DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claims 1-17 are under consideration.
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 03/02/2026 has been entered.
Rejections Maintained/New Rejections Necessitated by Amendment
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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.
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.
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.
Claim(s) 1-17 are rejected under 35 U.S.C. 103 as being unpatentable over Bryant (Bryant, et al., US 2006/0275305 A1; Published 12/07/2006, of record) in view of Agatsuma (Agatsuma, et al., US 10,227,417 B2; issued 3/12/2019; priority to 12/25/2013 by way of JP 2013-267548, of record) and Hirsch (Hirsch, et al., British Journal of Cancer 2002 86:1449, of record)
Regarding the sequence limitations of claims 2-3, 8-9, 13, 15 and 17, SEQ ID NOs: 6 and 5 of Bryant are a 100% match for AAs 1-449 of SEQ ID NO: 1 and AAs 1-214 of SEQ ID NO: 2, respectively (Bryant, ¶ 0144). Regarding the sequence limitations of claims 5, 10, 14 and 16, Bryant also teaches antibody variants with a C-terminal lysine (same as instant SEQ ID NO: 1 and 2 in their entirety) (Bryant, ¶ 0145). Regarding the conjugate limitations of claims 1, 7 and 17, Bryant also teaches that the methods of Bryant may also be performed with immunoconjugates comprising the antibody of Bryant linked to cytotoxins (Bryant, ¶ 0258-301). Regarding the DAR limitations of claims 5-6, 11-12 and 17, Bryant teaches that the ADCs of Bryant have DARs from 1 to 20 (Bryant, ¶ 0289). Regarding the maleimidocaproyl crosslinker limitations of claims 1, 7 and 17, Bryant teaches maleimidocaproyl crosslinkers (Bryant, ¶ 0292). Bryant also teaches linkers comprising tetrapeptides (Bryant, ¶ 0291).
Bryant does not teach ADCs comprising the maleimidocaproyl crosslinkers with DAR between 1 and 20 also comprise a GGFG-NH-CH2-O-CH2-C(=O)-NH-exatecan linker-drug moiety. Bryant does not teach that the resultant ADCs are administered to patients having non-small cell lung cancer.
Agatsuma teaches of anti-TROP2 antibody drug conjugates (Agatsuma, Abstract). Agatsuma teaches that the ADCs of Agatsuma comprise linker-drug moieties with the structure: maleimidocaproyl-GGFG-NH-CH2-O-CH2-C(=O)-NH-exatecan (Agatsuma, claim 1). Agatsuma also teaches that the ADCs of Agatsma are administered in methods of treating various cancers (Agatsuma, claim 6).
Hirsch teaches that of 238 NSCLC patients screened, 16% were found to overexpress HER2 (Hirsch, Abstract).
It would be prima facie obvious to one of ordinary skill in art to modify the trastuzumab ADCs of Bryant to comprise the GGFG-NH—CH2-O-CH2-C(=O)-NH-exatecan linker-drug moiety of Agatsuma and, in view of the teachings of Hirsch, use the resultant ADC in a method of treating NSCLC. One of ordinary skill in the art would be motivated to use such an ADC to better treat NSCLC. Bryant teaches that ADCs comprising trastuzumab linked via maleimidocaproyl crosslinkers further comprising tetrapeptide linkers and a wide range of drug moieties are useful in methods of treating cancers. Agatsuma teaches a specific peptidic linker/drug moiety known to be effective vs tumors. Swapping the peptidic linker/drug moiety of Bryant for the GGFG-NH-CH2-O-CH2-C(=O)-NH-exatecan linker-drug moiety of Agatsuma would therefore be a prima facie obvious simple substitution of one art element for another to yield predictable results. The teachings of Hirsch would also lead one of ordinary skill to understand that replacing the Trop2 antibodies of Agatsuma with HER2 would result in an ADC capable of treating NSCLC because Hirsch teaches that HER2 is often overexpressed in NSCLC. One of ordinary skill in the art would have a reasonable expectation of success swapping the peptidic linker/drug moiety of Bryant for the GGFG-NH-CH2-O-CH2-C(=O)-NH-exatecan linker-drug moiety of Agatsuma because: 1) Bryant teaches that ADCs comprising trastuzumab linked via maleimidocaproyl crosslinkers further comprising tetrapeptide linkers and a wide range of drug moieties may be used in methods of treating breast cancer and 2) Agatsuma teaches that the GGFG-NH-CH2-O-CH2-C(=O)-NH-exatecan linker-drug moiety of Agatsuma is an acceptable linker-drug moiety for anti-cancer ADCs and 3) Hirsch teaches that HER2 is often overexpressed in NSCLC, making HER2-targeting ADCs capable of treating NSCLC.
