CTNF 18/687,571 CTNF 89188 DETAILED ACTION 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. 12-151 AIA 26-51 12-51 Status of Claims Claims 1, 2, 13, 15, 17-20, 25-27, 29, 31, 33, 35, and 58-61 as amended on 1/14/2025 are currently pending and under consideration on the merits. Claim Rejections - 35 USC § 101 07-04-01 AIA 07-04 35 U.S.C. 101 reads as follows: Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title. Claims 1, 2, 13, 15, 17-20, 25-27, 29, 31, 33, 35, and 58-61 are rejected under 35 U.S.C. 101 because the claimed invention is directed to a judicial exception without significantly more. Claim 1 recites a method of assessing the efficacy of treatment for a generic bestrophinopathy in an eye of a subject having at least one mutant BEST1 allele, and then recites a step of assessing retinal function by ERG and correlating (in the terminal wherein clause) improved and/or maintained ERG amplitude(s) with the efficacy of treatment. The correlation is an abstract idea and thus the claim is directed towards an abstract idea (see M.P.E.P. § 2106.04(a)). This judicial exception is not integrated into a practical application because it only amounts to extra-solution activity. In this case, the administration of a generic rAAV comprising a generic nucleic acid encoding for a human BEST1 protein does not impose any meaningful limits on the claim, as the administration step is a precursor to all uses of the recited exception; see M.P.E.P. § 2106.04(d)(2). The claim(s) does/do not include additional elements that are sufficient to amount to significantly more than the judicial exception because the claim only recites elements that are routine and conventional in this art. Guziewicz ( PLoS One (2013), 8(10), e75666, 11 pages plus appended supplemental information; Reference U) teaches a method of assessing efficacy of treatment for a bestrophinopathy in an eye of a canine subject being a carrier for cmr1 (i.e. wherein the subject has at least one mutant BEST 1 allele) and control canine eyes, the method comprising treating the subject with a dose of a rAAV vector and wherein the rAAV vector comprises a nucleic acid encoding for the canine or human BEST1 protein (Materials and Methods on pages 7-10), reading in-part in claim 1. Guziewicz teaches that canine multifocal retinopathy (cmr) is an autosomal recessive disease caused by mutations in the BEST1 dog ortholog (the paragraph spanning pages 1-2) and envisions treating canine subjects suffering from cmr which could ultimately be translated to human BEST1 disorders (page 2, the paragraph starting “Over the last decade…”), reading in-part on claim 2. Guziewicz teaches that the rAAV2/2 vector serotype carrying either GFP reporter or BEST1 transgene under control of human VMD2 promoter was safe, and enabled specific transduction of the RPE cell monolayer that was stable for up to 6 months post injection (Abstract), reading on claim 2. Guziewicz teaches subretinal injection (Materials and Methods on pages 8-9), reading on claims 15 and 19. Guziewicz teaches that the human BEST1 is expressed in RPE cells (Fig. 5), reading on claim 17. Guziewicz teaches bleb formation in the retina following rAAV administration (page 2, left column, paragraph starting “A set of eighteen eyes...”) and monitoring bleb kinetics by in vivo retinal imaging in the fundus and with a cSLO/SD-OCT device (page 2, right column, paragraph starting “Subsequently, a modified vector construct…”, Fig. S3, and the paragraph spanning pages 9-10), reading in-part on claim 20, and reading in-part on the in vivo imaging of claims 58 and 59. Burgess ( The American Journal of Genetics (2008), 82, 19-31; Cite number 62 provided in the IDS dated 4/22/2024) teaches methods of measuring ERG activity in human subjects suffering from autosomal-recessive bestrophinopathy (ARB) caused by biallelic mutations in BEST1 (Abstract, Fig. 1 for biallelic BEST1 mutations, Fig. 3 and the paragraph starting “The retinopathy was present in all…” on page 22for ERG measurements), reading on claims 1 and 2. Burgess teaches full-field ERG (page 20, subheading “Patient Details), reading on claim 18. Burgess teaches measuring BWF a-waves and a mixed rod-cone response (Fig. 3 and 4, and noting that family 