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 .
Status of Application, Amendments and/or Claims
The amendment of 11 November 2025 has been entered in full. Claim 11 is amended. Claims 3, 5, 9, 10, 14, 15, 17, 19, 20, 26, 28, 30-45, and 47-54 are cancelled.
Claims 1, 2, 4, 6, 7, 8, 11-13, 16, 18, 21-25, 27, 29, 46, and 55 are under consideration in the instant application.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 11 November 2025 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Withdrawn Objections and/or Rejections
1. The objection to claim 11 as set forth at page 3 of the previous Office Action of 19 May 2025 is withdrawn in view of the amended claim (11 November 2025).
2. The rejection of claims 1, 2, 4, 6, 7, 8, 11-13, 16, 18, 21-25, 27, 29, 46, and 55 under 35 U.S.C. 103 as being obvious over Kinneer et al. (WO 2022/053650, published 17 March 2022 with priority to 11 September 2020), Johannes et al. (J Med Chem 64: 14498-14512, 2021), and Yap et al. (JCO Precision Oncol 6: e2100456, 09 February 2022) as set forth at pages 4-9 of the previous Office Action of 19 May 2025 is withdrawn in view of the submission of a statement under 35 U.S.C. §102(b)(2)(C) establishing that, not later than effective filing date of the claimed invention, the subject matter in Kineer et al. and the claimed invention were owned by the same assignee (MedImmune Limited) or subject to an obligation of assignment to the same assignee.
3. The rejection of claims 1, 2, 4, 6, 7, 8, 11-13, 18, 21-25, 27, 29, 46, and 55 under 35 U.S.C. 103 as being obvious over Schmidt et al. (WO 2022/053685, published 17 March 2022 with priority to 12 September 2020), Johannes et al. (J Med Chem 64: 14498-14512, 2021), and Yap et al. (JCO Precision Oncol 6: e2100456, 09 February 2022) as set forth at pages 9-13 of the previous Office Action of 19 May 2025 is withdrawn in view of in view of the submission of a statement under 35 U.S.C. §102(b)(2)(C) establishing that, not later than effective filing date of the claimed invention, the subject matter in Schmidt et al. and the claimed invention were owned by the same assignee (MedImmune Limited) or subject to an obligation of assignment to the same assignee.
Maintained 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.
U.S Patent 11,795,225
4. Claims 1, 2, 4, 6, 7, 8, 11-13, 16, 18, 21-25, 27, 29, 46, and 55 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-38 of U.S. Patent No. 11,795,225 in view of Johannes et al. (J Med Chem 64: 14498-14512, 2021), and Yap et al. (JCO Precision Oncol 6: e2100456, 09 February 2022; cited on the PTO-892 of 09 September 2024). The basis for this rejection is set forth at pages 15-18 of the previous Office Action of 19 May 2025 and is reiterated herein for convenience.
Claims 1-4 of the ‘225 patent are directed to an antibody or antibody binding fragment which binds to B7-H4. The antibody CDR, VH chain, and VL chain amino acid sequences recited in claims 1-4 of the ‘225 patent are 100% identical to the same sequences recited in claims 1, 11, 12, 13, 29, and 46 of the instant application.
Claim 5 of the patent recites that the antibody is conjugated to a heterologous agent.
Claims 6 and 7 of the ’225 patent recites that the heterologous agent is a topoisomerase I inhibitor, meeting the limitation of instant claim 23.
Claim 10 of the ‘225 patent recites that the antibody is conjugated to a linker and cytotoxic agent of compound SG3932, SG4010, SG4057, and SG4052, as recited in instant claims 25 and 46.
Claim 17 of the ’225 patent recites an antibody-drug conjugate comprising (i) an antibody which binds to B7-H4 comprising: a HCDR1 comprising the amino acid sequence of SEQ ID NO: 7; a HCDR2 comprising the amino acid sequence of SEQ ID NO: 8; a HCDR3 comprising the amino acid sequence of SEQ ID NO: 9; and a LCDR1 comprising the amino acid sequence of SEQ ID NO: 10; a LCDR2 comprising the amino acid sequence of SEQ ID NO: 11; a LCDR3 comprising the amino acid sequence of SEQ ID NO: 12; (ii) a cleavable mp-PEG8-val-ala linker; and (iii) a cytotoxic agent wherein the cleavable mp-PEG8-val-ala linker and the cytotoxic agent are SG3932, and wherein the ADC has a drug antibody ratio (DAR) of about 8, meeting the limitations of instant claims 22-25, 27, and 46.
