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 .
Application Status
This action is written in response to applicant’s correspondence received 4 December 2025. Claims 1-11, 13, 15, and 17-29 are currently pending. Claims 1-11, 13, 15, 23-29 are withdrawn from prosecution as being drawn to non-elected subject matter. Accordingly, claims 17-22 are examined herein. The restriction requirement mailed 3 February 2025 is still deemed proper. Applicant's elected Group II, claims 17-22, without traverse in the reply filed 5 May 2025.
Applicant’s arguments, see Remarks, filed 4 December 2025, with respect to the previously pending 35 USC 102 rejection over the Michnick reference have been fully considered and are persuasive. The 35 USC 102 rejection of claims 17-18 and 20 has been withdrawn.
However, Applicant's arguments filed 4 December 2025 with respect to the previously pending 35 USC 103 rejection of record of Liu in view of Michnick, as described below, have been fully considered but they are not persuasive.
Drawings
Color photographs and color drawings are not accepted in utility applications unless a petition filed under 37 CFR 1.84(a)(2) is granted. Any such petition must be accompanied by the appropriate fee set forth in 37 CFR 1.17(h), one set of color drawings or color photographs, as appropriate, if submitted via the USPTO patent electronic filing system or three sets of color drawings or color photographs, as appropriate, if not submitted via the via USPTO patent electronic filing system, and, unless already present, an amendment to include the following language as the first paragraph of the brief description of the drawings section of the specification:
The patent or application file contains at least one drawing executed in color. Copies of this patent or patent application publication with color drawing(s) will be provided by the Office upon request and payment of the necessary fee.
Color photographs will be accepted if the conditions for accepting color drawings and black and white photographs have been satisfied. See 37 CFR 1.84(b)(2).
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claim(s) 17 and 21-22 is/are rejected under 35 U.S.C. 103 as being unpatentable over Liu (PG Pub No. US 2017/0121693 A1) in view of Michnick (Pg Pub No. US 2003/0049688 A1). This rejection is maintained.
Regarding claim 17, part i), Liu is drawn towards an invention concerned with systems that can be utilized for the targeting editing of nucleic acids (Abstract). Liu teaches the use of a vector (i.e., a nucleic acid) encoding a base editing complex ([0335]-[0336]). Liu teaches that the base editing complex comprises a Cas9 fused to a cytidine deaminase (i.e., a base editing complex) that can complex with a guide RNA (i.e., a targeting module sequence) such that the base editing complex can target and deaminate a nucleic acid of interest (i.e., the deaminase of Liu can be utilized to edit a targeted cytosine of interest on a nucleic acid bound by the targeting module) ([0040], [0345]; see FIG. 4).
Liu does not teach or suggest that the deaminase is split and each terminal of the split deaminase fused to one of two inducible binding members, wherein the binding members dimerize upon contact with a dimerization agent to reform the deaminase such that a target adenosine or cytosine of interest is edited (Claim 17).
However, one of ordinary skill in the art would have considered the teachings of Michnick as both references are common fields of endeavor pertaining to the study and use of deaminases.
Michnick is drawn towards an invention concerned with designing and implementing protein-fragment complementation assays (i.e., “PCAs”) to detect biomolecular interactions in vivo and in vitro (Abstract). Michnick teaches that the utility of PCA is not limited to detecting protein-protein interactions, but can be adapted to detecting interactions of proteins with DNA, RNA, or small molecules ([0226]). Michnick teaches the use of two complementary fragments of a DHFR enzyme, wherein one of the fragments of DHFR is fused to an FKBP12 receptor (i.e., a first member of a specific binding pair) while the other fragment is fused to FKBP12’s binding partner mTOR (i.e., a second member of a specific binding pair) ([0226]). Michnick teaches that the FKBP12-mTOR binding pair is induced by the addition of rapamycin such that, in the presence of rapamycin, the DHFR fragments are reassembled and able to exhibit DHFR activity (i.e., Michnick teaches that the binding pairs dimerize upon contact with a dimerization agent such that the enzyme complementary fragments fused to the binding pairs reforms and restores activity thereto) ([0226]). Michnick teaches that PCA can be applied to an adenosine deaminase and an in vivo assay developed for it because it can be used as a dominant selective marker in mammalian and bacterial cells where the gene has been knocked out ([0256], [0258]). Michnick teaches that three test systems of interacting proteins were utilized as binding pairs for the adenosine deaminases, including leucine zipper-forming sequences; the proteins raf and p21 and the induced oligomerization system; and FK506 binding protein (FKBP) and mTOR that interact through the macrocyclic immuno-suppressant compound rapamycin ([0258]). Michnick teaches that, for all of these systems, mammalian transient transfection plasmids were constructed and the test proteins were subcloned as fusions to adenosine deaminase complementary fragments (i.e., Michnick teaches the use of a nucleic acid encoding the complementary adenosine deaminase fragments that are fused to the first and second members of nucleic acids encoding the binding pair) ([0258]). Michnick teaches that PCA is advantageous because the two fragments can be placed under different inducible or constitutive promoters such that the expression levels of the PCA fragments can be controlled and expressed only in the presence of multiple different inducers ([0159]). Michnick teaches that using the two different inducible promoters to drive expression of the fragments can allow for expression levels that are dose dependent on two different inducers ([0161]).
