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 .
Claims status
Applicant’s reply filed 5/7/2026 is acknowledged.
Claims 51, 53-55 are cancelled. Claims 1-4,19, 21-22, 28-32, 36,3 9-50, 52 and 56-59 is/are currently pending with claims 1, 3-4, 21-22, 28-32, 36 and 39-43 is/are withdrawn. Claims 2, 19, 44-50, 52, 56-59 is/are under examination.
Withdrawn Objections
The objections presented herein represent the full set of objections currently pending in this application. Any objections not specifically reiterated are hereby withdrawn.
Claim Rejections - 35 USC § 112(d) - Withdrawn
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Rejection of Claims 50, 51, 53-56 under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, 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of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends is withdrawn in light of claim amendment or cancellation.
Claim Rejections - 35 USC § 112(a) - Withdrawn
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.
Written Description
Rejection of Claims 50, 51, 53-56 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 is withdrawn in light of claim amendment or cancellation.
Enablement/ Scope of Enablement
Rejection of Claims 50, 51 and 53-56 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, as failing to comply with the scope of enablement or full enablement requirement is withdrawn in light of claim amendment or cancellation.
Claim Rejections - 35 USC § 103 – Maintained, New for claim 56 necessitated by claim amendment
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Rejection of Claims 51, 53-55 under 35 U.S.C. 103 as being unpatentable over Priori (US 20210030894 A1, effective filing date April 5, 2018; ref of record) in view of Stanczyk et al (Journal of Cell Science, 2018; ref of record) in view of NP_000247.2, NCBI Reference Sequence of myosin-binding protein C, cardiac-type [Homo sapiens] (available online since June 5, 2007, ref of record) and NP_032679.2, NCBI Reference Sequence of myosin-binding protein C, cardiac-type [Mus musculus] (available online since March 23, 2007, ref of record) as evidenced by NCBI RNA Fundamentals (ref of record) is moot due to claim cancellation.
Claims 2, 19, 44-50, 52, 57-59 remain rejected and claim 56 is rejected under 35 U.S.C. 103 as being unpatentable over Priori (US 20210030894 A1, effective filing date April 5, 2018; ref of record) in view of Stanczyk et al (Journal of Cell Science, 2018; ref of record) in view of NP_000247.2, NCBI Reference Sequence of myosin-binding protein C, cardiac-type [Homo sapiens] (available online since June 5, 2007, ref of record) and NP_032679.2, NCBI Reference Sequence of myosin-binding protein C, cardiac-type [Mus musculus] (available online since March 23, 2007, ref of record) as evidenced by NCBI RNA Fundamentals (ref of record).
Regarding claim 2, Priori teaches a method of treating catecholaminergic polymorphic ventricular tachycardia (CPVT), an inherited arrhythmia, in a patient which arises due to gain-of function mutation in RYR2 gene ( = mutation that results in increased protein function as required for claim 2; [0003], lines 1-4, 18-21, Example 1).
Regarding claims 48-50, 52, 56, Priori teaches CPVT which is an inherited arrhythmia that can result in heart failure and is caused by gain-of-function mutation (i.e. excessive protein activity) in RYR2 gene and the RYR2 protein functions to release Ca2+ during diastolic phase ([0003], lines 1-4, 18-21). Therefore, Priori teaches a method of treating a cardiac disorder as required for claims 2, 48-50, 52, 56.
Priori’s method comprises delivering to a patient a transgene encoding calsequestrin 2 (CASQ2) gene via viral gene therapy ([0003], lines 4-10). Vector taught include “plasmids, DNA vectors, RNA vectors, virions, or other suitable replicon (e.g., viral vector) ([0088], line 6 and [0110]). In their examples, Priori use recombinant AAV 2/9 vector ([0111], [0143], [0148]). Therefore, Priori teaches a method of treating a cardiac disorder associated with RYR2 gene mutations that increase RYR2 function, the method comprising administering to a subject a viral vector such as rAAV comprising a nucleotide sequence encoding a polypeptide. Priori teaches CASQ2 as the polypeptide.
