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 .
Priority
Receipt is acknowledged of certified copies of papers required by 37 CFR 1.55.
Information Disclosure Statement
The IDS filed 02/13/2024 has been considered by the Examiner.
Status of Claims
Claims 1, 3-6, 8, 12-21, 24-26 are under examination.
Claim 2, 7, 9-11, 22-23, and 27-46 are cancelled.
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.
Rejections maintained:
Claims 1, 3-4, 8, 12, 13-16, 17-18, 21, and 24-26 are rejected under 35 U.S.C. 103 as being unpatentable over Gilbert et al. (Cell, 2013) in view of Li et al. (Nature Letters, 2009) and Ross. (BD Biosciences Research Grant Program, 2014).
Regarding claim 1, Gilbert et al. teach reprogramming of cells and precise targeting of genes. Gilbert et al. further teach CRISPR-associated catalytically inactive dCas9 protein for RNA-guided DNA targeting (page 442, summary). Gilbert et al. teach the fusion of dCas9 to effector domains with distinct regulatory functions enables stable and efficient transcriptional repression or activation in human cells, with the site of delivery determined solely by a co-expressed short guide (sg)RNA (Summary, page 442). Gilbert et al. teach activation of gene expression in human cells with dCas9 with four fused copies of the transcription activator VP16 or a single copy of p65 activation domain (AD) to dCas9 (page 443, final paragraph). Gilbert et al. teach programmable dCas9 can repress or activate transcription in human cells. Gilbert et al. further teach dCas9 fusion proteins can functionally mimic multiple native protein interactions, including the KRAB domain of Kox1, VP16, and p65AD (page 448, first paragraph). Gilbert et al. teach that the sgRNA molecules are used to target the transcription factor to the desired gene. Gilbert et al. teach the simple constitutive dCas9 system can be coupled to more complex inducible systems for precise temporal and spatial control, enabling refined analysis of chromatin remodeling processes during cell development and differentiation (page 448, paragraph 2).
Gilbert et al. have enabled a critical component of the instant invention, the use of a synthetic transcription factor comprising (i) a fusion polypeptide that contains an enzymatically inactive Cas9 molecule and transcriptional activation domain such as VP64 or p65 and (ii) a guide RNA that binds to the promoter of a target gene and the fusion polypeptide. Furthermore, Gilbert et al. have suggested reprogramming somatic cells using their system.
Gilbert does not teach the DNA-binding segment binds a promoter region of an endogenous pluripotency factor gene of the mammalian somatic cells. Gilbert et al. do not teach that activation/expression of certain pluripotency genes. Gilbert does not specifically teach an induced pluripotent stem cell (iPSC), and/or transdifferentiate the mammalian somatic cell to a target cell different in cell type from said mammalian somatic cell.
Li et al. teach that activation/expression of certain pluripotency genes including oct4, sox2, kIf4, c-myc and repression of other pluripotency genes like p16Ink4a and p19Arf are required for reprogramming somatic cells into induced pluripotent stem cells (page 5, Generation of mouse iPS cells). Li et al. teach the culture period from about 2 days to about 14 days (page 5, Generation of mouse iPS cells).
It would have been obvious to one of ordinary skill in the art at the time the invention was made to have combined the teachings of Gilbert et al. for reprogramming of cells and precise targeting of genes utilizing CRISPR-associated catalytically inactive dCas9 protein for RNA-guided DNA targeting with the teachings of Li et al. for specific reprogramming of differentiated cells into induced Pluripotent Stem (iPS) cells via regulation of pluripotency genes. Combining these prior art elements according to known methods would yield predictable results, since all of the claimed elements were known in the prior art. It would have been obvious to use a combination of these known related elements in a method for reprogramming and regulating gene expression. The skilled artisan would have had a reasonable expectation of success in combining the teachings of Gilbert et al. and Li et al. because each of the critical elements had been enabled prior to the filing of the instant application and combining the various elements would be within the capability of one of ordinary skill in the art.
Gilbert et al. and Li et al. do not teach the use of synthetic transcription factors in order to regulate expression of pluripotency genes.
Ross teaches a method of activating expression of pluripotency gene using a technology based on engineered nucleases composed of sequence-specific DNA-binding domains fused to a non-specific cleavage module.