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to substitute the nucleic acid encoding the cytidine deaminase of Liu for the nucleic acid encoding the split adenosine deaminase of Michnick because it would have merely amounted to a simple combination of prior art elements according to known methods to yield predictable results. A person of ordinary skill in the art would have been motivated to do so in order to have greater control over the conditions in which the split deaminase is expressed and functional via the use of two different inducible promoters, each linked to a different fragment of the split adenosine deaminase, that are expressed in the presence of two different inducers. A person of ordinary skill in the art would have had a reasonable expectation of success because Liu teaches the use of a deaminase, present within a base editing system, that can deaminase nucleotide bases present within a target DNA while Michnick teaches the use of a deaminase that can be split and reconstituted via two inducible dimers in order to deaminate target nucleosides.
Therefore, one of ordinary skill in the art would have expected the split adenosine deaminase of Michnick to act similarly to the cytidine deaminase of Liu when present within the base editing system of Liu because both deaminases have similar functions wherein a target nucleoside or nucleotide is deaminated.
Regarding claim 21, Liu teaches that the target site can be present within DNA ([0040], [0345]; see FIG. 4).
Regarding claim 22, Liu teaches that the nucleic acid encoding the base editing complex may be combined with an activity buffer ([0380]).
Claim(s) 19 is/are rejected under 35 U.S.C. 103 as being unpatentable over Liu (PG Pub No. US 2017/0121693 A1) in view of Michnick (Pg Pub No. US 2003/0049688 A1) as applied to claims 17 and 21-22 above, and further in view of Kloban ("Improving cytidine and adenine base editors by expression optimization and ancestral reconstruction." Nature biotechnology 36.9 (2018): 843-846) as evidenced by Addgene 112093 (“pCMV_BE4max”; Addgene plasmid No. 112093, published 2018), Inobe ("Rapamycin-induced oligomer formation system of FRB–FKBP fusion proteins."; Journal of bioscience and bioengineering 122.1 (2016): 40-46), Choi ("Structure of the FKBP12-rapamycin complex interacting with binding domain of human FRAP." Science 273.5272 (1996): 239-242), and Minskaia ("Protein coexpression using FMDV 2A: effect of “linker” residues." BioMed research international 2013.1 (2013): 291730). This is a new rejection necessitated by amendment.
Regarding claim 19, it is noted that the instant specification teaches that the claimed constructs were cloned into the scaffold of a BE4max vector from a previously published Addgene Plasmid #112093 (Instant specification; pg. 24). It is noted that the difference between the claimed constructs and the previously published Addgene Plasmid #112093 is the insertion of an insert cassette comprising dimerization domains linked to different split deaminases (Instant specification; pg. 7; see Fig. 6B below). It is noted that the instant specification teaches that the claimed split A3A BE4max construct comprises, 5’ to 3’ and unique when compared to the Addgene Plasmid 112093 (i.e., described below), a Myc tag, an NLS, an N-terminal of an APOBEC3A protein, an FRB domain, a T2A linker, an FKBP12 domain, and the C-terminal of the APOBEC3A protein (Instant specification; pg. 7; see Fig. 6B below).
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Liu further teaches that the Cas9 fusion protein may be encoded on a vector ([0033]). Liu further teaches that the deaminase may be an APOBEC3A deaminase ([0013]). Liu teaches that the deaminase may comprise an NLS at the N-terminus of the deaminase ([0219]). Liu teaches that the NLS may comprise a sequence tag selected from a Myc-tag ([0218]). Liu teaches that the Cas9 may be a Cas9 nickase (i.e., an nCas9) ([0012]).