Claims 14 and 30 of the ‘225 patent recite treating cancer by administering the B7-H4 antibody-drug conjugate. Claims 33 and 34 of the ‘225 patent recite that the cancer has a homologous recombination DNA repair defect, wherein such defect is defined by the presence of a BRCA1 mutation.
The difference between the claims of the ‘225 patent and the claims of the instant application is that the claims of the ‘225 patent do not recite that the composition comprising the B7-H4 antibody-drug conjugate or methods of cancer treatment by administering the B7-H4 antibody-drug conjugate further comprise an additional agent, wherein the additional agent is a PARP1 inhibitor.
Johannes et al. disclose that PARP inhibitors have demonstrated widespread success as a therapeutic class for the treatment of a variety of cancers (page 14498, column 1). Johannes et al. indicate that BRCA mutant tumors are sensitive to PARP1/PARP2 inhibitors (page 14499, column 1, 1st paragraph). Johannes et al. state that in spite of their success, PARP1/2 inhibitors have shown significant hematological toxicities, including anemia, neutropenia, and thrombocytopenia (page 14499, column 1, 2nd paragraph). Johannes et al. teach the generation of compound 25, “AZD5305”, a potent and selective PARP1 inhibitor, with excellent in vivo efficacy and reduced effects on human bone marrow progenitor cells (abstract; page 14504 through page 14505, column 1 and column 2 (last full paragraph above “conclusions”). Johannes et al. disclose that AZD5305 is a next-generation PARP inhibitor with multiple clinical options, including combination approaches (page 14506, bottom of column 1 through column 2).
Yap et al. teach that tumors characterized by homologous recombination deficiency, such as BRCA1/2-mutated cancers, are sensitive to inhibition of poly(ADP-ribose) polymerases (PARPs) (page 1, column 1, 1st paragraph). Yap et al. also disclose that in human tumor cell lines, topoisomerase I (Topo1) inhibitors have demonstrated synergy with PARP inhibitors (page 1, column 1, 2nd paragraph). Yap et al. state that PARP inhibition may augment Topo1-mediated DNA damage or delay repair (page 1, column 1, 2nd paragraph). Yap et al. review the SEASTAR study, which investigated the combination of (i) PARP inhibitor, rucaparib, and (ii) sacituzumab govitecan (SG), a conjugate of SN-38 (the active metabolite in topoisomerase inhibitors irinotecan and topotecan) and a humanized anti-Trop-2 antibody (page 1, 2nd and 3rd paragraphs). Yap et al. state that the results provide “proof-of-concept clinical evidence supporting further development of PARP1 inhibitors in combination with ADCs carrying Topo1-inhibitor payloads” (page 5, column 2). Yap et al. also teach that combination with other selective PARP inhibitors, such as PARP1-targeted inhibitor AZD5305, may improve tolerability (page 5, column 2).
It would have been obvious to the person of ordinary skill in the art at the time the invention was made to modify the composition comprising a B7-H4 antibody-topoisomerase I drug conjugate and methods of treating cancer by administering the B7-H4 antibody-topoisomerase I drug conjugate as recited by the claims of the ‘225 patent in combination with a PARP1 inhibitor, such as ADZ5305, as taught by Johannes et al. and Yap et al. The person of ordinary skill in the art would have been motivated to make that modification to generate synergism between the topoisomerase inhibitor present in the antibody-drug conjugate of the ‘225 claims and the PARP1 inhibitor, to in turn enhance anti-tumor efficacy and improve patient tolerability (see Joannes et al., abstract; page 14504 through page 14505, column 1 and column 2 (last full paragraph above “conclusions”);; Yap et al., page 1, column 1, 2nd paragraph; page 5, column 2). The person of ordinary skill in the art reasonably would have expected success because (i) PARP inhibitors had widespread success as a therapeutic class for the treatment of a variety of cancers, including BRCA1/BRCA2 mutated tumors, at the time the instant invention was made (see Johannes et al; page 14498, column 1); (ii) “AZD5305” is a potent and selective PARP1 inhibitor, with excellent in vivo efficacy, reduced effects on human bone marrow progenitor cells, and multiple clinical options (including combination approaches) (see Johannes et al. abstract; page 14504 through page 14505, column 1 and column 2 (last full paragraph above “conclusions”; (page 14506, bottom of column 1 through column 2); and (iii) topoisomerase I (Topo1) inhibitors have demonstrated synergy with PARP inhibitors (see Yap et al., page 1, column 1, 2nd paragraph; page 5, column 2).