It would have been obvious to one of ordinary skill in the art at the time the invention was made to have combined the teachings of Gilbert et al. and Li et al. for a method of regulating pluripotency genes with the teachings of Ross for engineered synthetic gRNAs. The combination of these known prior art elements according to known methods to would yield predictable results. It would have been obvious to use a combination of these gene expression regulation elements in a method of reprogramming somatic cells into iPSCs. The skilled artisan would have had a reasonable expectation of success in combining the teachings of Gilbert et al., Li et al., and Ross because each of the critical elements had been enabled prior to the filing of the instant application and combining the various elements would be within the capability of one of ordinary skill in the art.
Regarding claim 3 Li et al. teach the mammalian somatic cells (fibroblasts and keratinocytes) are human cells (page 4, paragraph 3).
Regarding claim 4, Li et al. teach the mammalian somatic cells are fibroblasts (page 4, paragraph 3).
Regarding claim 8, Li et al. teach the mechanisms involved in the reprogramming of differentiated cells into induced pluripotent stem (iPS) cells by Oct4, Klf4 and Sox2 (page 1 abstract). Li et al. teach that activation/expression of certain pluripotency genes oct4, sox2, kIf4, c-myc and repression of other pluripotency genes are required for reprogramming somatic cells into induced pluripotent stem cells (page 5, Generation of mouse iPS cells).
Regarding claims 12 and 13, Gilbert et al. teach, activation of gene expression in human cells with dCas9, with a single copy of p65 activation domain (AD) to dCas9 (page 443, final paragraph).
Regarding claim 14, Li et al. teach contacting cells with a second transcription factor that represses a pluripotent factor gene (page 1, abstract). Gilbert, Li, and Ross make obvious contacting the cells second synthetic transcription factor that represses expression of a second endogenous pluripotency factor gene.
Regarding claim 15, Li et al. teach the second pluripotency factor genes being repressed are p16Ink4a and p19Arf (page 1, abstract).
Regarding claim 16, Gilbert et al. further teach dCas9 fusion proteins can functionally mimic multiple native protein interactions, including the KRAB domain (page 448, first paragraph).
Regarding claim 17, Gilbert et al. teach human cells demonstrated that local chromatin context is a crucial determinant of KRAS-mediated silencing (page 448, CRISPRI Efficiently and Specifically Represses Transcription in Human Cells). Gilbert et al. teach a dCas9-KRAB fusion protein efficiently silences GFP expression (page 447, Figure 4).
Regarding claim 18, Gilbert, Li, and Ross make obvious contacting the cells with at least one expression vector that represses expression of a second endogenous pluripotency factor gene. Gilbert et al. teach introduction of an expression vector contain a sgRNA expression plasmid and dCas9 the transcriptional modulator (page 444, Figure 1B).
Regarding claim 21, Gilbert et al. teach cells were transfected with the transcriptional modulator dCas9 expression plasmid and a sgRNA plasmid (page 449, Cell Culture, DNA Transfections, Viral Production, and Fluorescence Measurements for CRISPRi in Human Cells).
Regarding claim 24, Ross specifically points to a method of activating expression of pluripotency gene using a dCas9-fusion protein and gRNAs directed to oct4, sox2, klf4, c-myc and Nanog (page 2, paragraph 1).
Regarding claim 25, Ross teach introduction of (i) dCas9 genetically fused with a transactivation domain. Ross teach five single guide RNA (sgRNA) target sites of 20 bp followed by the protospacer adjacent motif sequence NGG, where N is any nucleotide, (ii) in the promoter of the Oct4, (iii) in the promoter of the Sox2 gene, and (iv) in the promoter of the Klf4 gene (page 2, paragraph 1).
Regarding claim 26, Ross specifically points to a method of activating expression of pluripotency gene using a dCas9-fusion protein and gRNAs directed to oct4, sox2, klf4, c-myc and Nanog (page 2, paragraph 1).
Rejections maintained:
Claims 19 and 20 rejected under 35 U.S.C. 103 as being unpatentable over Gilbert et al. (Cell, 2013) in view of Li et al. (Nature Letters, 2009) and Ross. (BD Biosciences Research Grant Program, 2014) as applied to claims 1 and 18 above, and further in view of Wu (US2014/0273226 A1).