2 has generalized rod- and cone-system dysfunction as set forth in the legend of Fig. 3), reading on claims 25 and 26 and reading in-part on claim 35. Burgess teaches that one of the subjects suffering from ARB shows subretinal fluid between the RPE cells and neurosensory retinal as measured by OCT (Fig. 2L), reading on claims 58 and 59. Yardley ( Invest Ophthalmol Vis Sci. 2004;45: 3683–3689); Reference V) teaches that Autosomal Dominant Vitreoretinochoroidopathy (ADVIRC) is caused by mutations in WMD2 (i.e. BEST1) , which encodes for bestrophin (Abstract), reading on claim 13. Bui ( Invest Ophthalmol Vis Sci. 2005;46:202–213; Reference W) teaches methods of characterizing retinal function during elevated intraocular pressure, the method comprising measuring the scotopic a-wave response the scotopic b-wave response, and photopic b-wave response at intensities of at -6.1-2.7 log cd*s/m 2 , (Abstract, Figure 1, and Data Analysis on pages 20-4-205), reading on claims 27, 29, 31, and 33. Davidson ( The American Journal of Genetics (2009), 85, 581-592; Reference X) teaches that subjects suffering from Retinitis Pigmentosa and harboring missense mutations in Bestrophin-1 were evaluated by fundoscopy and further suffer from retinal gliosis (page 584, paragraph starting “Family 1 is a …”, and Fig. 2A and 2B), reading on claim 60. Hippert ( PLoS One (2015), 10(3), e0120415, 27 pages; Reference U 2) teaches methods of assessing Gfap, vimentin and chondroitin sulphate proteoglycan (CSPG) levels and outer limiting membrane (OLM) integrity over time in four murine models of inherited photoreceptor degeneration (Abstract), reading in-part on claim 61. Hippert teaches methods of detecting Gfap in Muller glia and apical processes within the ONL (Fig. 2B iii, vi; Fig. 2C i-vi; Fig. 2E i-vi; generally noting the downward extension of Gfap+ Muller glia processes relative to as compared to wildtype mice in Fig 2A; The paragraph starting “Degeneration occurs…” on page 7 through paragraph ending “…(Fig. 3C vii).” on page 8, and the paragraph spanning pages 9-10), reading on claim 61. 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. 07-20-02-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 1, 2, 15, 17-20, 25, 26, 35, 58, and 59 are rejected under 35 U.S.C. 103 as being unpatentable over Guziewicz et al. ( PLoS One (2013), 8(10), e75666, 11 pages plus appended supplemental information; Reference U) in view of Burgess et al. ( The American Journal of Genetics (2008), 82, 19-31; Cite number 62 provided in the IDS dated 4/22/2024) . Guziewicz teaches a method of assessing efficacy of treatment for a bestrophinopathy in an eye of a canine subject being a carrier for cmr1 (i.e. wherein the subject has at least one mutant BEST 1 allele) and control canine eyes, the method comprising treating the subject with a dose of a rAAV vector and wherein the rAAV vector comprises a nucleic acid encoding for the canine or human BEST1 protein (Materials and Methods on pages 7-10), reading in-part in claim 1. Guziewicz teaches that canine multifocal retinopathy (cmr) is an autosomal recessive disease caused by mutations in the BEST1 dog ortholog (the paragraph spanning pages 1-2) and envisions treating canine subjects suffering from cmr which could ultimately be translated to human BEST1 disorders (page 2, the paragraph starting “Over the last decade…”), reading in-part on claim 2. Guziewicz teaches that the rAAV2/2 vector serotype carrying either GFP reporter or BEST1 transgene under control of human VMD2 promoter was safe, and enabled specific transduction of the RPE cell monolayer that was stable for up to 6 months post injection (Abstract), reading on claim 2. Guziewicz teaches subretinal injection (Materials and Methods on pages 8-9), reading on claims 15 and 19. Guziewicz teaches that the human BEST1 is expressed in RPE cells (Fig. 5), reading on claim 17. Guziewicz teaches bleb formation in the retina following rAAV administration (page 2, left column, paragraph starting “A set of eighteen eyes...”) and monitoring bleb kinetics by in vivo retinal imaging in the fundus and with a cSLO/SD-OCT device (page 2, right column, paragraph starting “Subsequently, a modified vector construct…”, Fig. S3, and the paragraph