Co-pending Application 18/467,137
5. Claims 1, 2, 4, 6, 7, 8, 11-13, 16, 18, 21-25, 27, 29, 46, and 55 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 46-69 of copending Application No. 18/467,137 in view of Johannes et al. (J Med Chem 64: 14498-14512, 2021), and Yap et al. (JCO Precision Oncol 6: e2100456, 09 February 2022; cited on the PTO-892 of 09 September 2024). The basis for this rejection is set forth at pages 20-23 of the previous Office Action of 19 May 2025 and is reiterated herein for convenience.
Claims 45-58 of the ‘137 application are directed to an antibody or antibody binding fragment which binds to B7-H4 and wherein the antibody or antigen binding agent is conjugated to a heterologous agent. The antibody CDR, VH chain, and VL chain amino acid sequences recited in the clams of the ‘137 application are 100% identical to the same sequences recited in claims 1, 11, 12, 13, 29, and 46 of the instant application.
Claims 49-54 of the ‘137 application recite that the heterologous agent is SG3932, SG4010, SG4057, or SG4052, as recited in instant claims 25 and 46.
Claims 55-57 of the ‘137 application recite that the ADC has a drug to antibody ration (DAR) of about 8, meeting the limitations of instant claim 27.
Claims 58-65 of the ‘137 application recite a method of treating cancer comprising a cancer cell which expresses B7-H4 comprising administering to a subject the ADC, meeting the limitations of instant claim 1.
Claims 60-69 of the ‘137 application recite that the cancer is selected from breast cancer (including HR+, HER2+, and TNBC), ovarian cancer, endometrial cancer, hematological cancer, cholangiocarcinoma, NSCLC, pancreatic cancer, gastric cancer, or a cancer that has a homologous recombination DNA repair defect (such as the presence of a BRCA1 mutation), meeting the limitations of instant claims 6-8 and 55.
The difference between the claims of the ‘137 application and the claims of the instant application is that the claims of the ‘137 application do not recite that the composition comprising the B7-H4 antibody-drug conjugate or methods of cancer treatment by administering the B7-H4 antibody-drug conjugate further comprise an additional agent, wherein the additional agent is a PARP1 inhibitor.
Johannes et al. disclose that PARP inhibitors have demonstrated widespread success as a therapeutic class for the treatment of a variety of cancers (page 14498, column 1). Johannes et al. indicate that BRCA mutant tumors are sensitive to PARP1/PARP2 inhibitors (page 14499, column 1, 1st paragraph). Johannes et al. state that in spite of their success, PARP1/2 inhibitors have shown significant hematological toxicities, including anemia, neutropenia, and thrombocytopenia (page 14499, column 1, 2nd paragraph). Johannes et al. teach the generation of compound 25, “AZD5305”, a potent and selective PARP1 inhibitor, with excellent in vivo efficacy and reduced effects on human bone marrow progenitor cells (abstract; page 14504 through page 14505, column 1 and column 2 (last full paragraph above “conclusions”). Johannes et al. disclose that AZD5305 is a next-generation PARP inhibitor with multiple clinical options, including combination approaches (page 14506, bottom of column 1 through column 2).
Yap et al. teach that tumors characterized by homologous recombination deficiency, such as BRCA1/2-mutated cancers, are sensitive to inhibition of poly(ADP-ribose) polymerases (PARPs) (page 1, column 1, 1st paragraph). Yap et al. also disclose that in human tumor cell lines, topoisomerase I (Topo1) inhibitors have demonstrated synergy with PARP inhibitors (page 1, column 1, 2nd paragraph). Yap et al. state that PARP inhibition may augment Topo1-mediated DNA damage or delay repair (page 1, column 1, 2nd paragraph). Yap et al. review the SEASTAR study, which investigated the combination of (i) PARP inhibitor, rucaparib, and (ii) sacituzumab govitecan (SG), a conjugate of SN-38 (the active metabolite in topoisomerase inhibitors irinotecan and topotecan) and a humanized anti-Trop-2 antibody (page 1, 2nd and 3rd paragraphs). Yap et al. state that the results provide “proof-of-concept clinical evidence supporting further development of PARP1 inhibitors in combination with ADCs carrying Topo1-inhibitor payloads” (page 5, column 2). Yap et al. also teach that combination with other selective PARP inhibitors, such as PARP1-targeted inhibitor AZD5305, may improve tolerability (page 5, column 2).
