DETAILED ACTION
Notice of Pre-AIA or AIA Status
1. The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claim Rejections - 35 USC § 112
2. The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
3. Claims 11 and 13 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
Claims 11 and 13 recite the phrases “wherein at least one step is carried out in” either living cells or animal models, respectively. Applicant’s original disclosure (claims 11 and 13 filed 22 December 2021) taught that “the method is carried out in living cells” and “the method is carried out in preclinical animal models.” Applicant’s specification provides no further detail or disclosure on “at least one step” of the method being carried out in either model organism. This limitation is not present in the original claims or specification, nor in any document to which this application claims priority, therefore these limitations constitute new matter.
4. Claim 13 is rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for certain steps of claim 1 to be carried out in preclinical animal models, does not reasonably provide enablement for most or all of the steps of claim 1 to be carried out in preclinical animal models. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
Applicant has amended claim 13 to recite the phrase the “method of claim 1, wherein at least one step is carried out in preclinical animal models.” It is noted here that the phrase “at least one step” encompasses more than one step, including all of the steps, being carried out in preclinical animal models. Certain steps, such as contacting the biotinylated substructure reagents with a streptavidin magnetic bead, performing a CuAAC reaction, and subjecting the RNA to reverse transcription and sequencing are not sufficiently enabled by the language in the specification. One having ordinary skill in the prior art would have knowledge related to performing portions of this method in preclinical animal models, such as the administration of RNA binding substructures to a patient (i.e., an animal) as discussed in Petter et al (United States Patent Application No. US 20200115372, effectively filed 06-01-2018; [0289]), which the applicant would be enabled for. However, practicing many of the steps and/or the entire method of claim 1 (which is currently encompassed by the claim language of amended claim 13) would be highly unpredictable, and the applicant provides no teaching or suggestion in their specification that would reduce that unpredictability or suggest how any of the required components (azide-biotin, CuAAC related click reagents, magnetic beads, etc.) would be delivered to appropriate sites within the animal model. There are no working examples in the literature or in the applicant’s specification, and therefore the method claimed cannot be practiced without undue experimentation.
5. The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
6. Claims 4 and 5 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
A. In claim 4, applicants provide a claimed formula of the alkyne moiety used in the formation of the substructure reagent. Based on applicant’s specification and claim 2, 4, and 5 the alkyne moiety is covalently conjugated to the substructure, and then the diazirine moiety is conjugated to the alkyne moiety. However, it is unclear how the diazirine moiety is conjugated to the alkyne moiety as claimed because the alkyne moiety comprises an Fmoc protecting group at the position indicated to react with the -COOH present on the diazirine. Additionally, claim 4 has been amended to recite the phrase “wherein the moiety comprising an alkyne group is a radical of a compound of formula…” and then provides the formula of the alkyne used in the synthesis of TGP-21-diaz. It is further unclear how this amendment is intended to limit the claim as written. There is no clear radical of the given compound that is used in the method of claim 1, and applicant’s specification neither discusses nor discloses a radical of this compound in the reaction to form TGP-21-daiz. The reaction of this amine with the -COOH group of TCP-21-acid and the deprotection of the Fmoc group do not proceed through a radical intermediate, and “the moiety” cited in claim 4 has antecedent basis to the substructure library in claim 1 prior to the CuAAC reaction with the biotin azide. It is unclear why this moiety of the substructure library would be a radical of the given formula, and therefore this claim is indefinite.
B. Claim 5 has been amended to recite the phrase “wherein the moiety comprising a diazirene group is a radical of a compound of formula…” and then provides the formula of the diazirene acid used in the synthesis of TGP-21-diaz. It is unclear how this amendment is intended to limit the claim as written. There is no clear radical of the given compound that is used in the method of claim 1, and applicant’s specification neither discusses nor discloses a radical of this compound in the reaction to form TGP-21-diaz. The crosslinking of diazirene moieties proceeds through a reactive carbene intermediate after photoactivation, but even so “the moiety” cited in claim 5 has antecedent basis to the substructure library prior to illumination with UV light. It is unclear why this moiety of the substructure library would be a radical of the given formula, and therefore the claim is indefinite.