Gilbert, Li, and Ross make obvious the method of nuclear reprogramming mammalian somatic cells. Gilbert, Li, and Ross make obvious mammalian somatic cells is contacted with at least one expression vector encoding said synthetic transcription factor.
Regarding claim 19, Gilbert, Li, and Ross make obvious the method for nuclear reprogramming mammalian somatic cells and further an expression vector. Gilbert, Li, and Ross do not teach the expression vector is a non-viral, episomal vector.
Wu teaches engineered CRISPR/Cas9 systems for genomic modification and regulation of gene expression in mammalian cells (cover page, abstract). Wu teaches a single vector system that expresses both a Cas9 nuclease and a guide RNA, thereby simplifying transfection protocols by requiring the transfection of only a single plasmid (page 16, paragraph 0168). Wu teaches the single vector system is an EBNA-based plasmid expression vector (page 14, paragraph 0138).
It would have been obvious to one of ordinary skill in the art at the time the invention was made to have combined the teachings of Gilbert, Li, and Ross for a method of nuclear reprogramming mammalian somatic cells with the teachings of Wu for an EBNA-based plasmid expression vector. Wu provides motivation by teaching that the all-in-one vectors simplify transfection protocols. One of skill in the art would have had a reasonable expectation of success at combining Gilbert, Li, and Ross and Wu et al. because both teach CRISPR/Cas9 systems for modification and regulation of gene expression in mammalian cells.
Regarding claim 20, Gilbert, Li, and Ross make obvious the method for nuclear reprogramming mammalian somatic cells and further an expression vector. Gilbert, Li, and Ross do not teach the expression vector encodes both said guide RNA and said transcriptional modulator.
Wu teaches engineered CRISPR/Cas9 systems for genomic modification and regulation of gene expression in mammalian cells (cover page, abstract). Wu teaches a single vector system that expresses both a Cas9 nuclease and a guide RNA, thereby simplifying transfection protocols by requiring the transfection of only a single plasmid (page 16, paragraph 0168). Wu teaches the all-in-one vectors were developed to be more efficient, affordable, and convenient (page 16, paragraph 0168).
It would have been obvious to one of ordinary skill in the art at the time the invention was made to have combined the teachings of Gilbert, Li, and Ross for a method of nuclear reprogramming mammalian somatic cells with the teachings of Wu for an all-in-one expression vector which encodes gRNA and the transcriptional modulator. Wu provides motivation by teaching that the all-in-one vectors were developed to be more efficient, affordable, and convenient. One of skill in the art would have had a reasonable expectation of success at combining Gilbert, Li, and Ross and Wu et al. because both teach CRISPR/Cas9 systems for modification and regulation of gene expression in mammalian cells.
Rejections maintained:
Claims 5 and 6 are rejected under 35 U.S.C. 103 as being unpatentable over Gilbert et al. (Cell, 2013) in view of Li et al. (Nature Letters, 2009) and Ross (BD Biosciences Research Grant Program, 2014) as applied to claims 1 and 3 above, and further in view of Ramos-Mejia et al (PLoS ONE, 2012).
Gilbert, Li, and Ross make obvious the method of nuclear reprogramming mammalian somatic cells.
Regarding claims 5 and 6, Gilbert, Li, and Ross make obvious the method of nuclear reprogramming. Gilbert, Li, and Ross teach fibroblasts as the starting somatic cells, but do not specifically teach cord blood cells. It was well known prior to the instant filing date that cord blood cells could be an alternative source for starting somatic cells during methods of producing iPSCs as evidenced by Ramos-Mejia. Ramos-Mejia et al. teach that both human fibroblasts and cord blood CD34+ cells can be reprogrammed to produce iPSCs. One of ordinary skill in the art would exchange the fibroblasts for cord blood cells. Ramos-Mejia teach fibroblasts and cord blood can be exchanged for one another in iPSC generation. Ramos-Mejia provide motivation teaching advantages of using cord blood cells as a source of somatic cells to reprogram into induced pluripotent stem cells. Ramos-Mejia teach that cord blood banks are a convenient source of this material which might be otherwise discarded. Ramos-Mejia teaches that these cord blood cells would have fewer somatic mutations than cells from adults. Therefore, there is some teaching, suggestion and motivation to use cord blood cells to produce iPS cells. Combining these known methods would yield predictable results, all of the claimed elements were known in the prior art and one skilled in the art could have combined the elements. It would be therefore predictably obvious to use a combination of these elements in a method of reprogramming cord blood cells into iPSCs. The skilled artisan would have had a reasonable expectation of success in combining the teachings of Gilbert et al. and Li et al. and Ramos-Mejia because cord blood cells have been used prior to the instant filing date to make iPSCs.
