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
Applicant’s remarks and amendments to the claims and specification filed April 17, 2026 are acknowledged. Claims 7, 16, 19, and 28 were amended. Claims 7-16, and 19-28 are pending and under consideration hereinafter.
Priority
Applicant’s priority claims to Application Nos. 63/111,916 and PCT/US2021/058699 are acknowledged. Claims 7-16, and 19-28 find support in Application No. 63/111,916. The effective filing date of all claims currently under examination is November 11, 2020, accordingly.
Withdrawn Rejections
Applicant’s amendments to the specification and claims are sufficient to overcome the objections to the same, which are withdrawn, accordingly.
Applicant’s remarks and amendments to the claims have been thoroughly reviewed, but are not found persuasive to place the claims in condition for allowance for the reasons that follow. Any rejection or objection not reiterated herein has been overcome by amendment.
Notice to Joint Inventors
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 Rejections - 35 USC § 103 – Kane, Reyes, Gabisonia, GenBank1, and GenBank2
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.
Claims 7-14, 16, 19-26, and 28 are rejected under 35 U.S.C. 103 as being unpatentable over Kane (Kane et al., 2006, Human Molecular Genetics, Vol. 15, No. 15, pg. 2285-2297; of record), Reyes (Reyes et al., 2008, Human Genetics, 123:665-667; of record), Gabisonia (Gabisonia and Recchia, 2018, Current Heart Failure Reports, 15:340-349; of record), GenBank1 (“Homo sapiens potassium inwardly-rectifying channel, subfamily J, member 11, mRNA (cDNA clone MGC:133230 IMAGE:40032947), complete cds,” GenBank: BC112358.1, available 21 Jan 2006; of record) and GenBank2 (“Mus musculus potassium inwardly rectifying channel, subfamily J, member 11 (Kcnj11), transcript variant 1, mRNA,” GenBank: NM_010602.3, available 6 July 2019; of record). The rejections that follow are maintained and modified as necessitated by Applicant’s amendments to the claims.
The specification states that the methods “can be used to slow, delay, or reverse heart failure (e.g., slow, delay, or reverse the development of heart failure) in a mammal (e.g., a human having, or at risk of developing heart failure based, at least in part, on the presence of a mutation (e.g., c.67G>A single nucleotide variant) in both copies of a KCNJ11 gene present in the human)” (pg. 25, lines 27-31). Claim 7 recites “treating a mammal developing heart failure… thereby slowing development of said heart failure within said mammal.” Claim 19 recites “treating a mammal having heart failure… thereby reversing said heart failure within said mammal.” Accordingly, claim 7 is interpreted as a method of slowing or delaying development of heart failure in a mammal developing heart failure, e.g., due to hypertension, coronary artery disease, presence of a particular genetic variant, etc. Claim 19 is interpreted as a method of reversing one or more symptoms of heart failure in a mammal which has heart failure.
Regarding claims 7 and 19, Kane teaches that heart failure is a “growing epidemic, with systemic hypertension a major risk factor for development of disease” (Abstract). Kane demonstrates that “knockout of the KCNJ11 gene, encoding [] Kir6.2” in a mammalian model of hypertension “predispose[s] to heart failure and death” (Abstract, see also results in at least Fig. 1-2). Kane teaches that their analysis demonstrates that “loss of channel function renders the heart vulnerable to heart failure,” and “presents KATP channel dysfunction as a novel channelopathy in heart failure” (pg. 2293, right col.). Kane concludes that “intact KCNJ11-encoded KATP channel is thus a required safety element preventing hypertension-induced heart failure” (Abstract). Kane teaches that genetic variants of KCNJ11 have been identified in population-based studies, but states that an association between mutations in KCNJ11 and cardiac disease had not been established at the time of publication, i.e., 2006 (pg. 2293, right col.).