Regarding claim 19, Priori teaches vectors such as “plasmids, DNA vectors, RNA vectors, virions, or other suitable replicon (e.g., viral vector)” ([0088], line 6). Compared to other types of RNA, such tRNA and rRNA etc, messenger RNAs are translated to form polypeptides therefore RNA vectors (as taught by Priori) that result in expression of a polypeptide are mRNA (See NCBI RNA Fundamentals in PTO-892). Therefore, Priori teaches RNA vectors that comprise mRNA nucleotide sequences.
Regarding claims 57-59, Priori teaches rAAV 2/9 i.e. a recombinant AAV vector with AAV9 serotype capsid (Example 1, [0111], [0143], [0148]).
Priori does not teach a polypeptide comprising C-terminal domain of MYBPC3 and thus does not teach polypeptides comprising the sequences of SEQ ID NOs: 3, 5, 11 or 13.
Stanczyk teaches MYBPC3 protein and its C-terminal fragments that interact with RYR2 protein (Figure 1, 2) and that MYBPC3 interaction with RYR2 suppresses RYR2 mediated spontaneous Ca2+ release (Figure 5). Stanczyk also teaches that functional alterations of RYRs are associated with several human diseases, specifically RYR2 mutations have a direct causative role in the heart rhythm disorders such as CPVT (page 1, right column, para 2). Their results show that c-terminal domains of MYBPC3 (domain C5-C10) interact with N-terminal domains of RYR2 and this interaction inhibits RYR2 function (Figure 5) and they suggest that this interaction could be relevant for arrhythmic cardiomyopathies that are known to be caused by leaky RYR2 channel with increased spontaneous Ca2+ release (page 6, right column, para 1, line 1).
Furthermore, Stanczyk specifically teaches the binding between RYR2 and various MYBPC3 C-terminus fragments and, that the fragment containing C6-C8 domains has the strongest binding with RYR2 (Figure 2B). Figure 2A shows the structure of MYBPC3 C-terminus (amino acid 650-1274) and the various domains (C5 to C10 domains), including C6-C8 fragment (C6 domain starts at amino acid 770 and C8 domain ends at amino acid 1065). Table S1 lists primers that were used to extract the various MYBPC3 C-terminus fragments from human MYBPC3 cDNA to generate human MYBPC3 protein and its fragments used. Figure 5 shows that the c-terminal fragment of MYBPC3 (C6-C10) reduces RYR2 mediated spontaneous Ca2+ leak.
Regarding the amino acid sequences recited in claims 2, 44-47, SEQ ID No. 5 and 13 are a 501 amino acid fragment of MYBPC3 C-terminus comprising C6-C10 domains derived from mouse and human respectively. SEQ ID No. 3 and 11 are a 292 amino acid fragment of MYBPC3 C-terminus comprising C6-C8 domains derived from mouse and human respectively.
Although Stanczyk teaches the c-terminal fragment of MYBPC3 including the fragment C6-C8, Stanczyk does not explicitly teach the exact amino acid sequence of a MYBPC3 protein or its fragments.
NP_000247.2 (human) and NP_032679.2 (mouse) teach the sequence of human and mouse MYBPC3 protein. Using the teachings of Stanczyk regarding the structure of MYBPC3 C-terminus (amino acid 650-1274) that comprises the C6-C8 domains (amino acid 770-1065) and, the sequence of human and mouse MYBPC3 protein taught by NP_000247.2 (human) and NP_032679.2 (mouse), an ordinary artisan would derive polypeptide sequences identical to sequences recited in claims 44-47 (see sequence alignments below).
Therefore, it will be obvious to person of ordinary skill in the art before the effective filing date of the claimed invention to utilize the teaching of Stanczyk regarding MYBPC3-inhibition of RYR2 and modify the method of treatment of CPVT, taught by Priori, by substituting CASQ2 of Priori with MYBPC3 or its C-terminal fragments taught by Stanczyk. It would be further obvious to a person of ordinary skill in the art before the effective filing date, when combining Priori with Stanczyk, to use the human and/or mouse MYBPC3 polypeptide sequences taught by NP_000247.2 (human) and NP_032679.2 (mouse) that comprise sequences identical to SEQ ID No. 3, 5, 11 and 13.