spanning pages 9-10), reading in-part on claim 20, and reading in-part on the in vivo imaging of claims 58 and 59. Regarding claim 1, Guziewicz does not teach assessing retinal function by ERG. Regarding claim 2, Guziewicz does not teach treating subjects having two mutant BEST1 alleles. Regarding claim 18, Guziewicz does not teach full field ERG. Regarding claim 20, Guziewicz does not teach ERG monitoring of the subretinal bleb at the administration site. Regarding claim 25, Guziewicz does not teach measuring scotopic a-waves. Regarding claim 26, Guziewicz does not teach measuring a mixed rod-cone response. Regarding claim 35, Guziewicz does not teach comparing ERG amplitudes between a treated and untreated eye. Regarding claims 58 and 59, Guziewicz does not teach evaluating the treatment by formation of light-potentiated subretinal microdetachments. Burgess teaches methods of measuring ERG activity in human subjects suffering from autosomal-recessive bestrophinopathy (ARB) caused by biallelic mutations in BEST1 (Abstract, Fig. 1 for biallelic BEST1 mutations, Fig. 3 and the paragraph starting “The retinopathy was present in all…” on page 22for ERG measurements), reading on claims 1 and 2. Burgess teaches full-field ERG (page 20, subheading “Patient Details), reading on claim 18. Burgess teaches measuring BWF a-waves and a mixed rod-cone response (Fig. 3 and 4, and noting that family 2 has generalized rod- and cone-system dysfunction as set forth in the legend of Fig. 3), reading on claims 25 and 26 and reading in-part on claim 35. Burgess teaches that one of the subjects suffering from ARB shows subretinal fluid between the RPE cells and neurosensory retinal as measured by OCT (Fig. 2L), reading on claims 58 and 59. Regarding the ERG of claims 1, 18, 25, and 26, it would have been obvious to a person of ordinary skill in the art before the invention was filed to assess retinal function in the subjects of Guziewicz with the full-field ERG measurement methods of Burgess. A person of ordinary skill in the art would have had a reasonable expectation of success to do so because both Guziewicz and Burgess are in-part towards non-invasive methods of assessing retinal function in subjects suffering from human BEST1 mutations or the canine BEST1 ortholog. The skilled artisan would have been motivated to do so because Burgess teaches that ERG measurements are predictably advantageous to non-invasively assess retinal function, and so would improve upon the methods of Guziewicz to assess the retinal function of the subjects with rAAV comprising BEST1 of Guziewicz. Regarding claim 2, it would have been obvious to a person of ordinary skill in the art before the invention was filed to further treat canine or human subjects having two mutant BEST1 alleles according to Guziewicz A person of ordinary skill in the art would have had a reasonable expectation of success to do so because Guziewicz teaches that the rAAV2/2 vector serotype carrying either GFP reporter or BEST1 transgene under control of human VMD2 promoter was safe, and enabled specific transduction of the RPE cell monolayer that was stable for up to 6 months post injection, and because Burgess teaches that biallelic BEST1 mutations case retinopathy. The skilled artisan would have been motivated to do so because Guziewicz expressly considers the further treatment of treat canine or human subjects having two mutant BEST1 alleles. Regarding claim 20, it would have been obvious to a person of ordinary skill in the art before the invention was filed to further assess retinal function by ERG at the subretinal bleb in the subjects of Guziewicz with the full-field ERG measurement methods of Burgess. A person of ordinary skill in the art would have had a reasonable expectation of success to do so because both Guziewicz and Burgess are in-part towards non-invasive methods of assessing retinal function in subjects suffering from human BEST1 mutations or the canine BEST1 ortholog, and because Guziewicz teaches monitoring bleb kinetics by in vivo retinal imaging in the fundus and with a cSLO/SD-OCT device. The skilled artisan would have been motivated to do so because Burgess teaches that ERG measurements are predictably advantageous to non-invasively