Reyes examined the association between subjects homozygous for the c.67G>A variant of the KCNJ11 gene and cardiac disease using a “community-based cross-sectional cohort”(“A common single nucleotide polymorphism (67G>A) in human KCNJ11 corresponds to glutamic acid or lysine at residue 23 of Kir6.2” pg. 665, right col.; “we explored the relationship between this KATP channel polymorphism and subclinical heart disease in the community,” pg. 665, right col.; Table 1; pg. 666, left col.). Reyes teaches the c.67G>A variant of the KCNJ11 gene impairs KATP channel function (pg. 665, right col.). Reyes teaches that the “KK genotype,” i.e., homozygosity for the c.67G>A variant of the KCNJ11 gene, “was associated with greater left ventricular size among subjects with increased stress load due to hypertension” (Abstract; Fig. 1; “synergistic effect on LV size of KK genotype and LV mass, a marker of chronic cardiac stress load (Fig. 1), further validated the impact of Kir6.2 E23K on cardiac structure in hypertension,” pg. 666, right col.). Importantly, Reyes’ observations in hypertensive KK genotype subjects, and Kane’s observations in Kir6.2-KO mammals with respect to key predictors of heart failure are similar; both exhibit increases in left ventricular size and mass (see Kane, Fig. 3, “[h]ypertension is the most common risk factor for congestive heart failure, and LV enlargement is an established precursor of symptomatic ventricular dysfunction,” pg. 666, right col.; Reyes, Fig. 1, “[u]nderlying the pathogenesis of the heart failure syndrome is an extensive ventricular remodeling… in hypertension, the magnitude of left ventricular mass increase is a predictor of long-term prognosis and of the rate of decompensation to heart failure,” pg. 2287).
Based on Kane and Reyes, the skilled artisan would conclude that subjects homozygous for the c.67G>A variant of the KCNJ11 gene will have impaired KCNJ11-encoded KATP channel function, resulting in ventricular remodeling underlying the pathogenesis of heart failure. Kane teaches an “intact KCNJ11-encoded KATP channel is [] a required safety element preventing hypertension-induced heart failure.” Indeed, Kane demonstrates that treatment of Kir6.2-KO mammals with a pharmacological agent which bypasses dysfunctional KATP channel activity reverses ventricular remodeling, averts heart failure, and decreases mortality (Fig. 7; pg. 2290-2292). Thus, the skilled artisan would have been motivated to design treatment modalities which restore intact KCNJ11-encoded KATP channels for KK genotype subjects developing heart failure, or with heart failure. However, neither Kane nor Reyes teach or suggest administering to cardiac cells of mammalian subject a nucleic acid encoding a Kir6.2-E23 polypeptide, which is interpreted as a nucleic acid encoding a Kir6.2 polypeptide comprising a glutamic acid at residue 23 (pg. 2, lines 1-3).
Gabisonia teaches that “[t]he difficulty of pharmacologically targeting receptors and intracellular pathways involved in the pathogenesis of HF led investigators, many years ago, to propose cardiac gene therapy” comprising “cell-directed delivery of exogenous genes (transgenes) [that] produce “curative proteins able to compensate for pathological downregulations or to counteract detrimental molecular processes” (pg. 340, right col.). Gabisonia teaches multiple gene therapy strategies in which transgenes have been delivered to cardiac cells of mammalian and human subjects with or at risk of having heart failure (“SERCA2a gene transfer to cardiac cells… successful tests in isolated human cardiomyocytes, murine, and porcine models, this strategy was finally translated to the clinics with… CUPID… the first clinical trial of cardiac gene therapy for HF,” pg. 341; “AC6 gene transfer by adenoviral vectors” to “a swine model of HF,” and “intracoronary delivery of AC6 carried by adenoviral vectors… in patients with symptomatic HF… [t]his intervention improved LV function more than the standard HF therapy,” pg. 343, left col.; “SDF-1 direct trans-endocardial delivery with the plasmid vector in 17 subjects with ischemic cardiomyopathy… the treatment is more specifically effective in patients with very depressed ejection fraction, which might represent the target population in subsequent trials,” pg. 343).
