapy, and that utilizing BH3 mimicking proteins is a method of overcoming the treatment resistant in non-responder subjects. Hoos teaches that monitoring immunotherapy over time is important to ensure initial readings are not indicative of other activity and further that response can be measured by biomarker development. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to combine the teachings of Hu with the teachings of Lickliter, Garcia-Aranda, and Hoos with a reasonable expectation of success to develop the methods of monitoring the efficacy of immunotherapy, and treating cancer in non-responder subject with BCL-2 inhibitors to increase their sensitivity to immunotherapies, because Sabutoclax shows the ability to sensitize cancer cells, and combinations of BCL-2 with immunotherapies improve cellular cytotoxicity in a apoptosis dependent method, and the BCL-2 family of proteins is the main player in the intrinsic apoptosis process of cancer cells and modulation has a direct impact on treatment efficacy, and monitoring of response over time gives a more accurate understanding of immunotherapy efficacy, leading to a method of treatment of cancer, and monitoring of efficacy which improves outcome through targeting of the apoptotic pathway . 07-22-aia AIA Claim s 41, 44, 45, and 48 are rejected under 35 U.S.C. 103 as being unpatentable over Togayachi as applied to claim 1 above, and further in view of Chen, Lickliter, Garcia-Aranda, and Hoos . Togayachi fails to teach the further administering an immunotherapy such as a CAR, TCR, TIL, or checkpoint inhibitor of claim 48. Hu also fails to teach the method of treating cancer comprising determining if the subject is an immunotherapy responder or non-responder by determining the activity of a gene candidate and further if they are a responder treating them with an immunotherapy and if a non-responder treating them with the method of claim 1, of claims 44 and 45. Further, Hu fails to teach the method of monitoring the efficacy of an immunotherapy comprising detecting the expression of one or more genes selected from MCL1, BCL2A1, JUNB, and B3GNT2 in a subject at two or more timepoints and further if increase is observed it dictates a poor outcome and the methods of claim 1 are administered of claim 41. Lickliter, however in regards to claim 48 teaches how inhibiting a BCL2 gene (a gene which blocks apoptosis similar to B3GNT2, as evidenced by Chen (pg.9, lines 2-4)) in combination with an immunotherapy improves cancer treatment, as outlined above. Lickliter fails to teach the method of treating cancer comprising determining if the subject is an immunotherapy responder or non-responder by determining the activity of a gene candidate and further if they are a responder treating them with an immunotherapy and if a non-responder treating them with the method of claim 1, of claim 44 and 45. Lickliter also fails to teach the method of monitoring the efficacy of an immunotherapy comprising detecting the expression of one or more genes selected from MCL1, BCL2A1, JUNB, and B3GNT2 in a subject at two or more timepoints and further if increase is observed it dictates a poor outcome and the method of claim 1 is administered of claims 41. Garcia-Aranda, however in regards to claims 44 and 45 teaches immunotherapies directly and indirectly activate cellular apoptosis, and that tumor sensitivity to these immunotherapies depends on the level of expression of anti-apoptotic proteins as well as on their ability to activate apoptotic pathways as outlined above. Garcia-Aranda fails to teach the monitoring of immunotherapy by measurement of gene expression at two or more timepoint of claim 41 however, Hoos teaches that monitoring or immunotherapy response in cancer needs to be monitored over time because immunotherapies can cause an initial tumor burden increase caused by a surge of infiltrating immune cells which might not be indicative of inefficiency and more information is needed as outlined above. Thus, Togayachi discloses the knockout of B3GNT2 in multiple mice to enhance T cell mediated Immune response, and apoptosis. Lickliter teaches using Bcl-2 inhibitors in combination with adoptive cell therapy improves their efficacy. Garcia-Aranda teaches that the Bcl-2 protein family which includes BCL2A1 and MCL1 is an indicator of a subject response to immunotherapies, and measuring these apoptotic factors can determine the efficacy of an immunotherapy. Hoos teaches that monitoring immunotherapy over time is important to ensure initial readings are not indicative of other activity and further that response can be measured by biomarker development. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to substitute the use B3GNT2 inhibition of the teachings of Togayachi over the teachings of BCL2 protein inhibitions of Lickliter, Garcia-Aranda, and Hoos with a reasonable expectation of success to develop the methods of monitoring the efficacy of immunotherapy, and treating cancer in non-responder subject with B3GNT2 inhibitors to increase their sensitivity to immunotherapies, because B3GNT2 knockdown shows the ability enhance anti-tumor immunity, and combinations of apoptosis inducing gene modulation with immunotherapies improve cellular cytotoxicity in a apoptosis dependent method, and the B3GNT2 is a main player in the immune response of T cells and apoptosis of cancer cells and modulation has a direct impact on treatment efficacy, and monitoring of response over time gives a more accurate understanding of immunotherapy efficacy, leading to a method of treatment of cancer, and monitoring of efficacy which improves outcome through targeting of the apoptotic pathway . 07-22-aia AIA Claim s 54-56 are rejected under 35 U.S.C. 103 as being unpatentable over Fan as applied to claim 19 above, and further in view of Lickliter, Garcia-Aranda, and Hoos . Fan fails to teach the further administering an immunotherapy such as a CAR, TCR, TIL, or checkpoint inhibitor of claim 54. Hu also fails to teach the method of treating cancer comprising determining if the subject is an immunotherapy responder or non-responder by determining the activity of a gene candidate and further if they are a responder treating them with an immunotherapy and if a non-responder treating them with the method of claim 19, of claim 55. Further, Hu fails to teach the method of monitoring the efficacy of an immunotherapy comprising detecting the expression of one or more genes selected from MCL1, BCL2A1, JUNB, and B3GNT2 in a subject at two or more timepoints and further if increase is observed it dictates a poor outcome and the methods of claim 19 are administered of claim 56. Lickliter, however in regards to claim 54 teaches how inhibiting a BCL2 gene (a gene which blocks apoptosis of cells similar to JUNB) in combination with an immunotherapy improves cancer treatment, as outlined above. Lickliter fails to teach the method of treating cancer comprising determining if the subject is an immunotherapy responder or non-responder by determining the activity of a gene candidate and further if they are a responder treating them with an immunotherapy and if a non-responder treating them with the method of claim 19, of claim 55. Lickliter also fails to teach the method of monitoring the efficacy of an immunotherapy comprising detecting the expression of one or more genes selected from MCL1, BCL2A1, JUNB, and B3GNT2 in a subject at two or more timepoints and further if increase is observed it dictates a poor outcome and the method of claim 19 is administered of claims 56. Garcia-Aranda, however in regards to claim 55 teaches immunotherapies directly and indirectly activate cellular apoptosis, and that tumor sensitivity to these immunotherapies depends on the level of expression of anti-apoptotic proteins as well as on their ability to activate apoptotic pathways as outlined above. Garcia-Aranda fails to teach the monitoring of immunotherapy by measurement of gene expression at two or more timepoint of claim 56 however, Hoos teaches that monitoring or immunotherapy response in cancer needs to be monitored over time because immunotherapies can cause an initial tumor burden increase caused by a surge of infiltrating immune cells which might not be indicative of inefficiency and more information is needed as outlined above. Thus, Fan discloses the knockdown of JUNB in multiple myeloma cancer cells to enhance their antitumor immunity. Lickliter teaches using Bcl-2 inhibitors in combination with adoptive cell therapy improves their efficacy. Garcia-Aranda teaches that the Bcl-2 protein family which includes BCL2A1 and MCL1 is an indicator of a subject response to immunotherapies, and measuring these apoptotic factors can determine the efficacy of an immunotherapy. Hoos teaches that monitoring immunotherapy over time is important to ensure initial readings are not indicative of other activity and further that response can be measured by biomarker development. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to substitute the use JUNB inhibition of the teachings of Fan over the teachings of BCL2 protein inhibitions of Lickliter, Garcia-Aranda, and Hoos with a reasonable expectation of success to develop the methods of monitoring the efficacy of immunotherapy, and treating cancer in non-responder subject with JUNB inhibitors to increase their sensitivity to immunotherapies, because JUNB knockdown shows the ability to sensitize cancer cells, and combinations of apoptosis inducing gene modulation with immunotherapies improve cellular cytotoxicity in a apoptosis dependent method, and the JUNB is a main player in the intrinsic apoptosis process of cancer cells and modulation has a direct impact on treatment efficacy, and monitoring of response over time gives a more accurate understanding of immunotherapy efficacy, leading to a method of treatment of cancer, and monitoring of efficacy which improves outcome through targeting of the apoptotic pathway . 