Regarding the DAR limitations of claims 5, 6, 11-17, it would be prima facie obvious to one of ordinary skill in the art to start with the DAR of 1-20 taught by Bryant and arrive at the claimed DARs via routine experimentation, wherein the purpose of this routine experimentation is to find the optimal drug loading for the ADCs in question. In the case where the claimed ranges “overlap or lie inside ranges disclosed by the prior art” a prima facie case of obviousness exists. In re Wertheim, 541 F.2d 257, 191 USPQ 90 (CCPA 1976); In re Woodruff, 919 F. 2d 1575, 16 USPQ2d 1934 (Fed. Cir. 1990) See MPEP 2144.05. Further with respect to optimal dosing regimens, it is not inventive to discover such regimens by routine experimentation when general conditions of a claim are disclosed in the prior art. See in re Aller, 220 F.2d 545, 456, 105 USPQ 233, 235 (CCPA 1955) and MPEP 2144.05(11).
Response to Arguments
Applicant's arguments filed 03/02/2026 have been fully considered but they are not persuasive.
Applicant’s traverse of the 35 USC § 103 rejection focuses entirely on the argument that the Hirsch reference provides no basis for targeting HER2 in NSCLC or any cancer other than breast cancer. Applicant argues that the Hirsch reference states that “we do not currently know the level of HER2/neu protein expression or gene gain/amplification will have prognostic /therapeutic implications”. This argument is not convincing because the Hirsch reference still teaches that HER2 is overexpressed in 16% of NSCLC patients and overexpression of a known tumor associated antigen (TAA) in a certain type of cancer is a known desirable target when selecting a target that will direct ADCs to that type of cancer cell. The exact level of HER2 expression that will have therapeutic implication is a matter of routine experimentation and is not required to motivate one of skill in the art to use a HER2 targeting ADC to treat NSCLC in view of Hirsch. Please note, this rebuttal also applies to Applicant’s citation of p 1454, right column, lines 36-40, as it rests on the exact clinical implications of gene amplification levels.
Applicant’s citation of p 1454, right column, lines 57-61 is also not convincing because it deals on the subject of Hirsch’s inability to demonstrate a statistically significant difference in prognosis between high and low levels of HER2. This has nothing to do with whether or not an ADC would be directed to the NSCLC cells. Even an antigen with zero effect on prognosis could be used as a target antigen to direct ADCs to target cells if differential expression between cancerous/noncancerous cells is sufficient. Applicant’s citation of p 1454, right column, lines 26-30 and p 1454, right column, lines 33-36 are not persuasive because a comparison to breast cancer proves nothing. Hirsch still teaches that 16% of NSCLC overexpresses HER2 and overexpression of a TAA in a tumor is a critical parameter for ADC antibody target selection.
Applicant concludes reiterating that Hirsch teaches no statistically significant difference between HER2 levels and “prognostic/therapeutic implications” (point already addressed) and by stating that the Hirsch reference when taken as a whole teaches against the reasons for which it is cited. This is not persuasive because Hirsch teaches that previous work with lung cancer cell lines detected a positive correlation between HER2 expression levels by IHC and effectiveness of trastuzumab (a HER2 targeting antibody) based therapies in NSCLC and it is simply the clinical implications of exact levels of HER2 that remain unknown (Hirsch, 1455, ¶ 1). Using cell-based techniques to predict in vivo behavior is very routine in the art.
