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
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office Action.
Status of Claims
Claims 1-28 are currently pending, in the claims filed August 13, 2026. Claims 1, 4, 5, 7 and 12 have been amended by Applicants’ amendment filed 08-13-2026. No claims have been added or canceled by Applicants’ amendment filed 08-13-2026.
Applicant's election of Group I, claims 1-8, 12 and 13, directed to a method for purifying a target molecule; and Applicant’s election of Species with traverse as follows:
Species (A): further comprising panning the phage library against at least one antigen to generate a library of phage clones (claim 4),
Species (B): the quantity of polynucleotides comprising a single-chain variable fragment in the form of gapped, double-stranded vectors wherein the gap exposes the scFv as a single-stranded segment (scFv) (claim 45), and
Species (C)-(E): are directed to non-elected Groups, in the reply filed March 30, 2026 was previously acknowledged.
Claims 9, 10 and 14-28 were previously withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a non-elected invention, there being no allowable generic or linking claim.
Claims 2, 3, 6 and 8 were previously withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a non-elected species, there being no allowable generic or linking claim.
Applicant timely traversed the restriction (election) requirement in the reply filed on March 30, 2026.
The restriction requirement was deemed proper and was made FINAL.
The claims will be examined insofar as they read on the elected species.
A complete reply to the final rejection must include cancellation of nonelected claims or other appropriate action (37 CFR 1.144) See MPEP § 821.01.
Therefore, claims 1, 4, 5, 7, 12 and 13 are under consideration to which the following grounds of rejection are applicable.
Priority
The present application filed November 30, 2022 is a 35 U.S.C. 371 national stage filing of International Application PCT/US2021/035528, filed June 2, 2021, which claims the benefit US Provisional Patent Application 63033429, filed June 2, 2020.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on July 29, 2026 has been considered. An initialed copy of the IDS accompanies this Office Action.
Withdrawn Objections/Rejections
Applicants’ amendment and arguments filed August 13, 2026 are acknowledged and have been fully considered. The Examiner has re-weighed all the evidence of record. Any rejection and/or objection not specifically addressed below are herein withdrawn.
Claim Rejections - 35 USC § 103
The rejection of claims 1, 4, 5, 7, 12 and 13 is withdrawn under 35 U.S.C. 103 as being unpatentable over Tveita et al. (hereinafter “Tveita”) (US Patent No. 11186641, published November 30, 2021; effective filing date September 21, 2017) in view of Liu et. al. (hereinafter “Liu ‘496”) (US Patent No. 11542496, issued January 3, 2023); and further in view of Kramer (Nucleic Acids Research, 1984, 12(24), 9441-9456).
The combined references of Tveita and Liu do not specifically exemplify the steps of diversifying and further diversifying in a cell-free environment.
In view of the withdrawn claims, Applicant’s arguments are rendered moot.
Maintained Objections/Rejections
Claim Rejections - 35 USC § 112(b)
The rejection of claims 1, 4, 5, 7, 12 and 13 is maintained under 35 U.S.C. 112(b) as being indefinite for failing to particularly point out and distinctly claim the subject matter which applicant regards as the invention.
Claim 1 is indefinite for the recitation of the term “the library of phage or phagemid clones” such as recited in claim 1, lines 6-7 because it is unclear whether the term refers to a library of phage or phagemid clones as recited in line 2 that have not been contacted with AID, such that they are separately contacted with Pol h, or whether the term refers to a library of phage or phagemid clones that has previously been contacted with AID (e.g., treating the diversified library of phage or phagemid clones) with Pol h and, thus, the metes and bounds of the claim cannot be determined.
Claim 12 is indefinite for the recitation of the term “cooling the mixture” such as recited in claim 12, line 8 because claim 12, lines 4-7 recites denaturing, mixing, and forming a mixture, instant claim 12 does not recite heating, warming, etc. such that the mixture must then be cooled. Moreover, claim 12 depends from instant claims 1, 4 and 7, wherein none of claims 1, 4, and 7 recite heating and/or warming the mixture and, thus, the metes and bounds of the claim cannot be determined.