assess retinal function, and so would improve upon the methods of Guziewicz to assess the retinal function of the subjects with rAAV comprising BEST1 of Guziewicz. Regarding claim 35, it would have been obvious to a person of ordinary skill in the art before the invention was filed to further comparing ERG amplitudes between a treated and untreated eye in the subjects of Guziewicz with the full-field ERG measurement methods of Burgess. A person of ordinary skill in the art would have had a reasonable expectation of success to do so because both Guziewicz and Burgess are in-part towards non-invasive methods of assessing retinal function in subjects suffering from human BEST1 mutations or the canine BEST1 ortholog. The skilled artisan would have been motivated to do so because Burgess teaches that ERG measurements are predictably advantageous to non-invasively assess retinal function, and so would improve upon the methods of Guziewicz to assess the retinal function of the subjects with rAAV comprising BEST1 of Guziewicz relative to untreated/control subjects. Regarding claims 58 and 59, it would have been obvious to a person of ordinary skill in the art before the invention was filed to evaluate the treatment by formation of light-potentiated subretinal microdetachments (e.g. subretinal fluid during in vivo OCT imaging) in the subjects of Guziewicz. A person of ordinary skill in the art would have had a reasonable expectation of success to do so because Guziewicz and Burgess are both in-part directed towards in vivo retinal imaging by OCT, and because Burgess teaches that one of the subjects suffering from ARB shows subretinal fluid between the RPE cells and neurosensory retinal as measured by OCT. The skilled artisan would have been motivated to do so because the further detection of morphological improvements in the treated subjects of Guziewicz would predictably determine of Guziewicz’ treatment methods were or were not effective. Therefore, the invention as a whole would have been prima facie obvious to a person of ordinary skill before the invention was filed . 07-22-aia AIA Claim 13 is rejected under 35 U.S.C. 103 as being unpatentable over Guziewicz and Burgess as applied to claim 1 above, and further in view of Yardley et al. ( Invest Ophthalmol Vis Sci. 2004;45: 3683–3689); Reference V) . The teachings of Guziewicz and Burgess are relied upon above. Regarding claim 13, Guziewicz and Burgess do not teach he embodiment of Autosomal Dominant Vitreoretinochoroidopathy (ADVIRC). Yardley teaches that Autosomal Dominant Vitreoretinochoroidopathy (ADVIRC) is caused by mutations in WMD2 (i.e. BEST1) , which encodes for bestrophin (Abstract), reading on claim 13. It would have been obvious to a person of ordinary skill in the art before the invention was filed to substitute the human subjects having ADVIRC of Yardley for the cmr carrier subjects of Guziewicz in Guziewicz’s methods. A person of ordinary skill in the art would have had a reasonable expectation of success to do so because Guziewicz teaches that the rAAV2/2 vector serotype carrying either GFP reporter or BEST1 transgene under control of human VMD2 promoter was safe, and enabled specific transduction of the RPE cell monolayer that was stable for up to 6 months post injection, and because Burgess teaches that biallelic BEST1 mutations case retinopathy. The skilled artisan would have been motivated to do so because Guziewicz expressly considers the further treatment of treat canine or human subjects having mutant BEST1 alleles, and so the substitution would be predictably advantageous to treat the human subjects suffering from ADVIRC of Yardley. Therefore, the invention as a whole would have been prima facie obvious to a person of ordinary skill before the invention was filed . 