RESPONSE TO APPLICANT’S AMENDMENT
Applicant's amendment, filed 09/05/2025, is acknowledged.
Claims 1-6 and 8-20 are pending and under examination.
Applicant’s IDS, filed 09/05/2025, is acknowledged.
4. The following new grounds of rejection are necessitated by the amendment submitted 09/05/2025.
5. 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.
6. Claims 1-6 and 8-20 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of copending Application No. 17/791667 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the `667 application is directed to a complex comprising anti-transferrin receptor antibody, 6-D3 comprising identical CDR SEQ ID NOs: 49,50,51,52,29,53 and VH and VL SEQ ID NOs: 54/55 covalently linked to an oligonucleotide tht targets a muscle disease gene. Constructing claims in light of the specification the muscle disease genes including DMPK (see Table 1 of the specification). The `677 applicant also claims a method of treating a subject a muscle disease, the method comprising administering to the subject an effective amount of the complex. The claims of the `667 anticipates the instant claims.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Applicant’s arguments, filed 09/05/2025, have been fully considered, but have not been found convincing.
Applicant requests that these provisional rejections be held in abeyance until allowable subject matter is agreed upon.
The rejection is maintained until applicant address the rejection.
7. Claims 1-6 and 8-20 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of copending Application No. 17/794768, in view of US US Pat. 11576980 B2 or US 11497814 B2. Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the `667 application is directed to a complex comprising anti-transferrin receptor antibody, 6-D3 comprising identical CDR SEQ ID NOs: 49,50,51,52,29,53 and VH and VL SEQ ID NOs: 54/55 covalently linked to oligonucleotide that targets a pro-atrophy gene. The `677 applicant also claims a method of treating a subject having muscle atrophy, the method comprising administering to the subject an effective amount of the complex. The `768 application further claims methods of delivering an oligonucleotide to a cell expressing transferring receptor the claimed complex. Also the application claims methods of treating a subject having muscle atrophy.
The reference teachings differ from the claimed invention only in the recitation of that the oligonucleotide targets DMPK.
The `980 patent teaches and claims single-stranded antisense oligonucleotide (ASO) conjugates comprising an anti-transferrin receptor antibody or antigen binding fragment thereof conjugated to an ASO sequence that hybridizes to a target sequence in exons 1-13 of the human DMPK mRNA excluding the CUG repeats and mediates RNA interference against the human DMPK mRNA preferentially in a muscle cell in a subject wherein the ASO sequence is 8 to 30 nucleotides in length, herein mediation of RNA interference against the human DMPK mRNA modulates muscle atrophy or myotonic dystrophy in the subject, wherein the myotonic dystrophy is DM1, wherein the ASO sequence that hybridizes to the target sequence of the human DMPK mRNA is selected from a group consisting of SEQ ID NOs: 6111-8814, SEQ ID NOs: 11519-14222 (see issued clams 1-23 also col. 1 lines 45+, col, 151, lines 50+, Fig. 17-18).
.
The `814 patent teaches and claims methods of treating myotonic dystrophy in a subject in need thereof, comprising: administering to said subject a therapeutically effective amount of a small interfering RNA (siRNA) conjugate comprising an anti-transferrin receptor antibody or antigen binding fragment thereof conjugated to an siRNA that hybridizes to a target sequence in exons 1-13 of human DMPK mRNA excluding CUG repeats, wherein the siRNA is 8 to 30 nucleotides in length, thereby treating myotonic dystrophy in said subject, wherein the myotonic dystrophy is myotonic dystrophy type 1 (DM1). Further, the `814 patent claims small interfering RNA (siRNA) conjugates comprising an anti-transferrin receptor antibody or antigen-binding fragment thereof conjugated to an siRNA that hybridizes to a target sequence in exons 1-13 of human DMPK mRNA excluding CUG repeats and mediates RNA interference against the human DMPK mRNA preferentially in a muscle cell in a subject, wherein the siRNA is a double stranded RNA comprising a guide strand and a passenger strand, wherein mediation of RNA interference against the human DMPK mRNA modulates muscle atrophy or myotonic dystrophy in the subject, wherein the anti-transferrin receptor antibody or antigen binding fragment thereof binds to a transferrin receptor on cell surface of the muscle cell, wherein the myotonic dystrophy is DM1, wherein the guide strand of the siRNA is selected from a group consisting of SEQ ID NOs: 6111-8814, 11519-14222 or SEQ ID NOs: 3407-6110, 8815-11518 (see issued claims 1-30).