Claim Rejections - 35 USC § 103
7. 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.
8. Claims 1, 3, 5-6, 8-11, 14-16 and 17 are rejected under 35 U.S.C. 103 as being unpatentable over Petter et al (United States Patent Application No. US 20200115372, 07-31-2018) in view of Kumaravel et al (United States Patent Application No. US 20190270723, filed 11-30-2018), Velagapudi et al (Defining RNA-Small Molecule Affinity Landscapes Enables Design of a Small Molecule Inhibitor of an Oncogenic Noncoding RNA, ACS Central Science, 3, 205-216, published 03-06-2017), and Guan et al (United States Patent Application No. US 20160194696, published 07-07-2016).
Regarding claims 1 and 15, Petter teaches a library of small molecules (i.e., substructures) that bind RNA ([0307]). Petter teaches an RNA ligand (i.e., a substructure) that is covalently conjugated to a click group (i.e., an alkyne [0237]) and an RNA warhead (i.e., a molecule that covalently binds to an RNA; FIGs 2 and 45, [0177] and [0178]). Petter teaches that these substructures bind a target RNA (i.e., the RNA is contacted with the substructure library) and that the compound covalently modifieds one or more 2’-OH groups of the target RNA ([0174]). Petter teaches that these covalently modified RNA-substructure complexes are subjected to a Cu-catalyzed azide/alkyne click reaction to attach a biotin moiety (i.e., since the substructure comprises an alkyne moiety, the biotin moiety inherently comprises an azide moiety) to all RNAs that are ‘hooked’ to the substructure + warhead ([0332]). Petter teaches that all RNAs that are ‘hooked’ are subjected to a subsequent pull-down step by streptavidin ([0332]) and that this isolation is performed through the use of streptavidin magnetic beads ([0347]). Petter teaches that the bound RNA-substructure complex is ‘purified,’ ‘isolated,’ and ‘enriched’ by this pull-down technique, these processes inherently comprise the magnetic separation of beads from the supernatant ([0347]). Petter teaches that the pull-down protocol enables the sequencing of only those RNAs that have been covalently modified by a ‘hook’ (i.e., the ligands are identified as an RNA binding substructure [0349]). Petter teaches that the RNA is reverse transcribed to produce cDNA and sequenced and the small molecule-RNA binding site is indicated by mutations in the sequence where the RNA ligand is bound ([0330]). Petter additionally teaches that relevant RNA targets are miRNAs that affect the expression of human genes and that their expression levels vary between different disease settings (i.e., these are human miRNAs affect human gene expression; [0143]). Petter teaches that RNAs are produced by a human ([0226]).
Petter does not teach that the RNA warhead is a diazirene group, that the diazirene group is illuminated with UV light to convert to an active carbene that reacts covalently with the RNA, that the biotin moiety comprises a disulfide bond, measuring the radioactivity or fluorescence associated with each member of the library, cleaving the SMIRNA-RNA complex from the bead by reduction of the disulfide bond in the biotin linker, or that the presence of SMIRNA binding sites are determined by the presence of transcriptional stops.
However, Kumaravel et al teaches methods of determining the binding site and structure of RNAs bound to small molecule libraries (abstract and [0128]) wherein photoprobes such as Diazirine are used as a UV-dependent RNA binding warhead ([0059], [0066], and [0077]).
It would have been obvious to one having ordinary skill in the art to have simply substituted any of the RNA binding warheads taught by Petter with the UV-dependent diazirine taught by Kumaravel to prepare a photoactivatable RNA binder with a reasonable expectation of success. The ordinary artisan would have been motivated to make this substitution because Kumaravel teaches that such a warhead is unreactive prior to activation and thus a non-covalent RNA-ligand interaction is required for successful photoactivated modification ([0394]). One having ordinary skill in the art would have recognized that the known techniques in the cited references could have been combined with predictable results because the known techniques in the cited references predictably result in methods of using small molecule libraries comprising warheads that covalently react with RNA.