07-22-aia AIA Claim s 27, 29, 31, and 33 are rejected under 35 U.S.C. 103 as being unpatentable over Guziewicz and Burgess as applied to claim 1 above, and further in view of Bui et al. ( Invest Ophthalmol Vis Sci. 2005;46:202–213; Reference W) . The teachings of Guziewicz and Burgess are relied upon above. Regarding claim 27, Guziewicz and Burgess do not teach wherein the amplitude of the scotopic a-wave response is measured at one or more intensities of at least about -2.0 Log cd*s/m 2 . Regarding claim 29, Guziewicz and Burgess do not teach wherein the amplitude of the scotopic b-wave response is measured at one or more intensities of at least about -4.0 Log cd*s/m 2 . Regarding claim 31, Guziewicz and Burgess do not teach wherein the amplitude of the photopic (1Hz) b-wave response is measured at one or more intensities of at least about -1.0 Log cd*s/m 2 . Regarding claim 33, Guziewicz and Burgess do not teach wherein the amplitude of the photopic 29 Hz flicker response is measured at one or more intensities of at least about -2.0 Log cd*s/m 2 . Bui teaches methods of characterizing retinal function during elevated intraocular pressure, the method comprising measuring the scotopic a-wave response the scotopic b-wave response, and photopic b-wave response at intensities of at -6.1-2.7 log cd*s/m 2 , (Abstract, Figure 1, and Data Analysis on pages 20-4-205), reading on claims 27, 29, 31, and 33. Regarding claims (light) intensities and (photoreceptor) wave measurement response of claims 27, 29, 31, and 33, it would have been obvious to a person of ordinary skill in the art before the invention was filed to substitute the ERG measurement methods of Bui for the ERG measurement methods of Burgess to assess retinal function in the subjects of Guziewicz. A person of ordinary skill in the art would have had a reasonable expectation of success to do so because both Guziewicz and Burgess are in-part towards non-invasive methods of assessing retinal function in subjects suffering from human BEST1 mutations or the canine BEST1 ortholog ,and because Bui teaches detailed ERG methods at specific intensities to quantify the different waves of the photoreceptor response. The skilled artisan would have been motivated to do so because Bui teaches that ERG measurements are predictably advantageous to non-invasively assess retinal function, and so would improve upon the methods of Guziewicz to assess the retinal function of the subjects with rAAV comprising BEST1 of Guziewicz. Regarding the 29 Hz flicker response of claim 33, a prima facie case of obviousness exists where the claimed ranges and prior art ranges do not overlap but are close enough that one skilled in the art would have expected them to have the same properties. Titanium Metals Corp. of Amer. v. Banner, 778 F.2d 775, 227 USPQ 773 (Fed. Cir. 1985). In this case, Burgess teaches ERG methods measuring a photopic 30 Hz flicker response as one of several non-invasive methods for measuring retina function in subjects suffering from Autosomal-Recessive bestrophinopathy (ARG), and any difference of 1 Hz between the claim and Burgess must be held prima facie obvious as being similarly effective methods for detecting the photopic flicker response in the treated subjects of Guziewicz absent any showing to the contrary. Therefore, the invention as a whole would have been prima facie obvious to a person of ordinary skill before the invention was filed . 07-22-aia AIA Claim 60 is rejected under 35 U.S.C. 103 as being unpatentable over Guziewicz and Burgess as applied to claim s 1, 58, and 59 above, and further in view of Davidson et al. ( The American Journal of Genetics (2009), 85, 581-592; Reference X) . The teachings of Guziewicz and Burgess are relied upon above. Regarding claim 60, Guziewicz and Burgess do not teach performing in vivo retinal imaging to evaluate the treated subjects for reactive gliosis. Davidson teaches that subjects suffering from Retinitis Pigmentosa and harboring missense mutations in Bestrophin-1 were evaluated by fundoscopy and further suffer from retinal gliosis (page 584, paragraph starting “Family 1 is a …”, and Fig. 2A and 2B), reading on claim 60. It would have been obvious to a person of ordinary skill in the art before the invention was filed to further evaluate the subjects of Guziewicz for retinal gliosis in view of Davidson. A person of ordinary skill in the art would have had a reasonable expectation of success to do so because both Guziewicz and Davidson are in-part towards non-invasive methods of assessing retinal function in subjects suffering from human BEST1 mutations or the canine BEST1 ortholog. The skilled artisan would have been motivated to do so because Davidson teaches that in vivo retinal imaging by fundoscopy is predictably advantageous to detect retinal gliosis, and so would improve upon the methods of Guziewicz to assess the retinal function of the subjects with rAAV comprising BEST1 of Guziewicz. Therefore, the invention as a whole would have been prima facie obvious to a person of ordinary skill before the invention was filed . 