Claims 4, 5, 7 and 13 are indefinite insofar as they ultimately depend from instant claim 1.
Claim Rejections - 35 USC § 112(d)
The rejection of claim 12 is maintained under 35 U.S.C. 112(d) as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Claim 12 recites (in part): “denaturing and mixing a first double-stranded phage or phagemid vector…cooling the mixture in order to generate re-annealed vectors” in lines 4-8 because claim 12 depends from claims 1, 4 and 7, wherein claims 1, 4, 7 and 12 do not teach that the mixture is heated and/or warmed. Thus, claim 12 is an improper dependent claims for failing to further limit the subject matter of the claim upon which they depend, or for failing to include all the limitations of the claim upon which they depends.
Applicant may cancel the claim, amend the claim to place the claim in proper dependent form, rewrite the claim in independent form, or present a sufficient showing that the dependent claim complies with the statutory requirements.
New Objections/Rejections
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 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 set forth in Graham v. John Deere Co., 383 U.S. 1, 148 USPQ 459 (1966), that are applied 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.
Claims 1, 4, 5, 7, 12 and 13 are rejected under 35 U.S.C. 103 as being unpatentable over Bowers et al. (hereinafter “Bowers”) (US Patent No. 9260533, issued February 16, 2016) in view of Rhonda Bransteitter (hereinafter “Bransteitter”) (Dissertation, University of Southern California, 2005, 1-92) as evidenced by Honda et al. (hereinafter “Honda”) (US Patent Application Publication 2005037421, published February 17, 2005). This is a new rejection necessitated by amendment of the claims in the response filed 08-13-2026.
Regarding claim 1, Bowers teaches the generation of huge libraries of mutant poly-nucleotides that are subsequently screened for improved variants, usually through the expression of the encoded proteins within a living cells, such that from these libraries a few improved proteins can be selected for further optimization (col 3, lines 65-67; and col 4, lines 1-3). Bowers teaches in vitro somatic hypermutation (SHM) systems including: (1) an expression system designed to create SHM susceptible and/or SHM resistant DNA sequences, with a cell or cell-free environment; (2) polynucleotide libraries that are focused in size and specificity, which can be enriched for SHM; and (3) a process based on computational analysis of protein structure, intra-species and inter-species sequence variation, and the functional analysis of protein activity for selecting optimal epitopes that provide for the selection of antibodies with superior selectivity, cross species reactivity, and blocking activity (col 17, lines 14-48). Bowers teaches that the compositions that comprise a synthetic nucleic acid sequence has been modified to act as a substrate for AID mediated somatic hypermutation by the insertion of somatic hypermutation motifs including the insertion of one or more SHM codons, and/or the synthetic nucleic acid sequence has been modified to act as a substrate for AID mediated somatic hypermutation by the insertion of one or more WAC motif, WRC motif or a combination thereof (interpreted as a library of phage or phagemid clones, claim 1) (col 5, lines 4-15). Bowers teaches that Figure 53E shows that the spectrum of mutations generated by AID in the present in vitro tissue culture system mirror those observed in other studies and those seen during in vivo affinity maturation (interpreted as diversifying phage or phagemid clones with AID in a cell-free environment, claim 1) (col 16, lines 47-49; and Figure 53E). Bowers teaches that Figures 1 and 2 show the 20 most common codon transitions, observed in CDRs and FWs during SHM mediated affinity maturation and demonstrate how simple frame shifts can determine the two radically different patterns of mutagenesis seen in CDRs and FWs (interpreted as mutagenesis) (col 10, lines 64 and col 11, lines 1-4). Bowers teaches that the term "synthetic variable regions" refers to synthetic polynucleotide sequences that are substantially comprised of optimal SHM hot spots and hot codons that, when combined with the activity of AID and/or one or more error-prone polymerases, can generate a broad spectrum of potential amino acid diversity at each position, wherein error-prone polymerases include polymerase eta and polymerase theta (interpreted as further diversifying by contacting AID and pol eta, without a cell, claim 1) (col 23, lines 26-31; and col 45, lines 24-25). Bowers teaches that like WAC synthetic motif, the WRC synthetic motif presents preferred SHM hot spot codons that, when combined with the SHM activity of AID and one or more error-prone polymerases, generates a broad spectrum of