CTNF 18/504,041 CTNF 90090 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. DETAILED ACTION Claim 167-191 are pending. Claims 167-191 are under examination on the merits. Priority Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged. Claims 167-191 have an effective filing date of 12/13/2019, corresponding to PRO 62/948,097. Information Disclosure Statement The information disclosure statements (IDS) submitted on 03/04/2024 and 12/02/2025 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statements are being considered by the examiner. Notes on the Prior Art At the effective filing date of the invention, it was known in the art that LY6G6D is a marker for colorectal cancer (CRC). For example at the Abstract, Sewda et a. (Oncotarget, 7(14): 17773-17789, 2016) teach that “[p]rofiling of mRNA expression microarray data from patient tissues including adenoma, adenocarcinoma, and normal gastrointestinal tissues was used to identify potential CRC specific cell surface markers. Of the identified markers, six were selected for further validation (CLDN1, GPR56, GRM8, LY6G6D/F, SLCO1B3 and TLR4). Protein expression was confirmed by immunohistochemistry of patient tissues. Except for SLCO1B3, diffuse and low expression was observed for each marker in normal colon tissues. The three markers with the greatest protein overexpression were CLDN1, LY6G6D /F and TLR4 , where at least one of these markers was overexpressed in 97% of the CRC samples. GPR56, LY6G6D/F and SLCO1B3 protein expression was significantly correlated with the proximal tumor location and with expression of mismatch repair genes. Marker expression was further validated in CRC cell lines. Hence, three cell-surface markers were discovered that distinguish CRC from surrounding normal tissues (emphasis added).” At p. 17775, Sewda et al. teach that “[t]o confirm protein expression of the six markers selected above in CRC and normal colon tissues, immunohistochemistry (IHC) was performed for each marker using a tissue microarray containing colon adenoma, adenocarcinoma and normal colon tissue samples from patients (Figure 2).” As such Sewda et al. teach that anti-LY6G6D/F antibodies may be used in IHC experiments to detect LY6G6D/F. The prior art does not teach an anti-LY6G6D antibody that comprises the HCDRs 1-3 of SEQ ID NO(s): 4-6 and the LCDRs 1-3 of SEQ ID NO(s): 1-3. The instantly claimed anti-LY6G6D antibody is also not an obvious variant of any art-known anti-LY6G6D antibodies, and as such the claimed anti-LY6G6D antibody is free of the prior art. Claim Rejections Nonstatutory 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. Claims 167-170, 172, 176, 177, 179, 180-182, and 187 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 13, 23, 24, 34, and 35 and 41 of U.S. Patent No. 11,845,799. With respect to claims 167-170 and 187, although the claims at issue are not identical, they are not patentably distinct from each other, because both sets of claims recite an anti-LY6G6D antibody that comprises the VH of SEQ ID NO: 10, which comprises the HCDRs 1-3 of SEQ ID NO(s): 4-6, and the VL of SEQ ID NO: 11, which comprises LCDRs 1-3 of SEQ ID NO(s): 1-3. With respect to claim 172, given that the instantly claimed anti-LY6G6D antibody and that of U.S. Patent No. 11,845,799 comprise identical CDRs, said antibodies would be expected to exhibit the same functional characteristics, such as those recited in claim 172. With respect to claims 176, 177, and 179-181, conflicting claims 1, 23, 24, 34, and 35 recite an anti-LY6g6D/anti-CD3 bispecific antibody comprising an IgG isotype Fc region, as well as a bispecific antibody is a full-length antibody. With respect to claim 182, conflicting claim 13 recites nucleic acids that encode antibodies of the invention. 