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 .
DETAILED ACTION
Applicant's amendments and remarks filed on May 1, 2026 are acknowledged. Claims 1, 2, 4-8, 10, 15-17, and 20-24 have been canceled. Claims 3, 9, 12, 13, 25, 26, and 27 were amended. Claims 3, 9, 11-14, 18, 19, and 25-31 are pending.
Election/Restrictions
Applicant’s election without traverse of Group I (claims 1-28) and species: SEQ ID NO: 79 in the reply filed on December 30, 2025 is acknowledged.
Claims 29-31 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on December 30, 2025.
Claims 18 and 19 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected species, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on December 30, 2025.
Claims 3, 9, 11-14, and 25-28 are examined on the merits herein.
Priority
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Withdrawn Objections
In view of Applicant’s amendments and response, the objection to the drawings is withdrawn.
Withdrawn Rejections
In view of Applicant’s amendments and response, the 35 U.S.C 112(b) and Improper Markush Grouping rejections are withdrawn.
In view of Applicant’s amendments and response, the nonstatutory double patenting rejection of copending Application No. 17/449,290 is withdrawn.
Drawings
The drawings were received on May 1, 2026. These drawings are found acceptable by the examiner.
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.
The following is a new rejection, necessitated by the amendment to the claims in the reply filed May 1, 2026.
Claims 3, 9, 11-14, and 25-28 are rejected under 35 U.S.C. 103 as being unpatentable over Zhang et al. (US 2022/0186217; reference previously cited by the Examiner) in view of Kaye (US 9,506,058) and Aznarez et al. (US 11,096,956; reference previously cited by the Examiner).
Regarding claims 3, 9, 12-14, and 25-27, Zhang et al. teaches an oligonucleotide or an oligonucleotide composition capable of mediating skipping of an exon, e.g., exon 51, of the DMD gene [0005]. Zhang et al. teaches SEQ ID NO: 394 (designated as Db) which has a match to instant SEQ ID NO: 79 (designated as Qy) as shown in the alignment below.
Query Match 100.0%; Score 18; DB 1; Length 20;
Best Local Similarity 72.2%;
Matches 13; Conservative 5; Mismatches 0; Indels 0; Gaps 0;
Qy 1 GGTAAGTTCTGTCCAAGC 18
||:|||::|:|:||||||
Db 1 GGUAAGUUCUGUCCAAGC 18
Zhang et al. also teaches that chemical modifications (e.g., modifications of sugar, base, and/or internucleotidic linkages, and patterns thereof) can have a significant impact on oligonucleotide properties, e.g., exon skipping (e.g., of exon 51 of DMD), toxicities, stability, protein binding characteristics, etc. [0004].
Regarding claim 11, Zhang et al. teaches DMD oligonucleotides comprising one or more modified base moieties [0228].
Regarding claim 28, Zhang et al. teaches a pharmaceutical composition comprising a DMD oligonucleotide or a DMD oligonucleotide composition and a pharmaceutically acceptable carrier [0091].
However, Zhang et al. does not teach an antisense oligonucleotide consisting of the base sequence of SEQ ID NO: 79 containing a chemical modification of the sugar moiety of each of the nucleotides of the antisense oligonucleotide wherein the chemical modification of 4 or 6 sugar moieties is an LNA and the chemical modification of the sugar moiety of the nucleotides not comprising an LNA is 2’-OMe (claim 3).
Zhang et al. does not teach wherein the chemical modification of the sugar moiety of each of the two 5’ terminal nucleotides of the AON and each of the two 3’ terminal nucleotides of the AON is an LNA (claims 9 and 25). Zhang et al. also does not teach that each of the two 5’ terminal nucleotides of the AON, the 3’ terminal nucleotide of the AON, and the nucleotide at position six from the 5’ terminus of the AON is an LNA (claim 26). Zhang et al. also does not teach that each of the two 5’ terminal nucleotides of the AON, each of the two 3’ terminal nucleotides of the AON, and each of the nucleotides at position six and eleven from the 5’ terminus of the AON is an LNA (claim 27).