Liu in view of Michnick does not teach or suggest that the insertion cassette comprises, 5’ to 3’, an N-terminal of an APOBEC3A protein, an FRB domain, a T2A linker, an FKBP12 domain, and the C-terminal of the APOBEC3A protein in order to arrive at the claimed split A3A BE4max construct (Claim 19). Liu in view of Michnick does not teach or suggest the use of the claimed BE4max vector scaffold sequence into which the expression cassette was inserted in order to arrive at the claimed split A3A BE4max construct (Claim 19).
However, one of ordinary skill in the art would have considered the teachings of Kloban, Addgene 112093, Inobe, and Minskaia as both references are common fields of endeavor pertaining to the design of vectors encoding deaminases, Cas9 proteins, dimerization domains, and linkers.
Kloban, as evidenced by Addgene 112093, is directed towards a study concerned with expression optimization of an nCas9 through the use of a BE4max vector comprising, 5’ to 3’, an NLS, an adenosine deaminase, an nCas9, two UGIs, an NLS, and Amp R expression cassettes (pg. 884; see Figure 1 and pg. 4 of Addgene entry). Kloban teaches that the BE4max vector corrected pathogenic SNPs with substantially increased efficiency in a variety of mammalian cell types (Abstract). Regarding Addgene 112093, it is noted that the instant specification teaches that claimed constructs were generated via the insertion of the expression cassettes into the scaffold of the same BE4max vector from the previously published Addgene Plasmid #112093 (Instant specification; pg. 24).
Therefore, Kloban as evidenced by Addgene 112093 teaches that the BE4max scaffold vector was a beneficial and known vector in the prior art that comprises an expression cassette encoding a deaminase.
Choi is directed towards a study concerned with the mechanisms of how rapamycin induces the dimerization of FKBP12 and FRB binding domains (Abstract). Choi teaches that introducing rapamycin to the FKBP12 and FRB binding domains allowed for dimerization of the domains within a cell (pg. 239).
Therefore, Choi teaches that FKBP12 domains and FRB domains can be dimerized in the presence of rapamycin in a similar manner as the FKBP12-mTOR domains rendered obvious by Liu in view of Michnick.
Inobe is directed towards a study concerned with rapamycin-induced oligomer formation in FRB-FKBP fusion proteins (Abstract). Inobe teaches that a schematic of a nucleic acid encoding a fusion protein comprising FRB and FKBP that comprises, 5’ to 3’, an FRB domain, a linker, and an FKBP domain (pg. 41; see Fig. 1). Inobe teaches that fusion proteins comprising the FRB and FKBP domain were able to dimerize in the presence of rapamycin within a cell (pg. 40-41; see Fig. 1).
Therefore, Inobe teaches that a nucleic acid construct comprising 5’ to 3’, an FRB domain, a linker, and an FKBP domain may be encoded on a nucleic acid, expressed within a cell, and induced with rapamycin such that the FRB and FKBP domains dimerize.
Minskaia is directed towards a study concerned with protein coexpression using F2A and T2A linkers (Abstract). Minskaia teaches that T2A linkers were known in the art to be able to be inserted between two different proteins and cleaved such that the proteins linked by the F2A linker can separate from one another (pg. 4; see FIG. 1).
Therefore, Minskaia teaches that utilizing a nucleic acid encoding a cleavable T2A linker located between two different proteins was a known method of linking the two proteins.
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have arrived at the requirements of a Split A3A BE4max construct as defined by the specification as explained above because it would have merely amounted to a simple combination of prior art elements according to known methods to yield predictable results. Because Kloban teaches using the Addgene 112093 for a similar purpose as Liu, namely expression of Cas9, then one would have had a reasonable expectation of success in using this plasmid for Cas9 expression in the method of Liu. And because Kloban teaches that the efficiency was high, then one would have been motivated to have done so.
The Addgene 112093 plasmid already comprises an APOBEC3A cassette and the obviousness of making and using a split APOBEC3A fused to protein dimerization partners is discussed above as applied to claim 17. Accordingly, it would have further been obvious to have replaced the APOBEC3A cassette of Addgene 112093 with a cassette encoding a APOBEC3A N-terminus fused to a first member of a dimerization pair and a APOBEC3A C-terminus fused to a second member of a dimerization pair because it would have merely amounted to a simple substitution of one APOBEC3A cassette for another to yield predictable results. Since Michnick teaches using a split deaminase fused to a dimerization pair as discussed above as applied to claim 17, it would have been predictable to have similarly made and used a cassette encoding a split APOBEC3A fused to dimerization pairs in Addgene 112093.