Response to Arguments
Applicant's arguments filed 03/03/2026 have been fully considered but they are not persuasive.
Applicant’s Argument: Applicant argues that although obviousness can be established by modifying and/or combining the teachings of the prior art to produce the instant invention where there is some teaching, suggestion, or motivation to do so.
Examiner’s response: Gilbert et al. teach reprogramming of cells and precise targeting of genes. Gilbert et al. further teach CRISPR-associated catalytically inactive dCas9 protein for RNA-guided DNA targeting (page 442, summary). Gilbert et al. teach that the sgRNA molecules are used to target the transcription factor to the desired gene. The precise targeting of transcription factors to the desired gene would allow specific reprogramming of differentiated cells into induced Pluripotent Stem (iPS) cells via regulation of pluripotency genes. Li et al. provide motivation teaching genetic inhibition of the Ink4/Arf 1ocus has a profound positive impact on the efficiency of iPS generation, increasing both the kinetics of reprogramming and the number of emerging iPS colonies (cover page, abstract). Ross teaches a method of activating expression of pluripotency gene using a technology based on engineered nucleases composed of sequence-specific DNA-binding domains fused to a non-specific cleavage module. Ross provides motivation by teaching the technique allows the manipulation virtually any gene in a diverse range of cell types and organisms (page 1, paragraph 2).
Applicant’s Argument: Applicant argues that uncertainty is part of biological systems, and unpredictability or variation in a biological process is common. The present application provides a method to directly regulate the endogenous pluripotency factor gene on the genome of the mammalian somatic cell to reprogram the cell into the induced pluripotent stem cell.
Examiner’s response: While biological systems can be unpredictable, iPSCs have been well studied as provided by Ross. Ross teaches successful reprogramming of differentiated human cells into a pluripotent state was reported in 2007 (page 1, paragraph 2). Furthermore, as provided by Li there has been further research into the mechanisms involved in reprogramming differentiated cells (cover page, abstract).
Applicant’s argument: There is no teaching in Gilbert that a dCas9 with a guide RNA for pluripotency factor gene would have a targeting effect, and certainly not teaching that any targeting effect would be sufficient to induce pluripotency. Gilbert does not provide any guidance for which the skilled artisan would be able to determine/select suitable culturing conditions, such as culturing time and other conditions sufficient to induce pluripotency.
Examiner’s response: Gilbert teaches precise targeting of genes but does not further teach the target to induce pluripotency, however the combination of Gilbert, Li, and Ross sufficiently teach the limitations of the present application. Li et al. teach that activation/expression of certain pluripotency genes including oct4, sox2, kIf4, c-myc and repression of other pluripotency genes like p16Ink4a and p19Arf are required for reprogramming somatic cells into induced pluripotent stem cells (page 5, Generation of mouse iPS cells).
Applicant’s Arguments: Li reports introducing three exogenous transcription factors Oct4, Klf4 and Sox2 into cells to reprogram the cells, where repression or silencing of the Ink4/Arf locus is also necessary (see Li, online Methods, left column). Li uses vectors to express exogenous transcription factors and achieve the silencing function, while the claimed invention provides a means to induce endogenous genes. Li does report pluripotency was induced in 10-12 days using its exogenous expression from vectors.
Examiner’s response: Li et al. teach the human shINK4a-iPS expressed endogenous Sox2, Nanog, A.P, and SSEA.3 (page 4, paragraph 1). Furthermore, the inhibiting of the Ink4/Arf locus would induce endogenous genes. Ross further teaches approaches for the reprogramming of somatic cells that have been generated during the last few years include activation of endogenous genes encoding key regulators of cell fate (page 1, paragraph 2). Li et al. teach the culture period from about 2 days to about 14 days (page 5, Generation of mouse iPS cells).