Kumaravel additionally teaches the illumination of the RNA-contacted library with UV light under conditions to cause conversion of a diazirine group into a reactive carbene ([0393] and [0398]), which reacts covalently with the RNA with which the small molecule is non-covalently bound ([0116] and [0394]).
Additionally, Kumaravel teaches that covalent modification of the RNA by the small molecule compound comprising an RNA reactive warhead leads to transcriptional pausing (i.e., the generation of a transcriptional stop [0059]) and that this pattern of modification is sequenced to determine the distribution and location of modified nucleotides within the RNA ([0128] and [0488]).
It would have been obvious to one having ordinary skill in the art to have substituted the read-through transcription method taught by Petter with the transcriptional pausing method taught by Kumaravel with a reasonable expectation of success. The ordinary artisan would have been motivated to make this substitution in order to avoid the additional steps related to the optimization of reverse transcription reaction enabling efficient reverse transcriptase read-through as discussed by Petter ([0341]). In addition, one having ordinary skill in the art would have recognized that the known techniques in the cited references could have been combined with predictable results because the known techniques in the cited references predictably result in the identification of RNA modification sites by reverse transcription and sequencing.
As discussed fully above Petter teaches a method wherein a biotin moiety is clicked onto an RNA-small molecule complex, but Petter in view of Kumaravel does not teach that the biotin moiety comprises a disulfide bond nor do they teach the cleavage of said disulfide bond to free the complex from the bead.
However, Guan teaches a method wherein a chemoselective group on a DNA is reacted with a capture molecule that comprises biotin and a cleavable linker such as a disulfide bond. Guan teaches that the affinity moiety (i.e., biotin) is captured and subsequently released by reducing the disulfide bond ([0012]).
It would have been obvious to have modified the biotin pull-down group taught by Petter in view of Kumaravel with the cleavable disulfide bond taught by Guan to generate a cleavable pull-down linker with a reasonable expectation of success. The ordinary artisan would have been motivated to make this modification in order to selectively cleave the captured RNA complexes from beads after the pull-down step taught by Petter in order to collect the isolated RNAs for downstream sequencing. In addition, one having ordinary skill in the art would have recognized that the known techniques in the cited references could have been combined with predictable results because the known techniques in the cited methods predictably result in the pull-down of nucleic acids onto streptavidin beads.
Petter in view of Kumaravel and Guan does not teach that the RNA is either radiolabeled or fluorescently labeled nor do they teach the measuring of the radioactivity or fluorescence associated with each member of the library.
However, Velagapudi teaches a method wherein a radiolabeled RNA target is contacted with an RNA binding compound and pulled down onto streptavidin magnetic beads to show that the small molecule reacts with the RNA target, and that the amount of radioactivity on the beads was measured (pg. 214, column 2, ¶ 2).
It would have been obvious to one having ordinary skill in the art to have modified the RNA target with a radiolabel as taught by Velagapudi and to have substituted the generic step of quantitating the ability of the compound to bind the target RNA taught by Petter ([0271]) with measuring the on-bead radioactivity taught by Velagapudi to arrive at the instantly claimed invention with a reasonable expectation of success. The ordinary artisan would have been motivated to make such modifications in order quantify the ability of a given compound to bind a target RNA as taught by Petter ([0271]). In addition, one having ordinary skill in the art would have recognized that the known techniques in the cited references could have been combined with a reasonable expectation of success because the known techniques in the cited references relate to the pull-down and quantification of RNAs bound to small molecules.
Regarding claim 3, Petter teaches that miR-21 is an RNA target ([0144]) and that the target miRNA is a pre-miRNA (e.g., pre-miR-21; [0146]).
Regarding claim 5, Kumaravel teaches a photoreactive RNA modifying group having the given formula (Claim 13).