It is noted that Michnick teaches the FKBP12-mTOR binding pair, which is induced by the addition of rapamycin, but the split A3A-BE3max requires the use of the FRB and FKBP12 dimerization pair. However, it would have been obvious to have used a FRB and FKBP12 dimerization pair instead of the FKBP12-mTOR binding pair because it would have amounted to a simple substitution of one known protein dimerization pair inducible by rapamycin for another. Because each of these two protein dimerization pairs were used in a similar way as fusion proteins and were each known to be inducible by rapamycin, then it would have been predictable to have used FRB and FKBP12 as the protein dimerization members.
It further would have been obvious to have utilized a sequence encoding a T2A self-cleaving peptide in the split APOBEC3A cassette to separate the split APOBEC3A N and C terminal dimerization fusion proteins because it would have amounted to a simple combination of prior art elements according to known methods to yield predictable results. Since Minskaia teaches using the T2A self-cleaving peptide to similarly express separate proteins after translation, then it would have been predictable to have similarly used the T2A self-cleaving peptide to separate the split APOBEC3A N and C terminal dimerization fusion proteins in the Addgene 112093 plasmid.
Claim(s) 20 is/are rejected under 35 U.S.C. 103 as being unpatentable over Liu (PG Pub No. US 2017/0121693 A1) in view of Michnick (Pg Pub No. US 2003/0049688 A1) as applied to claims 17-19 and 21-22 above, and further in view of Chew (Nature methods 13.10 (2016): 868-874). This rejection is maintained.
Regarding claim 20, Liu in view of Michnick renders obvious claims 17-19 and 21-22 as described above.
Liu in view of Michnick does not teach or suggest the use of an AAV expression vector (Claim 20).
However, one of ordinary skill in the art would have considered the teachings of Chew as both references are common fields of endeavor pertaining to the use of nucleic acids encoding CRISPR proteins.
Chew is drawn towards a study concerned with a multifunctional AAV-CRISPR-Cas9 construct and its host response (Abstract). Chow teaches the use of an AAV that encodes a split Cas9 molecule that evokes host responses and does not induce cellular damage in vivo (Abstract). Chow teaches that the AAV encoding the split Cas9 molecule was able to be delivered to target cells and the construct used to edit target nucleic acids of interest (pg. 867; see Figure 1).
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to substitute the vector encoding the base editing complex of Liu in view of Michnick for an AAV that can encode CRISPR proteins, as described by Chew, because it would have amounted to a simple combination of prior art elements according to known methods to yield predictable results. A person of ordinary skill in the art would have had a reasonable expectation of success in the substitution of the vectors because both Liu in view of Michnick and Chew teach the use of expression vectors that can be utilized for the same purpose: successfully encoding and expressing a CRISPR systems in order to target and edit nucleic acids of interest.
Therefore, one of ordinary skill in the art would have expected the AAV vector of Chew would function similarly to the vector encoding and expressing the Cas9 and split deaminase rendered obvious by Liu in view of Michnick.
Response to Arguments
Applicant’s arguments, see Remarks, filed 4 December 2025, with respect to the previously pending 35 USC 102 rejection over the Michnick reference have been fully considered and are persuasive. The 35 USC 102 rejection of claims 17-18 and 20 has been withdrawn.
However, Applicant's arguments filed 4 December 2025 with respect to the previously pending 35 USC 103 rejection of record of Liu in view of Michnick, as described below, have been fully considered but they are not persuasive.
In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning (Remarks; pg. 13), it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
Applicant alleges that the split deaminase of Michnick functions in a different manner and is insufficiently described (Remarks; pg. 13). Applicant alleges that the adenosine deaminases of Michnick “are highly unrelated to the DNA deaminase enzymes in base editors, although they seem to share a name. These adenosine deaminases act on nucleosides, not on DNA. The adenosine deaminases described in Michnick would never work in a base editor, which has to act on DNA. At the time of this patent filing (2003), DNA deaminase enzymes did not yet 'exist' - their activities were just being discovered” (Remarks; pg. 10).