Gabisonia emphasizes throughout that the choice of the target gene and delivery vector are imperative to success of gene therapy methods (Abstract; pg. 340). Gabisonia teaches that this challenge is not unique, as other therapeutic approaches are also “plagued by similar problems,” and suggests that the field is activity overcoming these challenges by identifying “new molecular targets with remarkable curative potential,” and designing vectors with improved therapeutic profiles (Abstract; pg. 341, right col.; Conclusions). Gabisonia concludes that investigators in the area of heart failure gene therapy “should persist in their efforts” (Conclusions).
Finally, GenBank1 and GenBank2 teach nucleic acids encoding mammalian and human Kir6.2 polypeptides, respectively, wherein each comprises a glutamic acid at residue 23 (“/translation= “MLSRKGIIPEEYVLTRLAEDPAE…,” BC112358.1; “/translation = “MLSRKGIIPEEYVLTRLAEDPAE…,” NM_010602.3). Thus, nucleic acids encoding the recited polypeptide were also known in the prior art.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have administered a nucleic acid encoding a Kir6.2-E23 polypeptide to cardiac cells of a mammalian or human subject having or developing heart failure, and identified as having a c.67G>A nucleotide variant in both copies of a KCNJ11 gene, to thereby treat the subject by slowing the development of or reverse heart failure. It would have amounted to administering a known nucleic acid encoding a wildtype polypeptide, to a subject homozygous for a known mutation in the gene encoding the polypeptide, which predisposes to heart failure, by known means to yield predictable results.
Based on Kane and Reyes, the skilled artisan would conclude that subjects homozygous for the c.67G>A variant of the KCNJ11 gene (“KK genotype”) will have impaired KCNJ11-encoded KATP channel function, resulting in ventricular remodeling underlying the pathogenesis of heart failure. Kane teaches an “intact KCNJ11-encoded KATP channel is [] a required safety element preventing hypertension-induced heart failure,” and thus, the skilled artisan would be motivated to design treatment modalities which restore expression of an “intact KCNJ11-encoded KATP channel” in KK genotype subjects at risk of or having heart failure. Kane demonstrates that treatment of Kir6.2-KO mammals with a pharmacological agent which bypasses dysfunctional channel activity reverses ventricular remodeling, averts heart failure, and decreases mortality (Fig. 7; pg. 2290-2292). Kane’s study was published in 2006, which is well before the gene therapy strategies taught by Gabisonia. The skilled artisan would have recognized that a known nucleic acid encoding a wildtype Kir6.2 polypeptide, i.e., Kir6.2-E23 taught by GenBank1 or GenBank2, could be delivered to cardiac cells in vivo by means taught by Gabisonia. The skilled artisan would reasonably predict that such a method would restore expression of an “intact KCNJ11-encoded KATP channel” in the recipient cardiac cells (i.e., meeting the “wherein” limitations of the claims), and treat KK genotype subjects at risk of developing, or having heart failure, based on the successful examples of heart failure gene therapy taught by Gabisonia, and the success of Kane’s pharmacological treatment in Kir6.2-KO mammals.
Regarding claims 8 and 20, the methods rendered obvious above comprise a human subject.
Regarding claims 9 and 21, the methods rendered obvious above comprise cardiac cells.
Regarding claims 10 and 22, the Kir6.2-E23 polypeptide taught by GenBank1 is a human Kir6.2-E23 polypeptide.
Regarding claims 11-12, and 23-24, Gabisonia teaches gene therapy strategies in which nucleic acids are administered to cardiac cells in the form of a viral vector, including adeno-associated viral vectors and adenoviral vectors (“AAV,” pg. 341, 343, Conclusions; “adenoviral vectors,” pg. 343, left col.). The obviousness of administering a Kir6.2-E23 polypeptide taught by GenBank1 or GenBank2 to cardiac cells in a mammalian or human subject via a method taught by Gabisonia is described above in paragraph 9 and applied here.