potential amino acid diversity at each position (Figure 6), wherein error-prone polymerases include polymerase eta and polymerase theta (interpreted as further diversifying by contacting phage clones with AID and Pol eta in a cell free environment, claim 1) (col 45, lines 24-25; and col 120, lines 36-40). Bowers teaches in vitro expression and hypermutation systems including cell free systems that enable the transcription, or coupled transcription and translation of DNA templates and, in certain embodiments, enable the on-going mutagenesis via SHM, wherein such in vitro translation systems can be used in combination with ribosome display to enable the ongoing mutagenesis and selection of proteins; and in vitro translation systems include for example the classical rabbit reticulocyte system, as well as novel cell free synthesis systems, (J. Biotechnol. (2004) 110 (3) 257-63; Biotechnol Annu. Rev. (2004) 10 1-30), wherein systems for ribosome display are described for example in Villemagne et al., J. Imm. Meth. 2006 313 (1-2) 140-148) (interpreted as cell free systems, claim 1) (col 146, lines 30-42). Bowers teaches that a phage library can be created by inserting the synthetic or semi-synthetic libraries described above into gene 3 of M12 or T7 phage (interpreted as creating a phage library) (col 146, lines 47-49). Bowers teaches biopanning, wherein an immobilized target molecule of interest, such as an antigen, and specifically bound phages are recovered and amplified by infection into Escherichia coli host cells; and the target molecule of interest such as a receptor (e.g., polypeptide, carbohydrate, glycoprotein, nucleic acid) is immobilized by covalent linkage to a chromatography resin to enrich for reactive phage by affinity chromatography) and/or labeled for screen plaques or colony lifts, then amplified phages can be sequenced for deduction of the specific peptide sequences (interpreted as creating phage libraries; and transfecting a library into microbes, claim 1) (col 146, lines 53-64). Bowers teaches in vitro affinity maturation, wherein selected cells isolated by FACS sorting were grown up for use as substrates for affinity maturation, such that cells expressing heavy and light chains as described above can then be transfected with an expression vector containing an inducible, cold AID polynucleotide sequence using standard transfection conditions as described above, such that three days post transfection, selective pressure is exerted, and a new stable cell population is propagated that includes the inducible AID expression vector (interpreted as diversifying by contacting a phage clones with AID in a cell free environment; and transfecting the further diversified library, claim 1) (col 212, lines 46-56). Bowers teaches that this population of cells is grown up, and AID expression is induced via the addition of tetracycline or an analog thereof for about 6 to 24 hours, which allowed the cells to expand for about 2 to 5 days, and then selected using the HEL protein or peptide coupled beads as described above, wherein cells that preferentially and/or selectively bind to the HEL protein or peptides with a higher affinity are selected and allowed to expand; and if required, another round of AID induction and mutagenesis is repeated, as described above, and again cells that exhibit improved, selective, and high affinity binding, are retained for further propagation and growth (col 212, lines 57-67). Bowers teaches identifying DNA hot spots/cold spots for SHM, wherein DNA sequences that promote or discourage SHM were identified in the following manner: no assumptions were made regarding the size of the SHM hot and cold motif; and likewise, the position of a mutation relative to the site of the motif was allowed to vary, such that for each mutation, identified as described above, a nucleotide 'window' was selected around the site, usually 9 or 15 nucleotides in length, likely to encompass any motif responsible for recruiting SHM machinery (activation-induced cytidine deaminase (AID) and error-prone polymerases), such that within each X-mer nucleotide window, wherein all motifs of length k were exhaustively searched, where an occurrence includes those sequences that vary at up to c positions within the k-mer motif (interpreted as diversifying the library of phage of phagemid clones; contacting the library with AID and DNA polymerase h, claim 1) (col 222), lines 1-15). Bowers teaches that analysis of mutations originating from SHM in antibodies undergoing affinity maturation led to several important insights, wherein nucleotide sequences are used at hot spots to attract the SHM machinery (see for example, Tables 2, 3, 6 and 9), and these hot spots are positioned specifically with regard to the codon reading frame (interpreted as affinity maturation, claim 1) (col 222, lines 52-57).