Zhang et al. also does not teach wherein all cytosine bases are 5-methylcytosine bases (claims 12, 25, 26, and 27) or wherein all thymine bases are uracil bases (claim 13). Zhang et al. also does not teach a fully phosphorothioate backbone (claims 14, 25, 26, and 27).
Kaye teaches antisense molecules capable of binding to a selected target site in the human dystrophin gene to induce exon skipping [abstract]. Kaye also teaches that Duchenne muscular dystrophy (DMD) is caused by a defect in the expression of the protein dystrophin [column 2, third full paragraph]. The continuous progression of DMD allows for therapeutic intervention at all stages of the disease; however, treatment is currently limited to glucocorticoids, which are associated with numerous side effects. Consequently, developing better therapies to treat the underlying cause of this disease is imperative [column 3, first paragraph]. Kaye teaches that an antisense oligonucleotide of sufficient length has a minimal number of nucleotides to be capable of specifically hybridizing to exon 51 of the human dystrophin gene. In one embodiment, an oligonucleotide of sufficient length is from 15 to about 25 nucleotides in length [column 26, first paragraph].
Aznarez et al. teaches that any component of an antisense oligonucleotide (ASO) (e.g., a nucleobase, sugar moiety, backbone) may be modified in order to achieve desired properties or activities of the ASO or reduce undesired properties or activities of the ASO. In some embodiments, the ASO comprises 2′MOE modifications and a phosphorothioate backbone [column 119, first full paragraph]. Further, Aznarez et al. teaches that ASOs comprised of 2’-O-(2-methoxyethyl) (MOE) phosphorothioate-modified nucleotides have significantly enhanced resistance to nuclease degradation and increased bioavailability [column 119, second full paragraph]. Aznarez et al. also teaches that in some examples each monomer of the ASO is modified in the same way, for example each linkage of the backbone of the ASO comprises a phosphorothioate linkage or each ribose sugar moiety comprises a 2′O-methyl modification [column 118, last paragraph]. In some embodiments, the antisense oligomer comprises a phosphorodiamidate morpholino, a locked nucleic acid, a peptide nucleic acid, a 2′-O-methyl, a 2′-Fluoro, or a 2′-O-methoxyethyl moiety. Further, in some embodiments, each sugar moiety is a modified sugar moiety [column 6, first paragraph]. Aznarez et al. also teaches that the nucleobase of an ASO may be any naturally occurring, unmodified nucleobase such as adenine, guanine, cytosine, thymine and uracil, or any synthetic or modified nucleobase (e.g., 5-methylcytosine or 5,6-dihydrouracil) such that it is capable of hydrogen bonding with a nucleobase present on a target pre-mRNA [column 116, second full paragraph].
It would have been obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to design an antisense oligonucleotide consisting of the base sequence of SEQ ID NO: 79 using the design principles taught by Zhang et al. and Kaye because it would have amounted to applying known design principles for an antisense oligonucleotide to induce exon skipping of the DMD gene to yield predictable results. The skilled artisan would have had a reasonable expectation of success in designing antisense oligonucleotides because as evidenced by Zhang et al. and Kaye it was well within the purview of the skilled artisan, and routine in the art to design antisense oligonucleotides to induce exon skipping of the DMD gene.
Although Aznarez et al. does not explicitly teach the number of LNAs to incorporate in the antisense oligonucleotide or the specific positions of the LNAs, it would have been obvious to try because Kaye taught that Duchenne muscular dystrophy (DMD) is caused by a defect in the expression of the protein dystrophin and treatment is currently limited to glucocorticoids which are associated with numerous side effects and developing better therapies to treat the underlying cause of this disease is imperative. It would have been obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to modify the antisense oligonucleotide of Zhang et al. and Kaye and arrive at the instantly claimed modifications because Aznarez et al. taught that any component of an antisense oligonucleotide (ASO) (e.g., a nucleobase, sugar moiety, backbone) may be modified in order to achieve desired properties or activities of the ASO or reduce undesired properties or activities of the ASO. One of ordinary skill in the art would have been motivated to do so because it would have amounted to combining known prior art elements to yield predictable results.