Regarding claim 6, Velagapudi teaches that the radioactive label on the target RNA is 32P (pg. 214, column 2, ¶ 2).
Regarding claim 8, Petter teaches that the term RNA means synthetic oligoribonucleotides ([0226]).
Regarding claim 9, Petter teaches that the RNA is produced by a virus ([0226]) and that nucleic acid junctions (i.e., structural motifs to which these small molecule libraries bind) are ubiquitously found in viral genomes ([0532]).
Regarding claim 10, Petter teaches that a target RNA is present in a cell lysate (i.e., in vitro; [0226]).
Regarding claim 11, Petter teaches that small molecule lead identification is performed against RNA targets in cells ([0321]).
Regarding claim 14, Petter teaches the screening of a library of small molecules ([0307] and [0312]) against an RNA target, and teaches multiple RNA targets of interest ([0144]). Kumaravel teaches the screening of RNA-small molecule binding at different concentrations in parallel in a plate format ([0531]).
Petter in view of Kumaravel, Guan, and Velagapudi does not specifically teach the method of claim 1 performed in parallel for a plurality of RNA sequences and candidate RNA-binding small molecules.
It would have been obvious to one having ordinary skill in the art to any one or more of the RNA targets and potential small molecule ligands taught by Petter using the 96-well plate format taught by Kumaravel. The ordinary artisan would have been motivated to make such a modification because Petter specifically teaches that their method is useful for screening large libraries of RNA-binding ligands ([0312]) and Kumaravel specifically teaches a plate-based method of screening multiple RNA/ligand mixtures in parallel ([0531]). In addition, the ordinary artisan would have recognized that the known techniques in the cited references could have been combined with predictable results because the known techniques in the cited references predictably result in the screening of RNA-ligand binding interactions.
Regarding claim 16, Velagapudi teaches the pull-down of 32P-labeled miR-18a hairpin via a biotinylated small molecule. MiR-18a is a naturally occurring RNA, and the 32P label is a non-naturally occurring modification (i.e., a semi-synthetic RNA; pg. 214, column 2, ¶ 2). It is noted here that the phrase “semi-synthetic” has no additional definitions or limitations in the applicant’s claims or specification, and is so broad as to encompass any RNA that has a what could be interpreted as a “natural” portion and a “synthetic” portion.
Regarding claim 17, Petter teaches that the term RNA means naturally-occurring oligoribonucleotides ([0226]).
9. Claim 7 is rejected under 35 U.S.C. 103 as being unpatentable over Petter et al (United States Patent Application No. US 20200115372, 07-31-2018) in view of Kumaravel et al (United States Patent Application No. US 20190270723, filed 11-30-2018), Velagapudi et al (Defining RNA-Small Molecule Affinity Landscapes Enables Design of a Small Molecule Inhibitor of an Oncogenic Noncoding RNA, ACS Central Science, 3, 205-216, published 03-06-2017), and Guan et al (United States Patent Application No. US 20160194696, published 07-07-2016) as applied to claim 1 above, and further in view of Domenyuk et al (United States Patent Application No. US 20180066262, published 03-08-2018).
Regarding claim 7, the method of claim 1 is discussed fully above and incorporated here. The combination of Petter, Kumaravel, Velagapudi and Guan does not teach that the RNA comprises a fluorescent label.
However, Domenyuk teaches a method of detecting and quantifying an RNA target and provides both radiolabels and fluorescent labels as detectable alternatives ([0402]).
It would have been obvious to one of ordinary skill in the art to have simply substituted the radiolabel taught by Velagapudi with the fluorescent label taught by Domenyuk to arrive at the instantly claimed invention with a reasonable expectation of success. One having ordinary skill in the art would have been motivated to make such a substitution in order to reduce experimental dependence on highly controlled reagents, such as radiolabels. In addition, the ordinary artisan would have recognized that the known techniques in the cited references could have been combined with predictable results because the known techniques in the cited references predictably result in the detection and quantification of RNA targets in pull-down assays.