It would have been obvious to the person of ordinary skill in the art at the time the invention was made to modify the composition comprising a B7-H4 antibody-topoisomerase I drug conjugate and methods of treating cancer by administering the B7-H4 antibody-topoisomerase I drug conjugate as recited by the claims of the ‘137 application in combination with a PARP1 inhibitor, such as ADZ5305, as taught by Johannes et al. and Yap et al. The person of ordinary skill in the art would have been motivated to make that modification to generate synergism between the topoisomerase inhibitor present in the antibody-drug conjugate of the ‘137 claims and the PARP1 inhibitor, to in turn enhance anti-tumor efficacy and improve patient tolerability (see Joannes et al., abstract; page 14504 through page 14505, column 1 and column 2 (last full paragraph above “conclusions”);; Yap et al., page 1, column 1, 2nd paragraph; page 5, column 2). The person of ordinary skill in the art reasonably would have expected success because (i) PARP inhibitors had widespread success as a therapeutic class for the treatment of a variety of cancers, including BRCA1/BRCA2 mutated tumors, at the time the instant invention was made (see Johannes et al; page 14498, column 1); (ii) “AZD5305” is a potent and selective PARP1 inhibitor, with excellent in vivo efficacy, reduced effects on human bone marrow progenitor cells, and multiple clinical options (including combination approaches) (see Johannes et al. abstract; page 14504 through page 14505, column 1 and column 2 (last full paragraph above “conclusions”; (page 14506, bottom of column 1 through column 2); and (iii) topoisomerase I (Topo1) inhibitors have demonstrated synergy with PARP inhibitors (see Yap et al., page 1, column 1, 2nd paragraph; page 5, column 2).
This is a provisional nonstatutory double patenting rejection.
Applicant’s arguments
(i) At the bottom of pages 12 and 13 of the Response of 11 November 2025, Applicant argues that Yap et al. describes the results of the SEASTAR study, which investigated the combination of a PARP inhibitor (rucaparib) and sacituzumab govitecan (SG), a conjugate of SN-38 and a humanized anti-Trop-2 antibody. Applicant asserts that in contrast, the present application is directed to methods of treating cancer comprising administering an antibody drug conjugate (ADC) which binds to a B7-H4 polypeptide and a PARP1 inhibitor. Applicant contends that the present application is directed to ADCs which bind to a completely different target, and which are structurally and functionally distinct from the ADC disclosed in Yap et al. Applicant states that there is no disclosure of an anti-B7-H4 ADC in Yap et al., nor any specific disclosure of any specific ADC targets other than Trop-2. Applicant asserts that the Trop-2-specific disclosures in Yap et al. are insufficient to support the broad suggestion that there is motivation or a reasonable expectation of success for the combination of any PAP inhibitor with any ADC bearing a Topo1-inhibitor payload.
Applicant’s arguments have been fully considered but are not found to be persuasive. Yap et al. teach that tumors characterized by homologous recombination deficiency, such as BRCA1/2-mutated cancers, are sensitive to inhibition of poly(ADP-ribose) polymerases (PARPs) (page 1, column 1, 1st paragraph). Yap et al. also disclose that in human tumor cell lines, topoisomerase I (Topo1) inhibitors have demonstrated synergy with PARP inhibitors (page 1, column 1, 2nd paragraph). Yap et al. review the SEASTAR study, which is a combination of a PARP inhibitor (rucaparib) and sacituzumab govitecan (SG), a conjugate of SN-38 and a humanized anti-Trop-2 antibody, and clearly state that the results provide “proof-of-concept clinical evidence supporting further development of PARP1 inhibitors in combination with ADCs carrying Topo1-inhibitor payloads” (page 5, column 2).