08-36 AIA Claim s 167-170, 172, 176, 177, 179, 180-182, and 187-191 rejected on the ground of nonstatutory double patenting as being unpatentable over claim s 1, 12, 13, 24, 34, and 35 and 41 of U.S. Patent No. 11,845,799 , in view of Sewda et al. (Oncotarget, 7(14): 17773-17789, 2016) . With respect to claims 167-170, 172, 176, 177, 179, 180-182, and 187, although the claims at issue are not identical, they are not patentably distinct from each other, as indicated above. Sewda et al. teach that “[p]rofiling of mRNA expression microarray data from patient tissues including adenoma, adenocarcinoma, and normal gastrointestinal tissues was used to identify potential CRC specific cell surface markers. Of the identified markers, six were selected for further validation (CLDN1, GPR56, GRM8, LY6G6D/F, SLCO1B3 and TLR4). Protein expression was confirmed by immunohistochemistry of patient tissues. Except for SLCO1B3, diffuse and low expression was observed for each marker in normal colon tissues. The three markers with the greatest protein overexpression were CLDN1, LY6G6D /F and TLR4 , where at least one of these markers was overexpressed in 97% of the CRC samples. GPR56, LY6G6D/F and SLCO1B3 protein expression was significantly correlated with the proximal tumor location and with expression of mismatch repair genes. Marker expression was further validated in CRC cell lines. Hence, three cell-surface markers were discovered that distinguish CRC from surrounding normal tissues … Hence, three cell-surface markers were discovered that distinguish CRC from surrounding normal tissues. These markers can be used to develop imaging or therapeutic agents targeted to the luminal surface of CRC (emphasis added).” At p. 17775, Sewda et al. teach that “[t]o confirm protein expression of the six markers selected above in CRC and normal colon tissues, immunohistochemistry (IHC) was performed for each marker using a tissue microarray containing colon adenoma, adenocarcinoma and normal colon tissue samples from patients (Figure 2). Proteins LY6G6D or LY6G6F were not distinguished from each other by the available antibodies. Table 1 reports the pathologist (A.S.L. and D.C.), scoring for protein expression of each marker.” As such Sewda et al. teach that anti-LY6G6D antibodies may be used in IHC experiments to detect LY6G6D. One of ordinary skill in the art would have thus been motivated to use the antibody of the instant claims as a means of detecting LY6G6D in a biological sample via IHC, because such a method would allow for the diagnosis of CRC, thus meeting the limitations of claim 191. Importantly at p. 17783, Sewda et al. teach that “[a]lthough there is potential for development of targeted drugs that modulate the function of these markers, these markers could also serve as ‘landing pads’ for delivery of targeted imaging or therapeutic agents to the cells and not necessarily to target the function of these proteins.” Based upon these teachings, one of ordinary skill in the art would have been motivated to prepare antibody-therapeutic agent immunoconjugates that target LY6G6D-expressing CRC cells with anti-cancer drugs. One of ordinary skill in the art would have thus been motivated to use the antibody of the conflicting claims as a means of delivering therapeutic agents to LY6G6D-expressing CRC cells, because there would have been a reasonable expectation that such a method would provide a therapeutic benefit to subjects having LY6G6D-expressing CRC, thus meeting the limitations of claims 188 and 189. Furthermore at p. 17774, Sewda et al. teach that proximal CRC lesions are more likely to exhibit microsatellite instability (MSI), and as such one of ordinary skill in the art would have been motivated to use the antibody of the instant claims as a means of delivering therapeutic agents to LY6G6D-expressing CRC cells exhibiting MSI, thus meeting the limitations of claim 190. Therefore the claimed invention is prima facie obvious over the conflicting claims in view of Sewda et al . 08-36 AIA Claim s 167-170, 172, 174-176, 177, 179, 180-182, and 187-191 rejected on the ground of nonstatutory double patenting as being unpatentable over claim s 1, 12, 13, 24, 34, and 35 and 41 of U.S. Patent No. 11,845,799 , in view of Yano et al. (Photodiagnosis and Photodynamic Therapy, 3: 177-183, 2006) . With respect to claims 167-170, 172, 176, 177, 179, 180-182, and 187, although the claims at issue are not identical, they are not patentably distinct from each other, as indicated above. Claims 188-191 are prima facie obvious over the conflicting claims in view of Sewda et al., as indicated above. Yano et al. teach that “we generated infrared ray fluorescence-labeled monoclonal antibodies and developed an infrared ray fluorescence endoscope capable of detecting the monoclonal antibodies to establish a novel diagnostic technique for gastrointestinal cancer. Although the whole IgG molecule has commonly been used for preparation of labeled antibodies, labeled IgG displays insufficient sensitivity and