Regarding claims 4 and 5, Bowers teaches in Figure 6, a series of mutation events that lead to the creation of amino acid diversity, starting from "preferred and SHM hot spot codons" AGC and TAC, as observed in affinity matured IGV heavy chain sequences, wherein 4200 primary and secondary SHM mutation events identified and analyzed from the NCBI database, starting from codons encoding asparagine and tyrosine, lead to a set of functionally diverse amino acids (interpreted as creating diversity of IgV genes, claims 4 and 5) (col 11, lines 55-62; and Figure 6). Bowers teaches that libraries of camelid-derived antibody variable regions, which maintain the in vivo diversity of the variable regions of a camelid, can be made by, for example, the methods disclosed in U.S. Patent Application Ser. No. 20050037421, published Feb. 17, 2005 (interpreted as a library of clones comprises a library of phage vectors inserted with a naïve IgV gene; and diversifying the naïve IgV gene, claim 4) (col 23, lines 66-67; and col 24, lines 1-3), wherein constructing a phage library by incorporating VHH genes obtained from tissue and blood of non-immunized camels into phage display vectors; and that naïve repertoires are included in the immunoglobulins of the IgM class is known in the art as evidenced by Honda (paragraphs [0036], lines 1-4; and [0040]). Bowers teaches that in order to prepare a composition of polynucleotides comprising a substantial portion of the immunological gene repertoire, a starting source material having the genes coding for the VH and VL polypeptides is required, wherein the source will be a heterogeneous population of antibody producing cells, i.e. B lymphocytes (B cells) (interpreted as encompassing naïve IgV genes, claims 4 and 5) (col 132, lines 39-44). Bowers teaches phage display and the use of phagemid vectors and phage vectors (col 43, lines 48-51; and col 44, lines 4-8 and 22-24).
Regarding claims 7 (in part) and 12 (in part), Bowers teaches that the term "phage vector" means a double stranded replicative form of a bacteriophage containing a heterologous gene and capable of replication, wherein the phage vector has a phage origin of replication allowing phage replication and phage particle formation, such that the phage is a filamentous bacteriophage, such as an M13, fl, fd, Pf3 phage or a derivative thereof, or a lambdoid phage, such as lambda, 21 , phi80, phi81 , 82, 424, 434, etc., or a derivative thereof (interpreted as phage vectors, claims 7 and 12) (col 44, lines 22-29). Bowers teaches that CDR3 region libraries are produced by cloning of the polynucleotides encoding the CDR3 regions of the VH chain and VL chain from a genetic repertoire comprised of polynucleotide coding strands, such as mRNA and/or the relevant coding region of genomic DNA, wherein the genetic repertoire is in the form of double-stranded genomic DNA, which is usually first denatured, typically, by melting, into single strands, such that the genomic DNA is subjected to a first primary extension reaction by treating (contacting) the DNA with a first polynucleotide synthesis primer having a pre-selected nucleotide sequence (interpreted as denaturing dsDNA denatured into single strands, claim 12) (col 135, lines 35-45).