Regarding claims 13-14, and 25-26, Gabisonia teaches gene therapy strategies in which nucleic acids are administered to cardiac cells in the form of a non-viral vector, including an expression plasmid (“plasmid DNA,” pg. 341, left col.; “plasmid vector,” pg. 343, right col.). The obviousness of administering a Kir6.2-E23 polypeptide taught by GenBank1 or GenBank2 to cardiac cells in a mammalian or human subject via a method taught by Gabisonia is described above in paragraph 9 and applied here.
Regarding claims 16 and 28, Gabisonia teaches gene therapy strategies in which nucleic acids are administered to cardiac cells via intracoronary injection (“intracoronary AAV1/SERCA2a,” pg. 341; “intracoronary infusion,” “intracoronary delivery,” pg. 341, 343). The obviousness of administering a Kir6.2-E23 polypeptide taught by GenBank1 or GenBank2 to cardiac cells in a mammalian or human subject via a method taught by Gabisonia is described above in paragraph 9 and applied here.
Claim Rejections - 35 USC § 103 – Kane, Reyes, Gabisonia, GenBank1 and GenBank2, in view of Tilemann
Claims 15 and 27 are rejected under 35 U.S.C. 103 as being unpatentable over Kane (Kane et al., 2006, Human Molecular Genetics, Vol. 15, No. 15, pg. 2285-2297; of record), Reyes (Reyes et al., 2008, Human Genetics, 123:665-667; of record), Gabisonia (Gabisonia and Recchia, 2018, Current Heart Failure Reports, 15:340-349; of record), GenBank1 (“Homo sapiens potassium inwardly-rectifying channel, subfamily J, member 11, mRNA (cDNA clone MGC:133230 IMAGE:40032947), complete cds,” GenBank: BC112358.1, available 21 Jan 2006; of record), and GenBank2 (“Mus musculus potassium inwardly rectifying channel, subfamily J, member 11 (Kcnj11), transcript variant 1, mRNA,” GenBank: NM_010602.3, available 6 July 2019; of record) as applied to claims 7-14, 16, 19-26, and 28 above, in further view of Tilemann (Tilemann et al., 2012, Circulation Research, 10:777-793; of record). The rejections that follow are maintained and modified as necessitated by Applicant’s amendments to the claims.
The teachings of Kane, Reyes, Gabisonia, GenBank1, and GenBank2 are described above and applied as to claims 7-14, 16, 19-26, and 28 therein.
None of Kane, Reyes, Gabisonia, GenBank1, or GenBank2 teach that the nucleic acid encoding the Kir6.2-E23 polypeptide is operably linked to a promoter sequence.
Tilemann also teaches gene therapy strategies for heart failure (“Recent advances in understanding of the molecular basis of myocardial dysfunction, together with the evolution of increasingly efficient gene transfer technology, have place heart failure within reach of gene-based therapy,” Abstract; “we will highlight new strategies for the treatment of heart failure by gene transfer, focusing on the vectors, targets, and delivery methods along with the recent clinical results from early clinical trials,” pg. 777, left col.; “Vectors Systems Used in Cardiovascular Gene Transfer,” Table 1). Tilemann teaches promoter sequences, which when operably linked to transgenes in vectors, drive expression of the transgene in the heart (“the use of cardiac specific promoters,” “the most commonly used promoter, the cytomegalovirus (CMV) promoter,” “the most promising promoter for cardiac-specific expression that is suitable for AAV vectors is… the chicken cardiac Troponin T promoter,” see “Transcriptional Targeting,” pg. 779-78). Tilemann teaches promoter sequences which are compatible with the delivery vectors of Gabisonia (“One promoter that was used in both adenoviral and AAV vectors…,” “the most promising promoter for cardiac-specific expression that is suitable for AAV vectors…,” pg. 780).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have operably linked the nucleic acid encoding the Kir6.2-E23 polypeptide in the method rendered obvious above to a promoter sequence in view of Tilemann. It would have amounted to combining a known element for expressing a transgene from a vector, in a vector expressing a transgene, by known means to yield predictable results. The skilled artisan would have expected that the promoter sequence and transgene would perform the same functions when combined as in their respective references; the promoter sequence would drive expression of a transgene, and the transgene would provide a template for production of the Kir6.2-E23 polypeptide. The skilled artisan would have had a reasonable expectation of success in using the combination in the obvious method because Tilemann is concerned with treating heart failure with gene therapy, and teaches a variety of known promoter sequences that promote transgene expression in the heart and are compatible with the delivery vectors of Gabisonia. The skilled artisan would have been motivated to operably link the nucleic acid encoding the Kir6.2-E23 polypeptide to a promoter sequence because as evidenced by Tilemann, and as is common knowledge in the art, a promoter sequence facilitates transgene expression, which is central to the obvious method above.