Response to Arguments
Applicant's arguments filed May 1, 2026 have been fully considered but they are not persuasive.
Applicant asserts that Zhang et al. and Aznarez et al. do not teach, suggest, or provide any reason to arrive at the AONs of the amended claims having the specific combination as recited in the claims. Applicant further asserts that Zhang et al. does not provide any suggestion to remove two of the nucleotides from SEQ ID NO: 394 let alone the specific nucleotides that would yield that of instant SEQ ID NO: 79. In addition, Applicant asserts that Zhang et al. discloses hundreds of oligonucleotide sequences and SEQ ID NO: 394 is merely one sequence listed among hundreds of sequences with no generic or exemplary disclosure to guide one of ordinary skill in the art toward selecting this particular sequence over another. Applicant points to Table 4J which demonstrates that WV-20102 (SEQ ID NO: 87) achieved the highest exon 51 skipping value at approximately 78% and 81% at 10 uM and WV-20119 (SEQ ID NO: 104) achieved approximately 79% and 80% at 10 uM. Therefore, Applicant asserts that one of ordinary skill in the art would select either SEQ ID NO: 87 or 104 to modify not SEQ ID NO: 394.
These arguments are not found persuasive. Zhang et al. taught that in some embodiments, provided technologies skip exon 51 in a target DMD transcript. A number of DMD oligonucleotides comprising various types of modified internucleotidic linkages, including many comprising non-negatively charged internucleotidic linkages (e.g., n001), which have various base sequences and/or target various nucleic acids (e.g., DMD transcripts of various genes) were prepared, and various useful properties, activities, and/or advantages were demonstrated [0499]. Zhang et al. also taught designing DMD oligonucleotides capable of mediating skipping of DMD exon 51 [0272]. Zhang et al. taught SEQ ID NO: 394 (designated as Db) which has a match to instant SEQ ID NO: 79 (designated as Qy) as shown in the alignment below.
Query Match 100.0%; Score 18; DB 1; Length 20;
Best Local Similarity 72.2%;
Matches 13; Conservative 5; Mismatches 0; Indels 0; Gaps 0;
Qy 1 GGTAAGTTCTGTCCAAGC 18
||:|||::|:|:||||||
Db 1 GGUAAGUUCUGUCCAAGC 18
Kaye taught antisense molecules capable of binding to a selected target site in the human dystrophin gene to induce exon skipping [abstract]. Kaye also taught that Duchenne muscular dystrophy (DMD) is caused by a defect in the expression of the protein dystrophin [column 2, third full paragraph]. The continuous progression of DMD allows for therapeutic intervention at all stages of the disease; however, treatment is currently limited to glucocorticoids, which are associated with numerous side effects. Consequently, developing better therapies to treat the underlying cause of this disease is imperative [column 3, first paragraph]. Kaye taught that an antisense oligonucleotide of sufficient length has a minimal number of nucleotides to be capable of specifically hybridizing to exon 51 of the human dystrophin gene. In one embodiment, an oligonucleotide of sufficient length is from 15 to about 25 nucleotides in length [column 26, first paragraph]. Therefore, it would have been obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to design an antisense oligonucleotide consisting of the base sequence of SEQ ID NO: 79 using the design principles taught by Zhang et al. and Kaye because it would have amounted to applying known design principles for an antisense oligonucleotide to induce exon skipping of the DMD gene to yield predictable results. The skilled artisan would have had a reasonable expectation of success in designing antisense oligonucleotides because as evidenced by Zhang et al. and Kaye it was well within the purview of the skilled artisan, and routine in the art to design antisense oligonucleotides to induce exon skipping of the DMD gene. In addition, even though Zhang et al. discloses hundreds of oligonucleotide sequences, this is a finite number of sequences to test.