Double Patenting
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 1-17 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-12 of U.S. Patent No. 11,795,236 B2 in view of Hirsch (Hirsch, et al., British Journal of Cancer 2002 86:1449, of record).
Regarding the ADC structure limitations of claims 1, 7 and 17, patented claims 1 teach methods of treating HER2-expressing cancer comprising administration of ADCs with structures identical to the instant claimed structure. Regarding the sequence limitations of claims 2-4, 8-10 and 17, patented SEQ ID NOs: 1 and 2 recited in patented claims 2-4, 8-10 and 17are the same as instant SEQ ID NOs: 1 and 2, with patented claims 2-3, 8-9 and 17 being directed to AAs 1-449 of SEQ ID NO: 1 and patented claims 4 and 10 being directed to the full-length sequences. Regarding the DAR limitations of claims 5-6 and 11-17, patented claim 11 teaches that the DAR of the ADC is between 2 and 8 and patented claim 12 teaches that the DAR of the ADC is between 3 and 8.
The ‘236 patent does not teach that the ADC of the ‘236 patent is administered in a method of treating NSCLC.
Hirsch teaches that of 238 NSCLC patients screened, 16% were found to overexpress HER2 (Hirsch, Abstract).
It would be prima facie obvious to combine the anti-HER2 ADC of the ‘236 patent and administer it in a method of treating NSCLC in view of Hirsch. One of ordinary skill in the art would be motivated to do this in order to better treat NSCLC. One of ordinary skill in the art would have a reasonable expectation of success doing this because Hirsch teaches HER2 is overexpressed often in NSCLC, making anti-HER2 ADCs a possible treatment for NSCLC.
Response to Arguments
Applicant's arguments filed 03/02/2026 have been fully considered but they are not persuasive.
Applicant reiterates the arguments related to the Hirsch reference used to traverse the 35 USC § 103 rejection above, which have already been addressed. Applicant also argues that the ADCs of the reference patents and the ADCs of the instant claims are distinct chemical species, citing Eli Lilly and Co. v Teva Parenteral Meds., Inc., and, as such, there is no overlap between the scope of the instant claims and because of this there is no possibility for unjustified timewise extension of the reference patents. This argument is not convincing because the ADCs of the reference patent and the ADC of the instant claims are not “distinct chemical species” but rather species that that share an interchangeable part—namely the drug-linker moiety. It is routine in the art to re-use drug-linker moieties known to be effective by attaching them to different antibodies to arrive at different ADCs. As such, there is overlap in claimed subject matter by way of the shared drug-linker moieties.
Claims 1-17 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-8 of U.S. Patent No. 11,008,398 B2 in view of Hirsch (Hirsch, et al., British Journal of Cancer 2002 86:1449, of record) and Bryant (Bryant, et al., US 2006/0275305 A1; Published 12/07/2006, of record).
Regarding the ADC structure limitations of claims 1, 7 and 17, patented claim 1 teaches anti-TROP2 ADCs comprising linker-drug moieties that are identical to the instant claimed linker-drug moiety. Regarding the DAR limitations of claims 5-6 and 11-17, patented claim 2 teaches that the DAR of the ADC is between 2 and 8 and patented claim 3 teaches that the DAR of the ADC is between 3 and 8.
The ‘398 patent does not teach that the linker-drug moiety of the ‘398 patent is conjugated to an anti-HER2 antibody comprising either AAs 1-449 of instant SEQ ID NO: 1 and SEQ ID NO: 2 or SEQ ID NO:1 and SEQ ID NO: 2. The ‘398 patent does not teach that the ADC of the ‘398 patent is administered in a method of treating NSCLC.
