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/Claims
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Applicant’s response filed on 19 September, 2025 has been considered. The following rejections and/or objections are either newly applied as necessitated by amendment or are reiterated and are the only rejections and/or objections presently applied to the instant application.
Claims 8, 11-12, 15-16, 30-33 and 35-44 were previously pending. Claims 30-33, 35, and 38-39 remain withdrawn from consideration as being drawn to a non-elected invention.
Applicant has amended no claims. Applicant has cancelled no claims. Applicant has only added new claim 45 which depends from pending claim 8.
Therefore, claims 8, 11-12, 15-16, 36-37, and 40-45 are pending and are the subject of the present Official Action.
Priority
Applicant’s claim for the benefit of a prior-filed application, provisional application 62/332,297 and PCT application PCT/US17/31351 filed on 05 May, 2016 and 05 May, 2017, respectively, under 35 U.S.C 119(e) or under 35 U.S.C 120, 121 or 365(c) is acknowledged.
Accordingly, the effective priority date of the instant application is granted as 05 May, 2016.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 08 May, 2025, 02 July, 2025, and 23 September, 2025 were received. The submissions are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statements are being considered by the examiner.
Drawings
The drawings filed on 05 May, 2017 are accepted by the Examiner.
Maintained Rejections in view of Applicant’s Amendments/Arguments
Claim Rejections - 35 USC § 103
Claim 8 as written, is not limited to the specific pairs of gRNA sequences recited because claim 8 recites “comprising” and “a nucleotide sequence set forth in”. The claims are broadly interpreted as comprising the full length of the claimed gRNA of SEQ ID NO:1 and SEQ ID NO:2 and any nucleotide domain within that gRNA including a single nucleotide of the claimed SEQ ID NO:1 and SEQ ID NO:2). To the extent that the recitation of “a first gRNA molecule comprising a targeting domain that comprises a nucleotide sequence set forth in SEQ ID NO: 1,” the following rejection applies.
Claims 8, 11-12, 15-16, 36-37 and 40-44 remain rejected and new claim 45 is newly rejected under 35 U.S.C. 103 as being unpatentable over Gersbach et al. WO2014/197748, published 12/11/2014 (hereinafter “Gersbach”, reference of record) in view of Park et al. Bioinformatics 31.24 (2015): 4014-4016 (hereinafter “Park”, reference of record). This rejection is maintained in part and newly applied in part to address Applicant’s amendment to add new claim 45.
Gersbach describes CRSPR Cas9-based systems and viral based delivery methods for performing genomic alterations of genes in muscle tissues (Gersbach, [0003]). Gersbach describes targeting the human dystrophin gene (DMD gene) for treating patients with Duchenne muscular dystrophy (Gersbach, [0029]). Gersbach describes designing gRNA sequences which bind in the exon 45-55 mutational hotspot region of the dystrophin gene, such that gene editing could restore dystrophin expression from a wide variety of patient-specific mutations (Gersbach, [0050]). Gersbach specifically describes deleting exon 51 from the human genome using CRISPR/Cas9 gene editing and verifies this using end-point PCR primers which flank the locus (Gersbach, Fig 16, Fig 21 and 23). Gersbach describes deleting segments of exon 51 which correspond to the length segments described in instant claims 43-44 (Gersbach, [0187]). In Table 8, Gersbach describes Cas9 proteins derived from S. aureus (SaCas9) which may be mutated and which recognize a protospacer adjacent motif of NNGRRT (PAM sequence corresponding to instant SEQ ID NO: 24) for the deletion of exons 45-55, corresponding to the limitations described in instant claims 8-10 41-42, and 45 (Gersbach, Table 8 pg 97; [0008]). Gersbach describes the use of AAV vectors to deliver CRISPR constructs, including Cas9 and up to two gRNA expression cassettes within a single AAV vector, corresponding to the limitations described in claim 12 (Gersbach, [0188] and Fig 39). Although Gersbach describes the use of AAV-mediated CRISPR/SaCas9 gene editing for deleting segments of exon 51, Gersbach does not expressly describe a first gRNA comprising a nucleotide sequence set forth in SEQ ID NO: 1 and a second gRNA molecule comprising a nucleotide sequence set forth in SEQ ID NO: 2 as described in the elected embodiment of independent claim 8
However, techniques are known in the art for the rational design of gRNAs with targeting domains of 21 to 24 nucleotides in length directed to known mutational hotspots such as exon 51 of the DMD gene. For example, Park discloses a web-based tool called Cas-Designer for generating possible gRNA sequences for a given genomic knockout target and their potential off-target sites, including bulge-type sites (Park, abstract). Park provides embodiments for designing gRNAs compatible with various Cas9 endonucleases and PAM sequences, including 5’-NNGRRT-3’ PAM sequences for SaCas9 (Park, Implementation- gRNA selection).