10. Claims 12 and 18 is rejected under 35 U.S.C. 103 as being unpatentable over Petter et al (United States Patent Application No. US 20200115372, 07-31-2018) in view of Kumaravel et al (United States Patent Application No. US 20190270723, filed 11-30-2018), Velagapudi et al (Defining RNA-Small Molecule Affinity Landscapes Enables Design of a Small Molecule Inhibitor of an Oncogenic Noncoding RNA, ACS Central Science, 3, 205-216, published 03-06-2017), and Guan et al (United States Patent Application No. US 20160194696, published 07-07-2016) as applied to claim 1 above, and further in view of Hermann (Small molecules targeting viral RNA, WIREs RNA, 7, 726-743, published 2016).
Regarding claims 12 and 18, the method of claim 1 is discussed fully above and incorporated here. Petter teaches that nucleic acid junctions are ubiquitous in viral genomes ([0532]), that RNA targets are produced by a virus or bacterium ([0226]) and that the binding and subsequent covalent linking of small molecules to RNA is performed in cells ([0321]). The combination of Petter, Kumaravel, Velagapudi and Guan does not teach that the method of claim 1 performed in living cells wherein the living cells are virally- or bacterially- infected cells.
However, Hermann teaches a number of small molecule binders as therapeutic molecules targeting structured RNAs in virally-infected cells (pg. 731, column 2, ¶ 3) and bacterially infected cells (pg. 727, column 1, ¶ 3 and pg. 737, column 2 ¶ 1).
It would have been obvious to one having ordinary skill in the art to have applied the screening method taught by the combination of Petter, Kumaravel, Velagapudi and Guan to virally- or bacterially-infected cells as taught by Hermann to arrive at the instantly claimed invention with a reasonable expectation of success. The ordinary artisan would have been motivated to make this modification because Petter specifically discusses the benefits of performing RNA binding a covalently capture screening in cells due to the specificity or RNA folding and the presence of post-translational RNA modifications that occur in the cell ([0321]). In addition, one having ordinary skill in the art would have recognized that the known techniques in the cited references could have been combined with predictable results because the known techniques in the cited references predictably result in the identification of therapeutic small molecule RNA binders.
11. Claim 13 is rejected under 35 U.S.C. 103 as being unpatentable over Petter et al (United States Patent Application No. US 20200115372, 07-31-2018) in view of Kumaravel et al (United States Patent Application No. US 20190270723, filed 11-30-2018), Velagapudi et al (Defining RNA-Small Molecule Affinity Landscapes Enables Design of a Small Molecule Inhibitor of an Oncogenic Noncoding RNA, ACS Central Science, 3, 205-216, published 03-06-2017), and Guan et al (United States Patent Application No. US 20160194696, published 07-07-2016) as applied to claim 1 above, and further in view of Velagupudi et al (Design of a small molecule against an oncogenic noncoding RNA, PNAS, 113, 21, 5898-5903, published 24 May 2016; hereinafter referred to as Velagapudi2).
Regarding claim 13, Petter, Kumaravel, Velagapudi and Guan teach the method of claim 1 as discussed fully above and incorporated here. Petter teaches that lead target identification is performed in living cells ([0321]) but neither Petter, Kumaravel, Velagapudi nor Guam teach that at least one step of the method is carried out in preclinical animal models.
However, Velagapudi2 teaches that mice bearing a xenografted tumor are treated with an RNA binding small molecule (pg. 5901, column 1, ¶ 3).
It would have been obvious to have modified the method taught by Petter, Kumaravel, Velagapudi and Guan to have performed the step of ‘contacting the library comprising the plurality of substructure reagents with the RNA for which the RNA-binding substructure is sought” within the xenografted mouse tumor as taught by Velagapudi2 to arrive at the instantly claimed invention with a reasonable expectation of success. The ordinary artisan would have been motivated to make this combination in order to test the binding of the small molecule substructure library in an in vivo environment to see which substructures bound to RNAs present in the xenografted tumor taught by Velagapudi2. In addition, the ordinary artisan would have recognized that the known techniques in the cited references could have been combined with predictable results because the known techniques in the cited references predictably result in the binding of RNA targets with a small molecule library.