Applicant’s Arguments: Applicant argues both Gilbert and Li indicate the uncertainty of their processes. In contrast, the claimed invention successfully proves the conditions to induce pluripotency by overexpressing the endogenous pluripotency factor gene or repressing certain genes. Ross mentions that others may have been able to activate endogenous pluripotency factor genes but provides no details.
Examiner’s Response: Certainty is not a requirement of patentability. The combination of Gilbert, Li, and Ross make obvious the invention of the present application.
Applicant’s argument: Applicant Argues nothing in the combination of cited references suggests the ways to regulate endogenous pluripotency factor gene to obtain the pluripotency cell.
Examiner’s response: Li et al. teach that activation/expression of certain pluripotency genes including oct4, sox2, kIf4, c-myc and repression of other pluripotency genes like p16Ink4a and p19Arf are required for reprogramming somatic cells into induced pluripotent stem cells (page 5, Generation of mouse iPS cells).
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.
Rejections maintained:
Claims 1,3, 5, 6, 8, 12 and 13 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, and 8 of U.S. Patent No. 11655481. Although the claims at issue are not identical, they are not patentably distinct from each other.
Instant claim 1 is made obvious by claims 1 and 2 of U.S. Patent No. 11655481 the method of reprogramming a mammalian somatic cells comprising 2 to 7 guide RNAs reads on at least one guide RNA of the present application, which includes more than one guide RNA. Claim 1 further recite each guide RNA comprising a DNA-binding segment and a polypeptide-binding segment, wherein the DNA-binding segment binds the promoter region of the endogenous pluripotency factor gene; and a second nucleic acid encoding at least one transcriptional modulator which binds the polypeptide-binding segment of the gRNAs, wherein the transcriptional modulator comprises an enzymatically inactive Cas9 polypeptide (dCas9), wherein the dCas9 is fused to a transcriptional activation domain; and culturing the mammalian somatic cells for a period of from about 2 to about 14 days, under conditions sufficient to (i) reprogram the mammalian somatic cell to an induced pluripotent stem cell (iPSC), and/or (ii) transdifferentiate the mammalian somatic cell to a target cell different in cell type from said mammalian somatic cell.
Instant claim 3 is met by claim 2 of U.S. Patent No. 11655481. Claim 2 recites mammalian somatic cells are human cells.
Instant claim 5 is met by claim 3 of U.S. Patent No. 11655481. Claim 3 recites mammalian somatic cells are primary blood cells.
Instant claim 6 is met by claim 4 of U.S. Patent No. 11655481. Claim 4 recites blood cells are peripheral blood mononuclear cells (PBMCs) or cord blood mononuclear cells.
Instant claim 8 is met by claim 5 of U.S. Patent No. 11655481. Claim 5 recites the pluripotency factor gene is selected from the group consisting of oct3/4, sox2, klf4, c-myc, lin28, Nanog, glis-1, bcl2, and bclx.
Instant claim 12 is met by claim 1 U.S. Patent No. 11655481. Claim 1 recites the dCas9 is fused to a transcriptional activation domain.
Instant claim 13 is met by claim 6 U.S. Patent No. 11655481. Claim 6 recites the transcriptional activation domain is VP64 or p65.
Response to Arguments
Applicant's arguments filed 03/03/2026 have been fully considered but they are not persuasive.
Applicant’s Arguments: The Office rejected claims 1, 3, 5, 6, 8, 12, and 13 on the ground of obviousness-type double patenting as allegedly unpatentable over claims 1-6 and 8 of U.S. Patent No. 11,655,481 (the "'481 Patent"). Applicant respectfully requests that the obviousness-type double patenting rejection over the '481 Patent be held in abeyance until allowable subject matter can be determined and all remaining rejections have been withdrawn.
Examiner’s response: Obviousness-type double patenting rejections remain as applicant’s arguments did not refute the rejections as they stand.
Conclusion
THIS ACTION IS MADE FINAL. 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.
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/C.L.M./Examiner, Art Unit 1638
/Tracy Vivlemore/Supervisory Primary Examiner, Art Unit 1638
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