Therefore, it would have been prima facie obvious to one of ordinary skill in the art to use the rational gRNA design methodologies described by Park to design gRNAs comprising a nucleotide sequence set forth in SEQ ID NO: 1 and a second gRNA molecule comprising a nucleotide sequence set forth in SEQ ID NO: 2 and apply it to the CRSPR Cas9-based genomic editing systems for targeting the human dystrophin gene (DMD gene) for treating patients with Duchenne muscular dystrophy as described by Gersbach. It would have been a matter of applying known gRNA design methodologies to experiment with various gRNAs corresponding to the DMD gene targets. Park shows that there are predictable ways to experiment with many spacer sequences in order to minimize off target effects and improve cutting efficiencies (Park, Fig 1). Park outlines both computational approaches to predictably experiment and validate CRISPR target sites corresponding to known gene target sequences. One would have been motivated to do this since Gersbach expressly describes targeting the deletion of exon 51 within the DMD gene for treating patients with Duchenne muscular dystrophy using SaCas9 proteins which recognize NNGRRT PAM sequences (Gersbach, Table 8, pg 97 and [0188]).
Furthermore, since there are a finite number of possible gRNAs which could target the deletion of exon 51 within the DMD gene, it would have been obvious to derive a gRNA comprising a nucleotide sequence set forth in SEQ IDs NOs: 1 and 2 identified in claim 8 following the rational sgRNA design methodologies described by Park and to apply them to the spCas9 gene editing complex described by Gersbach. One would have a reasonable expectation of success given the well-established workflows for evaluating gRNAs and the relative interchangeability of different gRNAs in CRISPR-Cas9 systems. Accordingly, in the absence of evidence to the contrary, one of ordinary skill in the art would have considered the claimed invention to have been prima facie obvious before the effective filing date of the claimed invention.
Response to Traversal
Applicant argues against the asserted prima facie obviousness of the instantly pending claims by arguing (1) that claim 8 recites specific pairs of gRNAs, (2) that one of skill would not have relied on Park to readily disclose all proper guides because doing to would not be practicable, (3) that the references cannot and did not suggest the claimed gRNAs, (4) that there is no teaching or suggestion to combine the specific gRNAs into the pairs specifically claimed, and (5) that one of skill would not have had any expectation of success in the editing efficiency of the claimed gRNA pairs. These arguments have been fully considered but have not been found persuasive for the following reasons:
(1)/(4)/(5) Applicant argues “Independent claim 8 is directed to a vector encoding a first guide RNA molecule and a second gRNA molecule for use with an S. aureus Cas9 molecule. Claim 1 recites specific pairs of the gRNAs, and their specific sequences are recited. The Examiner concedes that Gersbach does not expressly describe the elected gRNAs of SEQ ID NOs: 1-2, but the Examiner relies on Park for allegedly describing "a web-based tool called Cas- Designer for generating possible gRNA sequences for a given genomic knockout target and their potential off-target sites, including bulge-type sites" (Office action at page 5). The Examiner further alleges that there is "a finite number of possible gRNAs which could target the deletion of exon 51 within the DMD gene," that there are "well-established workflows for evaluating gRNAs," and that different gRNAs are "interchangeable[ability]" in CRISPR-Cas9 systems, and therefore, it would be obvious to arrive at the claimed invention in view of Gersbach and Park (Office action at page 6). In contrast to the Examiner's assertion of the "relative interchangeability of different gRNAs in CRISPR systems" (Office action at page 6), Applicant submits that different gRNAs can have widely different effectiveness and off-target activities, such that different gRNAs are not necessarily interchangeable.” (Remarks, at 7), and “none of the cited references, alone or in combination, discloses, teaches, or suggests the specific combinations of gRNAs in the same vector as claimed. Gersbach discloses CRISPR/Cas systems and the dystrophin gene, but Gersbach does not teach or suggest the specific combinations of gRNAs as recited in the claims, as the Examiner concedes (Office action at page 5). Each intron of the dystrophin gene is hundreds of thousands of nucleotides in length. As indicated above, even with the teachings of Park, there is no teaching or suggestion in the combination of cited references to pursue the gRNAs with the specific sequences as claimed, but further, Park does not suggest pairs of gRNAs. There is no teaching or suggestion to combine these specific gRNAs into the pairs as specifically claimed.” (Remarks, at 8), and “Further, one of skill in the art would not have had any expectation of success in the editing efficiency of the claimed gRNA pairs. Park does not predict which target sequences would be cleaved most efficiently. The specific combination of gRNAs as claimed demonstrated exceptional editing efficiency, as detailed in the Examples, Table 1, and Figures 1 and 2 of the present application. This is a surprising technical effect that was not predicted or expected based on the disclosures of the cited references.” (Remarks, at 8).