MPEP 716.01(c) makes clear that arguments of counsel cannot take the place of evidence in the record. There is no teaching in Michnick that states that the split deaminase is not able to be used in a base editing system. Further, these arguments are not found persuasive because it is piecemeal analysis of the rejection which is based on a combination of references. One cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
Applicant alleges that one of ordinary skill in the art would not have been motivated to substitute the intact deaminase of Liu for a split deaminase that is linked to two different binding partners, as described in Michnick, based on the disclosure of Liu describing a working deaminase (Remarks; pg. 14). Applicant alleges that the oligomerization features of Michnick have been available since 2003 (while the Liu reference was published in 2017) and the oligomerization features of Michnick were not employed in the 2017 Liu reference, accordingly Applicant alleges that the motivation perceived by the examiner is not present (Remarks; pg. 14).
These arguments are not found persuasive because it is piecemeal analysis of the rejection which is based on a combination of references. One cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). Further, the PCA described in Michnick is advantageous because the two fragments can be placed under different inducible or constitutive promoters such that the expression levels of the PCA fragments can be controlled and expressed only in the presence of multiple different inducers, as described in the 35 USC 103 rejection above. Thus, one of ordinary skill in the art would have recognized that the PCA of Michnick is advantageous to utilize in the base editing system of Liu.
Allowable Subject Matter
Claim 18 is objected to as being dependent upon a rejected base claim, but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims.
Regarding claim 18, the claim recites an expression vector comprising the nucleic acid sequence encoding the base editing complex containing the split deaminase of claim 17 selected from A3A-seBE4max of SEQ ID NO: 55, evoA1-seBE4max of SEQ ID NO: 53, AID' seBEmax of SEQ ID NO: 54, and evoAlseBE4 max-IRES of SEQ ID NO: 56 (see Claim 18). It is noted that the instant specification teaches that the claimed SEQ ID NOs are expression vectors that comprise specific gene blocks with specific sequence requirements that were cloned into the scaffold of a BE4max vector from a previously published Addgene Plasmid #112093 (Instant specification; pg. 24). Therefore, it is noted that the difference between the claimed constructs and the previously published Addgene Plasmid #112093 is the insertion of the gene blocks comprising dimerization domains linked to different split deaminases (Instant specification; pg. 7; see Fig. 6A-6B). It is noted that the instant specification teaches that the split A3A deaminase gene block fragment consists of SEQ ID NO: 19, the split AID deaminase gene block consists of SEQ ID NO: 20, the split evoA1 deaminase gene block consists of SEQ ID NO: 21, and the split TadA deaminase block consists of SEQ ID NO: 22 (Instant specification; pg. 31-34). The instant specification teaches that the claimed gene blocks, when inserted into the previously published Addgene Plasmid, were able to induce targeted base editing in the presence of rapamycin (pg. 7-8; see Figure 7C).
Therefore, the instant specification provides adequate written description support for the claimed expression vector sequences and the utilization of the claimed expression vectors in methods of deaminating one or more bases in a target nucleic acid through the use of the claimed expression vectors.
Regarding the closest prior art with respect to the BE4max expression vector scaffold, the teachings of Kloban as evidenced by Addgene 112093 is discussed above as applied to claim 19.
Regarding the closest prior art with respect to the gene blocks consisting of the claimed SEQ ID NOs: 19-22, the closest prior art is “AB528063.1” (GenBank Accession No. AB528063.1; published 24 July 2016). AB528063.1 is directed towards a GenBank accession No. comprising a synthetic DNA vector encoding a Homo sapiens APOBEC3A gene for apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3A, without a stop codon (see pg. 3 of attached sequence alignment). However, AB528063.1 teaches that the DNA vector has 99% identity to a query coverage of only 39% of the disclosed SEQ ID NO: 19 comprising the split A3A gene block (see pg. 1 of attached sequence alignment).
Accordingly, the closest prior art discloses a sequence that has 39% identity to the disclosed SEQ ID NOs: 19-22 gene blocks utilized to arrive at the claimed SEQ ID NOs: 53-56. Accordingly, as described above, the claimed SEQ ID NOs: 53-56 are novel and non-obvious in view of the closest prior art.
Conclusion
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.
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 KYLE T REGA whose telephone number is (571)272-2073. The examiner can normally be reached M-R 8:30-4:30, every other F 8:30-4:30 (EDT/EST).
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Neil Hammell can be reached at 571-270-5919. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/KYLE T REGA/Examiner, Art Unit 1636
/NEIL P HAMMELL/Supervisory Patent Examiner, Art Unit 1636
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