Regarding claim 13, Bowers teaches that each polynucleotide sequences template variable domain is designed to include suitable unique restriction sites for sub-cloning, and ligation of CDRs and constant domains (interpreted as comprising one or more restriction enzyme sites, claim 13) (col 132, lines 27-29). Bowers teaches that the DNA homologs representative of the plurality of polynucleotides encoding the CDR3 regions produced by PCR amplification are typically in double-stranded form and have contiguous or adjacent to each of their termini a nucleotide sequence defining an endonuclease restriction site (col 137, lines 42-46).
Bowers does not specifically exemplify a quantity of gapped, dsDNA vectors (claims 7 and 12, in part).
Regarding claims 7 (in part) and 12 (in part), Bransteitter teaches that the Ig genes undergo diversification by three processes: V(D)J recombination, somatic hypermutation (SHM) and class switch recombination (CSR) (pg. 1, first full paragraph, lines 5-7). Bransteitter teaches that V(D)J recombination is the first step in generating antibody diversity and occurs throughout early B cell development in the bone marrow, wherein site-specific double-stranded (ds) DNA breaks are introduced between germline copies of V, D, and J segments in an Ig gene; subsequently, the fragments are reassembled to produce transcriptionally competent heavy or light chain genes (Figure 1), wherein diversity is created by the random joining of V, D, and J segments to one another and also through errors that are introduced at the junction sites before the breaks are sealed (interpreted as IgV genes; diversity; and dsDNA vectors comprising gaps, claims 7 and 12) (pg. 1, last partial paragraph; and pg. 2, first partial paragraph; and Figure 1). Bransteitter teaches that DNA-RNA hybrid, dsDNA and ssDNA were assayed for AID, wherein the assay used to detect AID deamination on the various substrates is depicted in the Figure 2-1, such that after incubating AID with a 32P 5’-end labeled DNA substrate (33-nt), UDG converts AID generated U to abasic sites (interpreted as further comprising restriction enzyme sites, claim 13) (interpreted as AID in a cell-free environment, claim 1) (pg. 10, last partial paragraph). Bransteitter teaches that RNAse A was added to the DNA-RNA hybrid substrate for 10 seconds to degrade the RNA and allow the complementary DNA strand to anneal to the remaining DNA strand (Figure 2-1) (interpreted as denaturing and annealing, claims 7 and 12) (pg. 11, first partial paragraph; and Figure 2-1). Bransteitter teaches that a second assay used to detect C → U deamination provided an independent confirmation of AID deaminating C on ssDNA in the presence of RNAse A (Fig 2-5), wherein this assay involved primer elongation-dideoxynucleotide termination, wherein the DNA substrates were denatured and annealed to a DNA primer strand complementary to the DNA strand containing the single target C (interpreted as denaturing and annealing; and ssDNA, claims 7 and 12) (pg. 11, first partial paragraph; and Figure 2-1). Bransteitter teaches that AID was incubated with phage M13mp2 circular DNA substrate containing a 230-nt target of the lacZa reporter sequence in a 365-nt, single-stranded gapped region (Figure 3.1), such that AID dC deamination events occurring on individual ssDNA lacZa reporter sequences are detected as C → T mutations (white and light blue plaques) in individual phage progeny after transfection into uracil glycosylase-deficient (Ung-) E. coli, wherein M13mp2 molecules that were not mutated appeared as dark blue plaques (interpreted as in vitro AID diversification; gaps; and phage, claim 1) (pg. 24, last partial paragraph). Bransteitter teaches that the action of AID shows a highly diverse clonal pattern of mutations, leaving many ssDNA molecules unmutated while introducing multiple mutations into a few molecules (pg. 26, last partial paragraph). Bransteitter teaches that 86 mutant phage clones were selected from the transcription dependent AID deamination reactions and performed a sequencing analysis, wherein of these clones, 68 contain only G → A or C → T mutations, characteristic of AID deamination on the non-transcribed and transcribed strands, wherein the other 18 clones have single