In response, it is noted that, as written, claim 8 as elected is not limited to the specific pairs of gRNA sequences recited because claim 8 recites “comprising” and “a nucleotide sequence set forth in” (reading on any gRNA having even a single nucleotide set forth in the recited sequences). Applicant is correct in observing that Gersbach does not expressly describe gRNAs having the sequence of SEQ ID NO: 1 and 2. However, neither does claim 8 recite this specific gRNA pair. Thus, this argument has been considered but is, respectfully, not found to be persuasive. Further, Gersbach describes Cas9 proteins derived from S. aureus (SaCas9) which recognize a protospacer adjacent motif of NNGRRT (PAM sequence corresponding to instant SEQ ID NO: 24) for the deletion of exons 45-55 (Gersbach, Table 8, pg 97). Although it’s true that different gRNAs can have widely different effectiveness and off-target activities, closely structurally related gRNAs targeting similar gene regions are indeed interchangeable within CRISPR gene editing systems, which is one of the main reasons the technology has gained widespread adoption. Further, as stated in the above rejection, a person having ordinary skill in the art would have had a reasonable expectation of success given the well-established workflows for evaluating gRNAs and the relative interchangeability of different gRNAs in CRISPR-Cas9 systems. Insofar as Applicant has argued a surprising technical effect, evidence of unexpected properties may be in the form of a direct or indirect comparison of the claimed invention with the closest prior art which is commensurate in scope with the claims. See In re Boesch, 617 F.2d 272, 205 USPQ 215 (CCPA 1980) and MPEP § 716.02(d) - § 716.02(e). An affidavit or declaration under 37 CFR 1.132 must compare the claimed subject matter with the closest prior art to be effective to rebut a prima facie case of obviousness. In re Burckel, 592 F.2d 1175, 201 USPQ 67 (CCPA 1979). In this case, no such affidavit is provided and Applicant merely argues that the surprising technical effect was not predicted or expected based on the disclosures of the cited references. Further, Applicant is reminded that claim 8 is not specific to SEQ ID NOs: 1 and 2 (the subject of table 1 and FIG.s 1 and 2) but rather, guide RNA molecules comprising a sequence set forth in said SEQ ID NOs. Accordingly, this argument has been fully considered but is not found persuasive.
(2)/(3) Applicant argues “Additionally, one of skill in the art would not consult Park when trying to find suitable gRNA sequences as claimed. Even if one of skill did consult Park, they would not choose or proceed with the gRNA sequences as claimed. The Cas-Designer of Park does not allow for identification of gRNAs for long nucleotide sequences such as that of the DMD gene. The human DMD gene is 2.4 million bp in length with 79 exons, and each intron and exon of the dystrophin gene is hundreds of nucleotides in length. For example, the exon 50/51 junction is approximately 45,500 bp, and the exon 51/52 junction is about 44,200 bp in length. However, Cas-Designer only searches target sequences that are a maximum of 1,000 bp (less than 1000 bp or FASTA files of less than 1 kb) for designing gRNAs. Therefore, one of skill would not have relied on Park to readily disclose all proper guides without continually running the program, which is not practicable.” (Remarks, at 8), and “Applicant submits that the program of Park was attempted by inputting genomic sequences that were only approximately 500 bp in length and included the elected gRNA of SEQ ID NO: 1 or 2. Even with this biased input, the program of Park never identified the gRNA of SEQ ID NO: 1 or 2 as a possible gRNA for the region. Therefore, Gersbach and Park cannot and did not suggest the claimed gRNAs.” (Remarks, at 8).