07-21-aia AIA Claim 61 is rejected under 35 U.S.C. 103 as being unpatentable over Guziewicz and Burgess as applied to claim 1 and 58 above, and further in view Hippert et al. ( PLoS One (2015), 10(3), e0120415, 27 pages; Reference U2) . The teachings of Guziewicz and Burgess are relied upon above. Guziewicz teaches methods of immunohistochemical staining of canine retinal tissue (Fig. 2), reading in-part on claim 61 Regarding claim 61, Guziewicz and Burgess do not teach evaluating the treated subjects for Muller glial trunks/projections penetrating ONL layer with astrogliosis. Hippert teaches methods of assessing Gfap, vimentin and chondroitin sulphate proteoglycan (CSPG) levels and outer limiting membrane (OLM) integrity over time in four murine models of inherited photoreceptor degeneration (Abstract), reading in-part on claim 61. Hippert teaches methods of detecting Gfap in Muller glia and apical processes within the ONL (Fig. 2B iii, vi; Fig. 2C i-vi; Fig. 2E i-vi; generally noting the downward extension of Gfap+ Muller glia processes relative to as compared to wildtype mice in Fig 2A; The paragraph starting “Degeneration occurs…” on page 7 through paragraph ending “…(Fig. 3C vii).” on page 8, and the paragraph spanning pages 9-10), reading on claim 61. It would have been obvious to a person of ordinary skill in the art before the invention was filed to further evaluate the subjects of Guziewicz for Muller glial trunks/projections penetrating ONL layer with astrogliosis in view of Hippert. A person of ordinary skill in the art would have had a reasonable expectation of success to do so because both Guziewicz and Hippert are in-part towards methods of immunohistochemistry for assessing retinal structure in subjects suffering from retinal disease. The skilled artisan would have been motivated to do so because Hippert teaches that Gfap immunohistochemistry is predictably advantageous to detect Muller glial trunks/projections penetrating ONL layer with retinal gliosis, and so would improve upon the methods of Guziewicz to assess the retinal function of the subjects with rAAV comprising BEST1 of Guziewicz. Therefore, the invention as a whole would have been prima facie obvious to a person of ordinary skill before the invention was filed. Conclusion No claims are allowed. No claims are free of the art. Any inquiry concerning this communication or earlier communications from the examiner should be directed to SEAN C BARRON whose telephone number is (571)270-5111. The examiner can normally be reached 7:30am-3:30pm EDT/EST (M-F). 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, Sharmila Landau can be reached at 571-272-0614. 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. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000. /Sean C. Barron/Primary Examiner, Art Unit 1653 Application/Control Number: 18/687,571 Page 2 Art Unit: 1653 Application/Control Number: 18/687,571 Page 3 Art Unit: 1653 Application/Control Number: 18/687,571 Page 4 Art Unit: 1653 Application/Control Number: 18/687,571 Page 5 Art Unit: 1653 Application/Control Number: 18/687,571 Page 6 Art Unit: 1653 Application/Control Number: 18/687,571 Page 7 Art Unit: 1653 Application/Control Number: 18/687,571 Page 8 Art Unit: 1653 Application/Control Number: 18/687,571 Page 9 Art Unit: 1653 Application/Control Number: 18/687,571 Page 10 Art Unit: 1653 Application/Control Number: 18/687,571 Page 11 Art Unit: 1653 Application/Control Number: 18/687,571 Page 12 Art Unit: 1653 Application/Control Number: 18/687,571 Page 13 Art Unit: 1653 Application/Control Number: 18/687,571 Page 14 Art Unit: 1653 Application/Control Number: 18/687,571 Page 15 Art Unit: 1653 Application/Control Number: 18/687,571 Page 16 Art Unit: 1653 Application/Control Number: 18/687,571 Page 17 Art Unit: 1653
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