Those of skilled in the art would have had a reason to substitute the oligonucleotide that targets a pro-atrophy gene taught by the `768 application with the oligonucleotide that targets MDPK-ASO taught by the `980 and `814 patents in the method of treating muscle atrophy because anti-transferrin receptor antibody enhances DMPK ASO delivery to muscle for treating muscle atrophy by targeting the transferrin receptor (TfR1) on muscle cells. Substituting a known element for another, to yield the known result, is obvious. See KSR, 550 U.S. at 416, 421 (2007).
8. Claims 1-6 and 8-20 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-2, 4-19, 24-25 of copending Application No. 17791670, in view of US Pat. 11576980 B2 or US 11497814 B2. Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the `667 application is directed to a complex comprising anti-transferrin receptor antibody, 6-D3 comprising identical CDR SEQ ID NOs: 49,50,51,52,29,53 and VH and VL SEQ ID NOs: 54/55 covalently linked to ovalently linked to a molecular payload that modulates the expression or activity of myostatin (MSTN), inhibin beta A (INHBA) and/or activin receptor type-1B, wherein in the oligonucleotide comprising an antisense strand comprising a region of complementarity to an MSTN target sequence. The `677 applicant also claims a method of treating muscle atrophy, the method comprising administering to the subject an effective amount of the complex. MSTN, INHBA and/or ACVR1B oligonucleotide and a method of treating muscle atrophy.
The reference teachings differ from the claimed invention only in the recitation of that the oligonucleotide targets DMPK.
The teachings of US Pat. 11576980 B2 or US 11497814 B2 have been discussed, supra.
Those of skilled in the art would have had a reason to substitute the MSTN, INHBA and/or ACVR1B oligonucleotide taught by the `670 application with the oligonucleotide that targets MDPK-ASO taught by the `980 and `814 patents in the method of treating muscle atrophy because anti-transferrin receptor antibody enhances DMPK ASO delivery to muscle for treating muscle atrophy by targeting the transferrin receptor (TfR1) on muscle cells. Substituting a known element for another, to yield the known result, is obvious. See KSR, 550 U.S. at 416, 421 (2007).
9. Claims 1-6 and 8-20 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 copending Application No. 17791701, in view of US Pat. 11576980 B2 or US 11497814 B2. Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the `701 application is directed to a complex comprising anti-transferrin receptor antibody, 6-D3 comprising identical CDR SEQ ID NOs: 49,50,51,52,29,53 and VH and VL SEQ ID NOs: 54/55 covalently linked an oligonucleotide that induces dystrophin (DMD) exon skipping, wherein in the oligonucleotide comprising an antisense strand comprising a region of complementarity to a DMD mRNA target sequence. The `701 applicant also claims a method of treating DMD.
The reference teachings differ from the claimed invention only in the recitation of that the oligonucleotide targets DMPK.
The teachings of US Pat. 11576980 B2 or US 11497814 B2 have been discussed, supra.
Those of skilled in the art would have had a reason to substitute the oligonucleotide that induces dystrophin (DMD) exon skipping taught by the `701 publication with the oligonucleotide that targets MDPK-ASO taught by the `980 and `814 patents in the method of treating muscle atrophy because anti-transferrin receptor antibody enhances DMPK ASO delivery to muscle for treating muscle atrophy by targeting the transferrin receptor (TfR1) on muscle cells. Substituting a known element for another, to yield the known result, is obvious. See KSR, 550 U.S. at 416, 421 (2007).
10. Claims 1-6 and 8-20 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 14 copending Application No. 17796418 , in view of US Pat. 11576980 B2 or US 11497814 B2. Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the `418 application is directed to a complex comprising anti-transferrin receptor antibody, 6-D3 comprising identical CDR SEQ ID NOs: 49,50,51,52,29,53 and VH and VL SEQ ID NOs: 54/55 covalently linked to a molecular payload. The `677 applicant also claims a method of treating a disease, the method comprising administering to the subject an effective amount of the complex.
The teachings of US Pat. 11576980 B2 or US 11497814 B2 have been discussed, supra.