In response, Applicant is reminded of the breadth of instant claim 8 discussed above. It is also noted that the perspective for the purpose of obviousness is from what a person having ordinary skill in the art would have understood, not “one of skill”. It has been held that one cannot show non-obviousness by attacking references individually where, as here, the rejections are based on combinations of references. In re Keller, 208 USPQ 871 (CCPA 1981). Further, the Examiner does not argue that Park expressly describes all proper guides, the Examiner instead argues that it would have been prima facie obvious to one of ordinary skill in the art to use the rational gRNA design methodologies described by Park to design a gRNA comprising a nucleotide sequence set forth in SEQ ID NO: 1 and a second gRNA molecule comprising a nucleotide sequence set forth in SEQ ID NO: 2 and apply them to the CRSPR Cas9-based genomic editing systems for targeting the human dystrophin gene (DMD gene) for treating patients with Duchenne muscular dystrophy as described by Gersbach. As stated above, one would have a reasonable expectation of success given the well-established workflows for evaluating gRNAs and the relative interchangeability of different gRNAs in CRISPR-Cas9 systems. Finally, no affidavit has been submitted and there is no evidence of record to support the assertion that “the program of Park was attempted” or to support the result of said asserted activity. The arguments of counsel cannot take the place of evidence in the record. In re Schulze, 346 F.2d 600, 602, 145 USPQ 716, 718 (CCPA 1965); In re Geisler, 116 F.3d 1465, 43 USPQ2d 1362 (Fed. Cir. 1997).
Nonstatutory Double Patenting
Claims 8, 11-12, 15-16, 36-37 and 40-44 remain rejected and claim 45 is newly rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-7 of US Patent Number 10,704,060 (reference of record) in view of Park (supra). Although the claims at issue are not identical, they are not patentably distinct from each other because the patented claims would make obvious claims 8, 11-12, 15-16, 36-37 and 40-45 of the instant invention if they were available as prior art in view of the disclosure of Park. This rejection is maintained.
The patented claims are drawn to a DNA targeting system for deleting exon 51 of a dystrophin gene (i.e. DMD gene) comprising Cas9 and at least one gRNA as well as AAV viral vectors for delivery as described in claim 1. Furthermore, claim 7 of the patented claims describe a Cas9 based DNA targeting system comprising two gRNAs corresponding to SEQ ID Nos: 65 and 69 or SEQ ID Nos: 679 and 69. Furthermore, the patented claims identify a SaCas9 PAM sequence of NNGRRT in Tables 6 and 8 which targets a frameshift in exon 51 of the dystrophin gene. Thus, the patented claims show that SaCas9 inherently recognizes a PAM sequence of NNGRRT.
However, techniques are known in the art for the rational design of gRNAs targeting known mutational hotspots such as exon 51 of the DMD gene. For example, Park discloses a web-based tool called Cas-Designer for generating possible gRNA sequences for a given genomic knockout target and their potential off-target sites, including bulge-type sites (Park, abstract). Park provides embodiments for designing gRNAs compatible with various Cas9 endonucleases and PAM sequences, including 5’-NNGRRT-3’ PAM sequences for SaCas9 (Park, Implementation- gRNA selection).
It would have been obvious to one of ordinary skill in the art to use the rational gRNA design methodologies described by Park to design gRNAs comprising a nucleotide sequence set forth in SEQ ID NO: 1 and a second gRNA molecule comprising a nucleotide sequence set forth in SEQ ID NO: 2 and apply them to the CRSPR Cas9-based genomic editing systems for targeting the human dystrophin gene (DMD gene) for treating patients with Duchenne muscular dystrophy as described by Gersbach. It would have been a matter of applying known gRNA design methodologies to experiment with various gRNAs corresponding to the DMD gene targets. Park shows that there are predictable ways to experiment with many spacer sequences in order to minimize off target effects and improve cutting efficiencies (Park, Fig 1). Park outlines both computational approaches to predictably experiment and validate CRISPR target sites corresponding to known gene target sequences. One would have been motivated to do this since Gersbach expressly describes targeting the deletion of exon 51 within the DMD gene for treating patients with Duchenne muscular dystrophy using SaCas9 proteins which recognize NNGRRT PAM sequences (Gersbach, Table 8 pg 97 and [0188]).