specificity, probably resulting from non-specific binding of the Fc fragment to target cells or interference between fluorochromes on the identical labeled antibody, which might be caused by molecular structure. In this in vitro study, we characterized an Fc-free fluorescence-labeled Fab fragment, which was expected to yield more specific binding to target cells than the whole IgG molecule.” See Abstract. One of ordinary skill in the art would have thus been motivated to prepare labeled Fab fragments of the claimed bispecific antibody for diagnosing LY6G6D-positive CRC (as taught by Sewda et al.) via infrared ray fluorescence endoscopy, as said labeled Fab fragments would be expected to provide more specific binding to target cells compared to labeled whole antibody fragments, thus meeting the limitations of claims 174 and 175. Therefore the claimed invention is prima facie obvious over the conflicting claims in view of Sewda et al. and Yano et al . 08-36 AIA Claim s 167-170, 172, 176, 177, 179, 180-182, and 187-191 rejected on the ground of nonstatutory double patenting as being unpatentable over claim s 1, 12, 13, 24, 34, and 35 and 41 of U.S. Patent No. 11,845,799 , in view of Chen et al. (US PAT 8,545,850, publication date: 10/01/2023) . With respect to claims 167-170, 172, 176, 177, 179, 180-182, and 187, although the claims at issue are not identical, they are not patentably distinct from each other, as indicated above. At column 7, Chen et al. teach that “[i]n one aspect, the invention provides methods for making an antibody of the invention. For example, the invention provides a method of making a CD79b antibody (which, as defined herein includes full length and fragments thereof), said method comprising expressing in a suitable host cell a recombinant vector of the invention encoding said antibody (or fragment thereof), and recovering said antibody.” One of ordinary skill in the art would have thus been motivated to use nucleic acids that encode the antibody of the conflicting claims to prepare vectors comprising said nucleic acids, incorporate said vectors into suitable host cells, culture said host cells, and recover the antibody of the conflicting claims, because such a method is an art-know means of preparing a desired antibody, thus meeting the limitations of claims 183-186. At columns 73 and 74, Chen et al. teach that humanized antibodies provide less of a human anti-mouse antibody response (HAMA) compared to non-humanized antibodies. One of ordinary skill in the art would have thus been motivated to prepare humanized antibodies of the conflicting claims, as said humanized antibodies would be expected to be less immunogenic, and thus, safer for administration, compared to non-humanized forms of the antibodies of the conflicting claims, thus meeting the limitations of claim 173. Therefore the claimed invention is prima facie obvious over the conflicting claims in view of Chen et al . Allowable Subject Matter 12-151-08 AIA 07-43 12-51-08 Claim 178 is objected to as being dependent upon a rejected base claim, but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims. Conclusion 12-151-07 AIA 07-97 12-51-07 Claim 171 is allowed. Any inquiry concerning this communication or earlier communications from the examiner should be directed to NELSON B MOSELEY II whose telephone number is (571)272-6221. The examiner can normally be reached on M-F, 9:00-6:00 EST. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Samira Jean-Louis, can be reached at 571-270-3503. 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 the Patent Application Information Retrieval (PAIR) system. Status information for published applications may be obtained from either Private PAIR or Public PAIR. Status information for unpublished applications is available through Private PAIR only. For more information about the PAIR system, see http://pair-direct.uspto.gov. Should you have questions on access to the Private PAIR system, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative or access to the automated information system, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000. /NELSON B MOSELEY II/Primary Examiner, Art Unit 1642 Application/Control Number: 18/504,041 Page 2 Art Unit: 1642 Application/Control Number: 18/504,041 Page 3 Art Unit: 1642 Application/Control Number: 18/504,041 Page 4 Art Unit: 1642
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