Response to Remarks - 35 USC § 103
Applicant’s remarks regarding the § 103 rejections raised in the prior action have been reviewed. Applicant indicates that claims 7 and 19 have been amended. Applicant summarizes the disclosures of the prior art references, and concludes that “the combinations of these references fail to teach or suggest that a mammal having a c.67G> A single nucleotide variant in both copies of a KCNJ11 gene is developing heart failure (as in claim 7 as amended herein) or is experiencing heart failure (as in claim 19).” Applicant “disagrees with Examiner’s assertions” regarding Kane and Reyes, and states that Kane “fails to mention any particular mutations with the KCNJ11 gene, and the Reyes reference suggests that a mammal having a Kir6.23 K23 polypeptide (encoded by 67A>G KCNJ11 variant) might develop “subclinical maladaptive cardiac remodeling”” (emphasis preserved). Applicant states that “[a]t best, the combination of Kane and Reyes [] suggests that a mammal having a Kir6.2 K23 polypeptide… might be developing cardiac remodeling, which might lead to heart failure” (emphasis preserved).
Applicant indicates that the ordinarily skilled artisan, “given this uncertainty,” “would not have been motivated to design a gene therapy technique to provide a replacement gene that might treat a mammal that might be developing heart disease” (emphasis preserved). Applicant indicates that “[b]ased on the teachings of the Kane and Reyes references,” the ordinarily skilled artisan would have had no reasonable expectation of successfully slowing development of heart failure, or reversing heart failure, within a mammal developing heart failure and having heart failure, and identified as having a c.67G>A single nucleotide variant in both copies of a KCNJ11 gene by administering a nucleic acid encoding a Kir6.2-E23 polypeptide. Applicant indicates that that Examiner has based their obviousness analysis on Applicant’s specification, which Applicant indicates “clearly demonstrates that the presence of a c.67G>A single nucleotide variant in both copies of a KCNJ11 gene (also referred to as a KK genotype) can be used to identify a mammal as having, or as developing heart failure.”
First, Examiner notes that the obviousness rejection was not based on the disclosures of Kane and Reyes alone, nor was the obviousness rejection based on only the selected statements within Kane and Reyes which Applicant references in their remarks. The obviousness rejection was based on the disclosures of Kane, Reyes, Gabisonia, and GenBank1 and GenBank2 as a whole, and in combination, as they would have been understood by the ordinarily skilled artisan. 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). For example, neither Kane nor Gabisonia were relied upon to “mention any particular mutations within the KCNJ11 gene.” Similarly, Reyes, which was relied upon to describe the particular mutation within the KCNJ11 gene, and provide evidence supporting that KK genotype mammals were at risk of heart failure, was not the only reference relied upon to provide a reasonable expectation of success, as will be further described below. Applicant’s remarks regarding the references individually, or regarding only the Kane and Reyes references, are not found convincing.