07-21-aia AIA Claim 46 is rejected under 35 U.S.C. 103 as being unpatentable over Henrich (2016) A Microplate- Based Nonradioactive Protein Synthesis Assay: Application to TRAIL Sensitization by Protein Synthesis Inhibitors PLoS ONE 11(10) e0165192 (hereafter Henrich) in view of Togayachi and Tsuboi et al. (2011) A novel strategy for evasion of NK cell immunity by tumors expressing core2 O-glycans The EMBO Journal (30) 3173-31852 (hereafter Tsuboi) . Henrich teaches a method of screening for inhibitors of protein synthesis which sensitize cancer to TRAIL immunotherapy. Further Henrich teaches the method uses the measurement of binding of an anti-cFLIP antibody, and an anti-GAPDH antibody both of which are fluorescently labeled to measure cFLIP expression (pg.3, lines 23-54). Overexpression of cFLIP is associated with TRAIL resistance (pg.8, lines 3-4). Henrich fails to teach the tumor cells having upregulated the inhibitor decreasing poly-N-acetyllactosamine and further the tumor cell overexpressing B3GNT2 and further detecting the binding of one CD2, 4-1BB, TREML2, or NKGD2 wherein the increased binding indicated reduced poly-N-acetyllactosamine. Togayachi, however, teaches that poly-N-acetyllactosamine is a regulator in cancer cell response to T cell immunity (pg.196 line 9- pg.197 line 2), and further teaches that B3GNT2 is the main polylactosamine synthase (pg.187, lines 20-21), and thus B3GNT2 overexpression is indicative of poly-N- acetyllactosamine expression. Togayachi fails to teach detecting the binding of one CD2, 4-1BB, TREML2, or NKGD2 wherein the increased binding indicated reduced poly-N-acetyllactosamine. Tsuboi, however, teaches that poly-N-acetyllactosamine and galectin-3 reduce NKGD2-FC binding to tumor cells disrupting anti-tumor immunity (pg.3179, col 1, lines 1-2). Thus, Henrich discloses a method of screening protein synthesis inhibitors including contacting a cancer cell overexpressing a gene with an agent and determining efficacy by measuring binding of fluorescently labeled antibodies, Togayachi motivates the use of poly-L-acetyllactosamine because it is a key regulator cancer cell response to T cell mediated immunity, and further monitoring it expression through B3GNT2 expression because B3GNT2 is a main synthase of poly-N-acetyllactosamine, and Tsuboi motivates the monitoring of inhibition by measuring of binding of NKGD2 because poly-N-acetyllactosamine expression is associated with decreased binding of NKGD2 on cancer cells and decreased anti-tumor immune response. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to combine the teachings of Henrich, Togayachi, and Tsuboi with a reasonable expectation of success to develop a method of screening for inhibitor which decrease poly-N-acetyllactosamine. Conclusion Any inquiry concerning this communication or earlier communications from the examiner should be directed to DASIA A ALDARONDO whose telephone number is (571)272-1977. The examiner can normally be reached on Monday – Thursday from 8am to 6pm. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Joanne Hama, can be reached at telephone number (571. The fax phone number for the organization where this application or proceeding is assigned is (571)273-8300. Information regarding the status of an application may be obtained from Patent Center. Status information for published applications may be obtained from Patent Center. Status information for unpublished applications is available through Patent Center to authorized users only. Should you have questions about access to the USPTO patent electronic filing system, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). Examiner interviews are available via a variety of formats. See MPEP § 713.01. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) Form at https://www.uspto.gov/InterviewPractice. /D.A.A/Examiner, Art Unit 1647 /JOANNE HAMA/Supervisory Patent Examiner, Art Unit 1647 Application/Control Number: 18/565,668 Page 2 Art Unit: 1647 Application/Control Number: 18/565,668 Page 3 Art Unit: 1647 Application/Control Number: 18/565,668 Page 4 Art Unit: 1647 Application/Control Number: 18/565,668 Page 5 Art Unit: 1647 Application/Control Number: 18/565,668 Page 6 Art Unit: 1647 Application/Control Number: 18/565,668 Page 7 Art Unit: 1647 Application/Control Number: 18/565,668 Page 8 Art Unit: 1647 Application/Control Number: 18/565,668 Page 9 Art Unit: 1647 Application/Control Number: 18/565,668 Page 10 Art Unit: 1647 Application/Control Number: 18/565,668 Page 11 Art Unit: 1647 Application/Control Number: 18/565,668 Page 12 Art Unit: 1647 Application/Control Number: 18/565,668 Page 13 Art Unit: 1647 Application/Control Number: 18/565,668 Page 14 Art Unit: 1647
Prosecution Insights