Although Yap et al. do not disclose an anti-B7-H4 ADC or any other specific ADC targets other than Trop-2, the antibody component of the ADC is simply the cancer cell-targeting mechanism. Yap et al. teach that Trop-2 is a cell surface antigen overexpressed in epithelial cancers and that targeted delivery of SN-38 (the active metabolite in topoisomerase inhibitors irinotecan and topotecan) to cancer cells through an antibody-drug conjugate is a rational and effective strategy for combination therapy with a PARP1 inhibitor to reduce off-target and additive toxicity (page 1, top of column 2). The person of ordinary skill in the art would have been motivated to modify the composition comprising a B7-H4 antibody-topoisomerase I drug conjugate and methods of treating cancer by administering the B7-H4 antibody-topoisomerase I drug conjugate as recited by the claims of the ‘225 patent or ‘137 application in combination with a PARP1 inhibitor to generate synergism between the topoisomerase inhibitor present in the antibody-drug conjugate of the ‘225 and ‘137 claims and the PARP1 inhibitor, to in turn enhance anti-tumor efficacy and improve patient tolerability (see Yap et al., page 1, column 1, 2nd paragraph; page 5, column 2). The skilled artisan reasonably would have expected success because topoisomerase I (Topo1) inhibitors have demonstrated synergy with PARP inhibitors and Yap et al. provide proof-of-concept clinical evidence supporting the development of PARP1 inhibitors in combination with ADCs carrying Topo1-inhibitor payloads (see Yap et al., page 1, column 1, 2nd paragraph; page 5, column 2).
(ii) At the bottom of page 12 through the top of page 13 of the Response of 11 November 2024, Applicant also argues that Johannes et al. cannot cure the deficiencies in Yap et al. Applicant states that Johannes et al. discloses that PARP inhibitors are a therapeutic call for the treatment of cancer and specifically indicates that AZD5305 as a potent and selective PARP1 inhibitor. Applicant submits that Johannes et al. does not teach or suggest the combination of a PARP1 inhibitor with other cancer treating agents, let alone ADCs. Applicant concludes that even in view of the cited references, a one skilled in the art would not have had a motivation to combine the alleged teachings of the ‘225 patent or ‘137 application with either Johannes et al. or Yap and would not have had a reasonable expectation of success.
Applicant’s arguments have been fully considered but are not found to be persuasive. As discussed previously, Johannes et al. disclose that PARP inhibitors have demonstrated widespread success as a therapeutic class for the treatment of a variety of cancers (page 14498, column 1). Johannes et al. indicate that BRCA mutant tumors are sensitive to PARP1/PARP2 inhibitors (page 14499, column 1, 1st paragraph). Johannes et al. state that in spite of their success, PARP1/2 inhibitors have shown significant hematological toxicities, including anemia, neutropenia, and thrombocytopenia (page 14499, column 1, 2nd paragraph). Johannes et al. teach the generation of compound 25, “AZD5305”, a potent and selective PARP1 inhibitor, with excellent in vivo efficacy and reduced effects on human bone marrow progenitor cells (abstract; page 14504 through page 14505, column 1 and column 2 (last full paragraph above “conclusions”). Johannes et al. disclose that AZD5305 is a next-generation PARP inhibitor with multiple clinical options, including combination approaches (page 14506, bottom of column 1 through column 2).
Therefore, it would have been obvious to the person of ordinary skill in the art at the time the invention was made to modify the composition comprising a B7-H4 antibody-topoisomerase I drug conjugate and methods of treating cancer by administering the B7-H4 antibody-topoisomerase I drug conjugate as recited by the claims of the ‘225 patent or ‘137 application in combination with a PARP1 inhibitor, such as ADZ5305, as taught by Johannes et al. and Yap et al. The person of ordinary skill in the art would have been motivated to make that modification to generate synergism between the topoisomerase inhibitor present in the antibody-drug conjugate of the ‘225 patent claims or ‘137 application claims and the PARP1 inhibitor, to in turn enhance anti-tumor efficacy and improve patient tolerability (see Joannes et al., abstract; page 14504 through page 14505, column 1 and column 2 (last full paragraph above “conclusions”);; Yap et al., page 1, column 1, 2nd paragraph; page 5, column 2). The person of ordinary skill in the art reasonably would have expected success because (i) PARP inhibitors had widespread success as a therapeutic class for the treatment of a variety of cancers, including BRCA1/BRCA2 mutated tumors, at the time the instant invention was made (see Johannes et al; page 14498, column 1); (ii) “AZD5305” is a potent and selective PARP1 inhibitor, with excellent in vivo efficacy, reduced effects on human bone marrow progenitor cells, and multiple clinical options (including combination approaches) (see Johannes et al. abstract; page 14504 through page 14505, column 1 and column 2 (last full paragraph above “conclusions”; (page 14506, bottom of column 1 through column 2); and (iii) topoisomerase I (Topo1) inhibitors have demonstrated synergy with PARP inhibitors (see Yap et al., page 1, column 1, 2nd paragraph; page 5, column 2).
Conclusion
No claims are allowable.
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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BEB
Art Unit 1647
27 February 2026
/BRIDGET E BUNNER/Primary Examiner, Art Unit 1647