Those of skilled in the art would have had a reason to substitute the payload taught by the `418 application with the oligonucleotide that targets MDPK-ASO taught by the `980 and `814 patents in the method of treating muscle atrophy because anti-transferrin receptor antibody enhances DMPK ASO delivery to muscle for treating muscle atrophy by targeting the transferrin receptor (TfR1) on muscle cells. Substituting a known element for another, to yield the known result, is obvious. See KSR, 550 U.S. at 416, 421 (2007).
11. Claims 1-6 and 8-20 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 copending Application No. 17791697, , in view of US Pat. 11576980 B2 or US 11497814 B2. Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the `667 application is directed to a complex comprising anti-transferrin receptor antibody, 6-D3 comprising identical CDR SEQ ID NOs: 49,50,51,52,29,53 and VH and VL SEQ ID NOs: 54/55 covalently linked to a molecular payload configured for inhibiting expression or activity of Double Homeobox 4 (DUX4), wherein in the molecular payload is the oligonucleotide. The `677 applicant also claims a method of treating a subject wone or more deletions of a D4Z4 repeat in chromosome 4 that is associated with facioscapulohumeral muscular dystrophy (FSHD), the method comprising administering to the subject an effective amount of the complex.
The teachings of US Pat. 11576980 B2 or US 11497814 B2 have been discussed, supra.
Those of skilled in the art would have had a reason to substitute the payload taught by the `697 application with the oligonucleotide that targets MDPK-ASO taught by the `980 and `814 patents in the method of treating muscle atrophy because anti-transferrin receptor antibody enhances DMPK ASO delivery to muscle for treating muscle atrophy by targeting the transferrin receptor (TfR1) on muscle cells. Substituting a known element for another, to yield the known result, is obvious. See KSR, 550 U.S. at 416, 421 (2007).
Applicant’s arguments, filed 09/05/2025, have been fully considered, but have not been found convincing.
Applicant requests that these provisional rejections be held in abeyance until allowable subject matter is agreed upon.
The rejection is maintained until applicant address the rejection.
12. No claim is allowed.
The prior art made of record and not relied upon is considered pertinent to applicant's disclosure.
US 20100016215 A1.
The `215 claims an antisense compound for use in treating myotonic dystrophy DM1 or DM2, comprising an antisense oligonucleotide having 8-30 bases, with at least 8 contiguous bases being complementary to the polyCUG or polyCCUG repeats in the 3'UTR region of dystrophia myotonica protein kinase (DMPK) mRNA in DM1 or DM2, respectively, and conjugated to the oligonucleotide, a cell-penetrating peptide having the sequence
US 20150064181 A
The `181 publication claims a conjugate comprising an antisense oligonucleotide that hybridizes to a DMPK transcript; and an antibody or antigen binding fragment selected from: monoclonal antibody 3E10, or a variant thereof that retains the cell penetrating activity of 3E10, or a variant thereof that binds the same epitope as 3E10, or an antibody that has substantially the same cell penetrating activity as 3E10 and binds the same epitope as 3E10, or an antigen binding fragment of any of the foregoing.
US Patent 11116843 B2
The `843 patent claims a method of reducing the expression of DMPK in skeletal muscle and cardiac muscle, comprising administering to a subject a duplex comprising a first oligomeric compound and a second oligomeric compound wherein the first oligomeric compound comprises a first modified oligonucleotide consisting of 10-30 linked nucleosides; and the second oligomeric compound comprises a second modified oligonucleotide consisting of 10-30 linked nucleosides and a conjugate group; wherein the conjugate group comprises a conjugate moiety and a conjugate linker, wherein the conjugate moiety is cholesterol; and wherein the conjugate linker comprises at least one cleavable moiety; and wherein the nucleobase sequence of the first oligomeric compound is complementary to the nucleobase sequence of the second oligomeric compound and to a DMPK mRNA.
13. Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). 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 extension fee 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 date of this final action.
14. Any inquiry concerning this communication or earlier communications from the examiner should be directed to MAHER M HADDAD whose telephone number is (571)272-0845. The examiner can normally be reached on Monday-Friday from7:00AM to 4:30PM. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Misook Yu, can be reached at telephone number 571-272-0839. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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October 9, 2025
/MAHER M HADDAD/ Primary Examiner, Art Unit 1644