Response to Arguments
12. Applicant’s enablement rejection under U.S.C. 112(a) was overcome by amendment to claim 13, however claim 13 has been further rejected with a scope of enablement rejection under U.S.C. 112(a).
The 112(b) rejections of claim 1 have been overcome by applicant’s arguments (Section V.a. of their remarks) and amendments to the claims.
The 112(b) rejections of claims 2, 7, 11, and 12 have been overcome by amendment to the claims.
The NSDP rejections over application 17/622,005 have been withdrawn because the reference application has been abandoned.
13. Applicant's remaining arguments filed 07 November 2025 have been fully considered but they are not persuasive.
Applicant has amended claim 4 to recite that “the moiety comprising an alkyne group is a radical of a compound of formula…” but it is unclear how this limitation is intended to limit the claim or increase clarity. Applicant’s specification provides no disclosure or teaching regarding a radical compound of this formula, and Fmoc deprotection chemistry does not proceed through a radical intermediate. Additionally, the “moiety comprising an alkyne group” of claim 1 has antecedent basis to a substructure covalently conjugated to a moiety comprising an alkyne group and a moiety comprising a diazirene group. No radical of this compound would be expected by a person of ordinary skill in the art within such a substructure reagent as claimed. Neither the Fmoc or amine groups as drawn would be present within a substructure reagent as claimed. Therefore this claim is indefinite and the rejection is maintained.
Applicant amended claim 1 to recite “the RNA is human RNA” however Petter teaches that RNA used in their method is human RNA as discussed fully above.
Applicant argues that one of ordinary skill in the art would not have expected the carbene moiety formed by diazirene to effectively react with RNA (remarks, pg. 16 ¶ 1). Applicant’s argument seems to suggest that Kumaravel’s teaching of diazirene warheads binding to aptamers (i.e., a highly structured RNA target) would not have led one having ordinary skill in the art to have a reasonable expectation of success that such a warhead would also bind highly structured naturally occurring RNAs. Petter teaches small molecules that bind to structured RNA targets and comprise an RNA binding moiety that covalently reacts with RNA (applicant’s remarks, pg. 16 ¶ 2). Kumaravel teaches small molecules that bind to structured RNA targets and comprises an RNA binding group that covalently reacts with RNA (applicant’s remarks, pg. 16 ¶ 3). As discussed fully above, it would have been obvious to one having ordinary skill in the art to have substituted the binding group taught by Petter with the photoactivatable binding group taught by Kumaravel to arrive at the instantly claimed invention with a reasonable expectation of success, with the motivation that photoactivation provides an additional level of control to such RNA binding experiments. Applicant’s arguments that diazirene was previously used to map protein structures and that RNAs are substantially different that proteins (remarks, pg. 15 ¶ 5) is not found persuasive because Kumaravel specifically teaches that diazirene warheads photo-crosslink small molecules to RNA. Therefore the rejection of claim 1 is maintained. Applicant’s additional arguments suggest that Domenyuk and Hermann fail to remedy the deficiencies of Petter, Kumaravel, Velagapudi and Guan, however since the rejection of claim 1 from which these claims depend was maintained, these rejections are also maintained.
14. 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.
Conclusion
15. No claims are allowed.
16. Claim 2 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.
17. Any inquiry concerning this communication or earlier communications from the examiner should be directed to BRIAN ELLIS YOUNG whose telephone number is (703)756-5397. The examiner can normally be reached M-F 0730 - 1700.
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/BRIAN ELLIS YOUNG/Examiner, Art Unit 1684
/JULIET C SWITZER/Primary Examiner, Art Unit 1682