Examiner’s conclusion of obviousness was not based upon improper hindsight reasoning as Applicant alleges. The obviousness rejection in the prior action and above 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. The information which Applicant alleges was only available in their disclosure, i.e., that KK genotype individuals are at risk of developing or having heart failure, was available in the prior art as it would be understood by the ordinarily skilled artisan. Specifically, Reyes identifies that hypertensive mammals homozygous for a 67G>A single nucleotide variant in the KCNJ11 gene (i.e., hypertensive “KK” genotype mammals) exhibit LV enlargement. The skilled artisan would know, at least based on Reyes and Kane, and their general knowledge in the field of cardiac disease, that “h]ypertension is the most common risk factor for congestive heart failure, and LV enlargement is an established precursor of symptomatic ventricular dysfunction” (Kane, pg. 666). The skilled artisan also would have known that "intact KCNJ11-encoded KATP channel is[] a required safety element preventing hypertension-induced heart failure” based on Kane, and that treatment of Kir6.2-KO mammals with a pharmacological agent which bypasses dysfunctional KATP channel activity reverses ventricular remodeling, averts heart failure, and decreases mortality (Fig. 7; pg. 2290-2292). The prior art provides the information relied upon by Applicant to allege improper hindsight reasoning. Applicant’s arguments related to improper hindsight reasoning are not found convincing.
The prior art also provides sufficient evidence that the skilled artisan would have had a reasonable expectation of success in treating a mammal developing heart failure, or having heart failure, and identified as having the “KK” genotype (i.e., homozygous for c.67G>A mutation in the KCNJ11 gene), by administering a nucleic acid encoding a Kir6.2 polypeptide which restores a functional Kir6.2 encoded by KCNJ11 (i.e., a Kir6.2-E23 polypeptide). The amendments to the claims do not modify the scope of the claims so as to overcome the rejections of record, which are maintained above, accordingly. The previous rejections considered the scope of the amended claims (see paragraph 10 of the prior action). The prior art provides sufficient evidence that the skilled artisan could have averted or reversed heart failure in a mammal with the KK genotype by restoring a functional Kir6.2 (i.e., Kir6.2-E23) encoded by a wildtype KCNJ11 gene. See paragraph 11 of the prior action describing the findings of Kane and Reyes, which support I) that mammals homozygous for the c.67G>A variant of KCNJ11 have impaired KCNJ11-encoded KATP channel function (i.e., Kir6.2 function), resulting in ventricular remodeling underlying heart failure, and importantly, I) that treatment of Kir6.2-KO mammals with a pharmacological agent which bypasses dysfunctional KATP function reverses ventricular remodeling, averts heart failure, and decreases mortality. Gabisonia establishes that cardiac gene therapy was a known, viable strategy to restore KCNJ11-encoded KATP channel function, which may be preferable to pharmacological interventions, and the sequences encoding mammalian Kir6.2-E23 were known as evidenced by GenBank. Together, the skilled artisan would have had the means and motivation, and a reasonable expectation of success, that delivering a nucleic acid encoding a Kir6.2-E23 polypeptide would slow or reverse heart failure in KK genotype mammals.
“Obviousness does not require absolute predictability of success.” Id. at 903, 7 USPQ2d at 1681. Applicant has not provided any evidence that there was no reasonable expectation of success. Indeed, Applicant’s remarks appear to concede that there was at least some degree of predictability (“At best, the combination of the Kane and Reyes references suggests that a mammal having a Kir6.2 K23 polypeptide (encoded by 67A>G KCNJ11 variant) might be developing cardiac remodeling, which might lead to heart failure,” see remarks). Applicant’s disclosure does not provide any working examples of the method that, for example, provide evidence that the prior art disclosures were not, in fact, predictable. See MPEP 2143.02. Applicant’s remarks regarding the amendments to the claims, or the alleged lack of predictability based on the prior art are not found convincing.
Conclusion
No claims are allowed.
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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/JENNA L PERSONS/Examiner, Art Unit 1637
/Jennifer Dunston/Supervisory Patent Examiner, Art Unit 1637
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