Applicant asserts that Aznarez et al. does not disclose or suggest exon skipping much less exon 51 skipping for treatment of DMD. Further, Aznarez et al.’s direct target genes do not include dystrophin. Thus, Applicant asserts that Aznarez et al.’s antisense oligomers are designed for an entirely different mechanism than exon 51 skipping for treatment of DMD. Therefore, one of ordinary skill in the art looking to achieve desired properties or reduce undesired properties of exon 51 skipping AONs for treatment of DMD would not look to Aznarez et al. for guidance.
These arguments are not found persuasive. Aznarez et al. is used in combination with Zhang et al. and Kaye to render obvious the instant claims because Zhang et al. taught an oligonucleotide or an oligonucleotide composition capable of mediating skipping of an exon, e.g., exon 51, of the DMD gene and chemical modifications (e.g., modifications of sugar, base, and/or internucleotidic linkages, and patterns thereof) that can have a significant impact on oligonucleotide properties, e.g., exon skipping (e.g., of exon 51 of DMD), toxicities, stability, and protein binding characteristics, Kaye taught antisense molecules capable of binding to a selected target site in the human dystrophin gene to induce exon skipping, and Aznarez et al. taught that any component of an antisense oligonucleotide (ASO) (e.g., a nucleobase, sugar moiety, backbone) may be modified in order to achieve desired properties or activities of the ASO or reduce undesired properties or activities of the ASO.
Applicant asserts that the AONs of the amended claims consisting of the base sequence of SEQ ID NO: 79 and having 4 or 6 LNAs and 2’-O-methyl sugar modifications on non-LNA nucleotides possess unexpectedly improved exon 51 skipping properties as compared to the closest prior art AON, drisapersen. Applicant points to Example 2 which identified AON #79B, #79C, and #79F as having the highest exon 51 skipping efficacy. Further, of these AONs with slightly different LNA profiles, AON #79C was most efficient (7.3%). Applicant also asserts that in subsequent in vitro comparative screening assays AON #79C was found to be 10-fold more effective than drisapersen; therefore, the AONs of the amended claims exhibit unexpectedly improved efficacy compared to the closest AON of the prior art.
These arguments are not found persuasive. In an assertion of unexpected results, one must compare the claimed subject matter with the closest prior art to be effective to rebut a prima facie case of obviousness. Although MPEP 716.02(e)(I) states that Applicants may compare the claimed invention with prior art that is more closely related to the invention than the prior art relied upon by the examiner, drisapersen is not more closely related to the invention than the prior art that was cited by the Examiner. Janssen et al. (Molecular Therapy Nucleic Acids 2019) discloses that drisapersen is a modified 2’O-methyl phosphorothioate antisense oligonucleotide [abstract]. Janssen et al. also teaches that the sequence of drisapersen is 5’-UCA AGG AAG AUG GCA UUU CU-3’ which targets dystrophin exon 51 [page 302, right column, first full paragraph]. Applicant also asserts that subsequent in vitro comparative screening assays found AON #79C to be 10-fold more effective than drisapersen; however, Applicant did not provide evidence to support these assertions.
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 3, 9, 11-14, and 25-28 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-13 of copending Application No. 18/179,064 (reference application) in view of Aznarez et al. (US 11,096,956). ‘064 SEQ ID NO: 4565 (designated as Db) has a 100% match to instant SEQ ID NO: 79 (designated as Qy) as shown in the alignment below.