Bryant teaches on the subject of anti-HER2 antibodies suitable for clinical use (Bryant, Abstract). Bryant teaches SEQ ID NOs: 6 and 5 of Bryant are 100% matches for AAs 1-449 of SEQ ID NO: 1 and SEQ ID NO: 2, respectively (Bryant, ¶ 0144). Bryant also teaches antibody variants with a C-terminal lysine on the heavy chain, with the resultant sequence being the same as instant SEQ ID NO: 1 (Bryant, ¶ 0145)
Hirsch teaches that of 238 NSCLC patients screened, 16% were found to overexpress HER2 (Hirsch, Abstract).
It would be prima facie obvious to combine the linker-drug moiety of the ‘398 patent, the anti-HER2 antibody of Bryant and administer it in a method of treating NSCLC in view of Hirsch. One of ordinary skill in the art would be motivated to do this in order to better treat NSCLC. One of ordinary skill in the art would have a reasonable expectation of success doing this because Bryant teaches well-characterized anti-HER2 antibodies suitable for clinical use, allowing one to make anti-HER2 ADCs using the linker-drug moiety of the ‘398 patent and Hirsch teaches HER2 is overexpressed often in NSCLC, making anti-HER2 ADCs a possible treatment for NSCLC.
Response to Arguments
Applicant's arguments filed 03/02/2026 have been fully considered but they are not persuasive.
Applicant reiterates the arguments related to the Hirsch reference used to traverse the 35 USC § 103 rejection above, which have already been addressed. Applicant also argues that the ADCs of the reference patents and the ADCs of the instant claims are distinct chemical species, citing Eli Lilly and Co. v Teva Parenteral Meds., Inc., and, as such, there is no overlap between the scope of the instant claims and because of this there is no possibility for unjustified timewise extension of the reference patents. This argument is not convincing because the ADCs of the reference patent and the ADC of the instant claims are not “distinct chemical species” but rather species that that share an interchangeable part—namely the drug-linker moiety. It is routine in the art to re-use drug-linker moieties known to be effective by attaching them to different antibodies to arrive at different ADCs. As such, there is overlap in claimed subject matter by way of the shared drug-linker moieties.
Claims 1-17 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-16 of U.S. Patent No. 10,227,417 B2 in view of Hirsch (Hirsch, et al., British Journal of Cancer 2002 86:1449, of record) and Bryant (Bryant, et al., US 2006/0275305 A1; Published 12/07/2006, of record).
Regarding the ADC structure limitations of claims 1, 7 and 17, patented claims 1 teach anti-TROP2 ADCs comprising linker-drug moieties that are identical to the instant claimed linker-drug moiety. Regarding the DAR limitations of claims 5-6 and 11-17, patented claim 2 teaches that the DAR of the ADC is between 2 and 8 and patented claim 3 teaches that the DAR of the ADC is between 3 and 8.
The ‘417 patent does not teach that the linker-drug moiety of the ‘417 patent is conjugated to an anti-HER2 antibody comprising either AAs 1-449 of instant SEQ ID NO: 1 and SEQ ID NO: 2 or SEQ ID NO:1 and SEQ ID NO: 2. The ‘417 patent does not teach that the ADC of the ‘398 patent is administered in a method of treating NSCLC.
Bryant teaches on the subject of anti-HER2 antibodies suitable for clinical use (Bryant, Abstract). Bryant teaches SEQ ID NOs: 6 and 5 of Bryant are 100% matches for AAs 1-449 of SEQ ID NO: 1 and SEQ ID NO: 2, respectively (Bryant, ¶ 0144). Bryant also teaches antibody variants with a C-terminal lysine on the heavy chain, with the resultant sequence being the same as instant SEQ ID NO: 1 (Bryant, ¶ 0145)
Hirsch teaches that of 238 NSCLC patients screened, 16% were found to overexpress HER2 (Hirsch, Abstract).