Furthermore, since there are a finite number of possible gRNAs which could target the deletion of exon 51 within the DMD gene, it would have been obvious to derive a gRNA comprising a nucleotide sequence set forth in SEQ IDs NO: 1 and 2 identified in claim 8 following the rational sgRNA design methodologies described by Park and apply it to the saCas9 gene editing complex described by Gersbach. One would have a reasonable expectation of success given the well-established workflows for evaluating gRNAs and the relative interchangeability of different gRNAs in CRISPR-Cas9 systems. Accordingly, in the absence of evidence to the contrary, one of ordinary skill in the art would have considered the claimed invention to have been obvious.
Response to Traversal
Applicant traverses the instant rejection by referring to previous arguments with respect to the obviousness rejection of Gersbach in view of Park.
Applicant is invited to review previous arguments. The rejection is maintained accordingly.
Claims 8, 11-12, 15-16, 36-37 and 40-44 remain rejected and claim 45 is newly rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3, 5, and 14-15 of US patent No. 12214054. This rejection was previously a provisional rejection over claims 5-6, 10, 13, 32 and 53 of co-pending Application No: 15/779,633 (US Patent Application Publication Number US 2018/0353615) in view of Park (supra) and is now converted into a non-provisional rejection on the ground of nonstatutory double patenting. Although the claims at issue are not identical, they are not patentably distinct from each other because the patented claims would render obvious the instant claims if they were available as prior art in view of the disclosure of Park. This rejection is maintained.
The patented claims are drawn to a pair of gRNAs for deleting exon 51 of a dystrophin gene (i.e. DMD gene) comprising Cas9 and at least one gRNA as well as AAV viral vectors for delivery as described in patented claim 1.
However, techniques are known in the art for the rational design of gRNAs targeting known mutational hotspots such as exon 51 of the DMD gene. For example, Park discloses a web-based tool called Cas-Designer for generating possible gRNA sequences for a given genomic knockout target and their potential off-target sites, including bulge-type sites (Park, abstract). Park provides embodiments for designing gRNAs compatible with various Cas9 endonucleases and PAM sequences, including 5’-NNGRRT-3’ PAM sequences for SaCas9 (Park, Implementation- gRNA selection).
It would have been obvious to one of ordinary skill in the art to use the rational gRNA design methodologies described by Park to design gRNAs a nucleotide sequence set forth in SEQ ID NO: 1 and a second gRNA molecule comprising s nucleotide sequence set forth in SEQ ID NO: 2 and apply them to the CRISPR Cas9-based genomic editing systems for targeting the human dystrophin gene (DMD gene) for treating patients with Duchenne muscular dystrophy as described by Gersbach. It would have been a matter of applying known gRNA design methodologies to experiment with various gRNAs corresponding to the DMD gene targets. Park shows that there are predictable ways to experiment with many spacer sequences in order to minimize off target effects and improve cutting efficiencies (Park, Fig 1). Park outlines both computational approaches to predictably experiment and validate CRISPR target sites corresponding to known gene target sequences. One would have been motivated to do this since Gersbach expressly describes targeting the deletion of exon 51 within the DMD gene for treating patients with Duchenne muscular dystrophy using SaCas9 proteins which recognize NNGRRT PAM sequences (Gersbach, Table 8 pg 97 and [0188]).
Furthermore, since there are a finite number of possible gRNAs which could target the deletion of exon 51 within the DMD gene, it would have been obvious to derive a gRNA comprising a nucleotide sequence set forth in SEQ IDs NO: 1 and 2 identified in claim 8 following the rational sgRNA design methodologies described by Park and apply it to the spCas9 gene editing complex described by Gersbach. One would have a reasonable expectation of success given the well-established workflows for evaluating gRNAs and the relative interchangeability of different gRNAs in CRISPR-Cas9 systems. Accordingly, in the absence of evidence to the contrary, one of ordinary skill in the art would have considered the claimed invention to have been obvious.