background mutations other than G → A or C → T that can have been generated during transcription because there was an increase in mutation frequency when only T7 RNA polymerase was added to the reaction (pg. 62, last partial paragraph, lines 1-7). Bransteitter teaches examination of the mutation spectrum of AID C → U deamination on an actively transcribed dsDNA template reveals that AID preferentially deaminates C in WRC hot spots while avoiding deamination of C in SYC cold spots during transcription (pg. 65, first full paragraph, lines 1-4). Bransteitter teaches that there is a stronger preference for deaminations at WRC hot spots in the transcription-dependent reaction (7-fold) than on naked ssDNA (4.6-fold), such that unlike gapped ssDNA, where AID has access to all possible cytosines at any given time, within a moving transcription bubble, AID must select between a limited number of C residues present in a short span of ssDNA that is only briefly exposed (pg. 72, last partial paragraph). Bransteitter teaches in Figure 5-6, somatic hypermutation V-region, wherein gap filling synthesis by pol h gives mutations at A:T bps (interpreted as pol h gap filling, claims 7 and 12) (pg. 74, Figure 5-6). Bransteitter teaches that gapped DNA was constructed by digesting double stranded M13mp2 DNA with PvuII, wherein the PvuII digestion yields a small 365-nt DNA fragment and linearized double stranded M13mp2, wherein the cut double stranded M13mp2 DNA is gel purified and denatured by heating to 70oC for 5 minutes, such that after the denaturing step, single stranded M13mp2 is added in at approximately 4-fold excess to the double stranded gapped M13mp2 DNA and placed on ice to allow annealing (interpreted as denaturing by heating, and reannealing by cooling, claims 7 and 12) (pg. 80, last partial paragraph; and pg. 81, first partial paragraph)
“It is prima facie obvious to combine prior art elements according to known methods to yield predictable results; the court held that, "…a conclusion that a claim would have been obvious is that all the claimed elements were known in the prior art and one skilled in the art could have combined the elements as claimed by known methods with no change in their respective functions, and the combination would have yielded nothing more than predictable results to one of ordinary skill in the art. KSR International Co. v. Teleflex Inc., 550 U.S. ___, ___, 82 USPQ2d 1385, 1395 (2007); Sakraida v. AG Pro, Inc., 425 U.S. 273, 282, 189 USPQ 449, 453 (1976); Anderson’s-Black Rock, Inc. v. Pavement Salvage Co., 396 U.S. 57, 62-63, 163 USPQ 673, 675 (1969); Great Atlantic & P. Tea Co. v. Supermarket Equipment Corp., 340 U.S. 147, 152, 87 USPQ 303, 306 (1950)”. Therefore, in view of the benefits of diversifying Ig genes that are dedicated to the production of B cell antibodies as exemplified by Bransteitter, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to modify the method of generating huge libraries of mutant polynucleotides through in vitro somatic hypermutation by AID and DNA polymerase eta as disclosed by Bowers, to include the methods of SHM targeted to IgV regions, AID targeting the WRC hot spot motif to generate of C deaminations, and/or producing additional mutations introduced through error-prone DNA polymerases including polymerase eta as taught by Bransteitter with a reasonable expectation of success in creating highly diversified libraries of phage or phagemid clones, the creation of secondary hot spot mutations including in WA motifs; and/or in screening the huge and diverse libraries against arbitrary antigens to identify variants with improved properties.
Thus, in view of the foregoing, the claimed invention, as a whole, would have been obvious to one of ordinary skill in the art at the time the invention was made. Therefore, the claims are properly rejected under 35 USC §103 as obvious over the art.
Conclusion
Claims 1, 4, 5, 7, 12 and 13 are rejected.
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 AMY M BUNKER whose telephone number is (313) 446-4833. The examiner can normally be reached on Monday-Friday (6am-2:30pm).
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/AMY M BUNKER/Primary Examiner, Art Unit 1684
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