Query Match 100.0%; Score 18; DB 1; Length 18;
Best Local Similarity 100.0%;
Matches 18; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 GGTAAGTTCTGTCCAAGC 18
||||||||||||||||||
Db 1 GGTAAGTTCTGTCCAAGC 18
‘064 SEQ ID NO: 4568 (designated as Db) has a 100% match to instant SEQ ID NO: 79 (designated as Qy) as shown in the alignment below.
Query Match 100.0%; Score 18; DB 1; Length 18;
Best Local Similarity 100.0%;
Matches 18; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 GGTAAGTTCTGTCCAAGC 18
||||||||||||||||||
Db 1 GGTAAGTTCTGTCCAAGC 18
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680
636
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However, ‘064 does not teach that each of the nucleotides of the AON contains a chemical modification of the sugar moiety. ‘064 also does not teach that 4 or 6 sugar moieties is an LNA, the specific positions of the LNA as recited in the instant claims, and the chemical modification of the sugar moiety of the nucleotides not comprising a LNA is 2’-OMe. ‘064 does not teach that all thymine bases are uracil bases.
Aznarez et al. teaches that any component of an antisense oligonucleotide (ASO) (e.g., a nucleobase, sugar moiety, backbone) may be modified in order to achieve desired properties or activities of the ASO or reduce undesired properties or activities of the ASO. In some embodiments, the ASO comprises 2′MOE modifications and a phosphorothioate backbone [column 119, first full paragraph]. Further, Aznarez et al. teaches that ASOs comprised of 2’-O-(2-methoxyethyl) (MOE) phosphorothioate-modified nucleotides have significantly enhanced resistance to nuclease degradation and increased bioavailability [column 119, second full paragraph]. Aznarez et al. also teaches that in some examples each monomer of the ASO is modified in the same way, for example each linkage of the backbone of the ASO comprises a phosphorothioate linkage or each ribose sugar moiety comprises a 2′O-methyl modification [column 118, last paragraph]. In some embodiments, the antisense oligomer comprises a phosphorodiamidate morpholino, a locked nucleic acid, a peptide nucleic acid, a 2′-O-methyl, a 2′-Fluoro, or a 2′-O-methoxyethyl moiety. Further, in some embodiments, each sugar moiety is a modified sugar moiety [column 6, first paragraph]. Aznarez et al. also teaches that the nucleobase of an ASO may be any naturally occurring, unmodified nucleobase such as adenine, guanine, cytosine, thymine and uracil, or any synthetic or modified nucleobase (e.g., 5-methylcytosine) such that it is capable of hydrogen bonding with a nucleobase present on a target pre-mRNA [column 116, second full paragraph].
It would have been obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to modify the antisense oligonucleotide of ‘064 wherein each of the nucleotides contains a chemical modification of the sugar moiety, wherein 4 or 6 sugar moieties is an LNA at specific positions, and the nucleotides not comprising an LNA is 2’-OMe because Aznarez et al. taught that any component of an antisense oligonucleotide (ASO) (e.g., a nucleobase, sugar moiety, backbone) may be modified in order to achieve desired properties or activities of the ASO or reduce undesired properties or activities of the ASO. One of ordinary skill in the art would have been motivated to do so because it would have amounted to combining known prior art elements to yield predictable results.
This is a provisional nonstatutory double patenting rejection.
Response to Arguments
Applicant's arguments filed May 1, 2026 have been fully considered but they are not persuasive.
Applicant has requested for the provisional nonstatutory double patenting rejection of 18/179,064 to be held in abeyance until allowable subject matter has been indicated at which point Applicant will take appropriate action. Thus, the nonstatutory double patenting rejection is maintained.
Conclusion
No claims are allowed.
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 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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to CHRISTINA TRAN whose telephone number is (571)270-0550. The examiner can normally be reached M-F 7:30 - 5:00pm.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Jennifer Dunston can be reached at (571) 272-2916. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/C.T./
Examiner, Art Unit 1637
/Jennifer Dunston/Supervisory Patent Examiner, Art Unit 1637
Prosecution Insights