Response to Traversal
Applicant traverses the instant rejection by referring to previous arguments with respect to the obviousness rejection of Gersbach in view of Park.
Applicant is invited to review previous arguments. The rejection is maintained accordingly.
Claims 8, 11-12, 15-16, 36-37 and 40-44 remain provisionally rejected and claim 45 is newly provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-18 of co-pending Application No: 16/858,689 (US Patent Application Publication Number US 2021/0002665) in view of Park (supra). Although the claims at issue are not identical, they are not patentably distinct from each other because the co-pending claims would render obvious the instant claims if they were available as prior art in view of the disclosure of Park. This rejection is maintained.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented. The co-pending claims are drawn to a DNA targeting system for deleting exon 51 of a dystrophin gene (i.e. DMD gene) comprising Cas9 and at least one gRNA as well as AAV viral vectors for delivery as described in claim 1.
However, techniques are known in the art for the rational design of gRNAs targeting known mutational hotspots such as exon 51 of the DMD gene. For example, Park discloses a web-based tool called Cas-Designer for generating possible gRNA sequences for a given genomic knockout target and their potential off-target sites, including bulge-type sites (Park, abstract). Park provides embodiments for designing gRNAs compatible with various Cas9 endonucleases and PAM sequences, including 5’-NNGRRT-3’ PAM sequences for SaCas9 (Park, Implementation- gRNA selection).
It would have been obvious to one of ordinary skill in the art to use the rational gRNA design methodologies described by Park to design gRNAs comprising a nucleotide sequence set forth in SEQ ID NO: 1 and a second gRNA molecule comprising a nucleotide sequence set forth in SEQ ID NO: 2 and apply it to the CRSPR Cas9-based genomic editing systems for targeting the human dystrophin gene (DMD gene) for treating patients with Duchenne muscular dystrophy as described by Gersbach. It would have been a matter of applying known gRNA design methodologies to experiment with various gRNAs corresponding to the DMD gene targets. Park shows that there are predictable ways to experiment with many spacer sequences in order to minimize off target effects and improve cutting efficiencies (Park, Fig 1). Park outlines both computational approaches to predictably experiment and validate CRISPR target sites corresponding to known gene target sequences. One would have been motivated to do this since Gersbach expressly describes targeting the deletion of exon 51 within the DMD gene for treating patients with Duchenne muscular dystrophy using SaCas9 proteins which recognize NNGRRT PAM sequences (Gersbach, Table 8 pg 97 and [0188]).
Furthermore, since there are a finite number of possible gRNAs which could target the deletion of exon 51 within the DMD gene, it would have been obvious to derive a gRNA comprising a nucleotide sequence set forth in SEQ IDs NO: 1 and 2 identified in claim 8 following the rational sgRNA design methodologies described by Park and apply it to the spCas9 gene editing complex described by Gersbach. One would have a reasonable expectation of success given the well-established workflows for evaluating gRNAs and the relative interchangeability of different gRNAs in CRISPR-Cas9 systems. Accordingly, in the absence of evidence to the contrary, one of ordinary skill in the art would have considered the claimed invention to have been obvious.
Response to Traversal
Applicant traverses the instant rejection by referring to previous arguments with respect to the obviousness rejection of Gersbach in view of Park.
Applicant is invited to review previous arguments. The rejection is maintained accordingly.
Amending the claims to recite “(i) a first gRNA molecule comprising a targeting domain that comprises the nucleotide sequence set forth in SEQ ID NO: 1, and a second gRNA molecule comprising a targeting domain that comprises the nucleotide sequence set forth in SEQ ID NO: 2; would advance prosecution.
Conclusion
No claim is 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 BRENDAN THOMAS TINSLEY whose telephone number is (703)756-5906. The examiner can normally be reached Mon-Fri 8:00-5:00.
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/BRENDAN THOMAS TINSLEY/Examiner, Art Unit 1634
/MARIA G LEAVITT/Supervisory Patent Examiner, Art Unit 1634