It would be prima facie obvious to combine the linker-drug moiety of the ‘417 patent, the anti-HER2 antibody of Bryant and administer it in a method of treating NSCLC in view of Hirsch. One of ordinary skill in the art would be motivated to do this in order to better treat NSCLC. One of ordinary skill in the art would have a reasonable expectation of success doing this because Bryant teaches well-characterized anti-HER2 antibodies suitable for clinical use, allowing one to make anti-HER2 ADCs using the linker-drug moiety of the ‘417 patent and Hirsch teaches HER2 is overexpressed often in NSCLC, making anti-HER2 ADCs a possible treatment for NSCLC.
Response to Arguments
Applicant's arguments filed 03/02/2026 have been fully considered but they are not persuasive.
Applicant reiterates the arguments related to the Hirsch reference used to traverse the 35 USC § 103 rejection above, which have already been addressed. Applicant also argues that the ADCs of the reference patents and the ADCs of the instant claims are distinct chemical species, citing Eli Lilly and Co. v Teva Parenteral Meds., Inc., and, as such, there is no overlap between the scope of the instant claims and because of this there is no possibility for unjustified timewise extension of the reference patents. This argument is not convincing because the ADCs of the reference patent and the ADC of the instant claims are not “distinct chemical species” but rather species that that share an interchangeable part—namely the drug-linker moiety. It is routine in the art to re-use drug-linker moieties known to be effective by attaching them to different antibodies to arrive at different ADCs. As such, there is overlap in claimed subject matter by way of the shared drug-linker moieties.
Claims 1-17 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-14 of U.S. Patent No. 11,633,493 B2 in view of Hirsch (Hirsch, et al., British Journal of Cancer 2002 86:1449, of record) and Bryant (Bryant, et al., US 2006/0275305 A1; Published 12/07/2006, of record).
Regarding the ADC structure limitations of claims 1, 7 and 17, patented claims 1 teach anti-B7H3 ADCs comprising linker-drug moieties that are identical to the instant claimed linker-drug moiety. Regarding the DAR limitations of claims 5-6 and 11-17, patented claim 2 teaches that the DAR of the ADC is between 2 and 8 and patented claim 3 teaches that the DAR of the ADC is between 3 and 8.
The ‘493 patent does not teach that the linker-drug moiety of the ‘493 patent is conjugated to an anti-HER2 antibody comprising either AAs 1-449 of instant SEQ ID NO: 1 and SEQ ID NO: 2 or SEQ ID NO:1 and SEQ ID NO: 2. The ‘493 patent does not teach that the ADC of the ‘493 patent is administered in a method of treating NSCLC.
Bryant teaches on the subject of anti-HER2 antibodies suitable for clinical use (Bryant, Abstract). Bryant teaches SEQ ID NOs: 6 and 5 of Bryant are 100% matches for AAs 1-449 of SEQ ID NO: 1 and SEQ ID NO: 2, respectively (Bryant, ¶ 0144). Bryant also teaches antibody variants with a C-terminal lysine on the heavy chain, with the resultant sequence being the same as instant SEQ ID NO: 1 (Bryant, ¶ 0145)
Hirsch teaches that of 238 NSCLC patients screened, 16% were found to overexpress HER2 (Hirsch, Abstract).
It would be prima facie obvious to combine the linker-drug moiety of the ‘493 patent, the anti-HER2 antibody of Bryant and administer it in a method of treating NSCLC in view of Hirsch. One of ordinary skill in the art would be motivated to do this in order to better treat NSCLC. One of ordinary skill in the art would have a reasonable expectation of success doing this because Bryant teaches well-characterized anti-HER2 antibodies suitable for clinical use, allowing one to make anti-HER2 ADCs using the linker-drug moiety of the ‘493 patent and Hirsch teaches HER2 is overexpressed often in NSCLC, making anti-HER2 ADCs a possible treatment for NSCLC.
Response to Arguments
Applicant's arguments filed 05/23/2025 have been fully considered but they are not persuasive.
Applicant’s arguments are centered around the fact that the antibody from the reference patent is not a HER-2 antibody, arguing heavily that the instant claimed ADC and the ADC of the reference patent are “separate and distinct”. This is simply not true. The reference patent teaches the exact drug-linker moiety of the instant claimed HER-2 targeting ADC attached to a different antibody. Attaching the same drug-linker moiety to different antibodies is routine in the art. Furthermore, the Hirsch reference provides sufficient motivation for one of skill in the art to view HER2 as a suitable target antigen for an ADC therapeutic and the Bryant reference provides an antibody of known structure that is capable of binding HER2. It is obvious to take the drug-linker moiety of the reference patent and attach it to the anti-HER2 antibody of Bryant and administer it for NSCLC in view of the teachings of Hirsch.
Claims 1-17 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-18 of U.S. Patent No. 9,808,537 B2 in view of Hirsch (Hirsch, et al., British Journal of Cancer 2002 86:1449, of record) and Bryant (Bryant, et al., US 2006/0275305 A1; Published 12/07/2006, of record).
Regarding the ADC structure limitations of claims 1, 7 and 17, patented claims 1 and 2 teach anti-ADC linker-drug moieties that are identical to the instant claimed linker-drug moiety. Regarding the DAR limitations of claims 5-6 and 11-17, patented claim 3 teaches that the DAR of the ADC is between 2 and 8 and patented claim 4 teaches that the DAR of the ADC is between 3 and 8.
The ‘537 patent does not teach that the linker-drug moiety of the ‘537 patent is conjugated to an anti-HER2 antibody comprising either AAs 1-449 of instant SEQ ID NO: 1 and SEQ ID NO: 2 or SEQ ID NO:1 and SEQ ID NO: 2. The ‘537 patent does not teach that the ADC of the ‘537 patent is administered in a method of treating NSCLC.
Bryant teaches on the subject of anti-HER2 antibodies suitable for clinical use (Bryant, Abstract). Bryant teaches SEQ ID NOs: 6 and 5 of Bryant are 100% matches for AAs 1-449 of SEQ ID NO: 1 and SEQ ID NO: 2, respectively (Bryant, ¶ 0144). Bryant also teaches antibody variants with a C-terminal lysine on the heavy chain, with the resultant sequence being the same as instant SEQ ID NO: 1 (Bryant, ¶ 0145)
Hirsch teaches that of 238 NSCLC patients screened, 16% were found to overexpress HER2 (Hirsch, Abstract).
It would be prima facie obvious to combine the linker-drug moiety of the ‘537 patent, the anti-HER2 antibody of Bryant and administer it in a method of treating NSCLC in view of Hirsch. One of ordinary skill in the art would be motivated to do this in order to better treat NSCLC. One of ordinary skill in the art would have a reasonable expectation of success doing this because Bryant teaches well-characterized anti-HER2 antibodies suitable for clinical use, allowing one to make anti-HER2 ADCs using the linker-drug moiety of the ‘537 patent and Hirsch teaches HER2 is overexpressed often in NSCLC, making anti-HER2 ADCs a possible treatment for NSCLC.
Response to Arguments
Applicant's arguments filed 03/02/2026 have been fully considered but they are not persuasive.
Applicant reiterates the arguments related to the Hirsch reference used to traverse the 35 USC § 103 rejection above, which have already been addressed. Applicant makes no further arguments specific to the NSDP rejection in view of the ‘537 patent.
Conclusion
Claims 1-17 are rejected.
No claims are allowed
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Sydney Van Druff whose telephone number is (571)272-2085. The examiner can normally be reached 10 am - 6 pm.
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, Julie Wu can be reached on 571-272-5205. 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.
/SYDNEY VAN DRUFF/Examiner, Art Unit 1643
/JULIE WU/Supervisory Patent Examiner, Art Unit 1643