Owing to Stanczyk’s teachings, an ordinary artisan would recognize that MYBPC3 and its C-terminal fragments suppress RYR2-mediated spontaneous Ca2+ release and would be motivated to use MYBPC3 and its C-terminal fragments to inhibit excess RYR2 function observed in CPVT which results from gain-of-function mutations in RYR2 (as taught by Priori). Furthermore, an ordinary artisan would be motivated to use sequences taught by NP_000247.2 (human) and NP_032679.2 (mouse) to generate viral vectors encoding human and/or mouse MYBPC3 polypeptide sequences because viral vectors with mouse sequences would be useful for preclinical studies with mouse models while human sequences would be useful for studies with human cells.
An ordinary artisan would reasonably expect to administer MYBPC3 or its C-terminal fragments as taught by Stanczyk to a subject using viral vectors to treat cardiac disorders because Priori teaches the design and delivery of transgenes using viral vectors to an animal subject which result in expression of the transgene in cardiac tissue and alleviation of cardiac dysfunction (Example 1) and Stanczyk teaches binding between RyR2 and MYBPC3 in human cardiac tissue (page 2, left column, para 3), human embryonic kidney cells (Figure 2) and porcine cardiac tissue (Figure 3) as well as inhibitory effect of MYBPC3 on RYR2 spontaneous activity in human embryonic kidney cells (Figure 5F). Thus, an ordinary artisan would reasonably except that using Priori’s viral vector and administration method to deliver c-MYBPC3 fragments would result in expression of c-MYBPC3 fragment in cardiac tissue wherein the fragments would be expected to bind RYR2 and modulate its function, as taught by Stanczyk. An ordinary artisan would reasonably expect to generate viral vectors encoding MYBPC3 or its C-terminal fragments as taught by Stanczyk using standard PCR techniques such as used by Stanczyk (Materials and Methods: Plasmid constructs) and sequences taught by NP_000247.2 (human) and NP_032679.2 (mouse).
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Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the effective time of filing of the invention, especially in the absence of evidence to the contrary.
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Response to Arguments
Applicant’s arguments filed 5/7/2026 with respect to the U.S.C. 103 rejection claim(s) 2, 19, 44-52, 57-59 have been considered but are unpersuasive.
First, Applicant argue that an ordinary artisan lacks motivation to combine the cited references (pages 9-10).
In support, Applicant allege that “the Examiner relies on the rationale of a simple
substitution of one known element for another to obtain predictable results under M.P.E.P. § 2143(1)(B)” which requires that substitution be predictable and this condition is not met (page 9-10, bridging para). Applicant also allege that Priori “explicitly teaches that intervention of pathways associated with RYR2 is not needed” pointing to [0095] and [0153] in Priori that states “dominant CPVT can be treated without the need to provide the patient with a functional RYR2, CALM1, or CALM3 protein or a transgene encoding the same" (emphasis added) and "Surprisingly, CASQ2 gene transfer alone, without the need for RYR2 delivery, was found to prevent the physiological sinus rhythm that triggers arrythmias due to adrenergic activation." (page 10, para 1).
In response, at first it must be noted that, KSR rationale (B) was not relied upon in the rejection. As detailed in the rejection, Priori and Stanczyk along with NP_000247.2 (human) and NP_032679.2 (mouse) provide sufficient teachings, suggestions and motivation to render the instant claims prima facie obvious. The rejection also details reasonable expectations of an ordinary artisan when combining the prior art references.
Regarding [0095] and [0153] in Priori, these statements do not suggest that according to Priori CPVT can be treated without any intervention to the entire RYR2-associated pathway. Instead, it means that according to Priori CPVT can be treated without the direct delivery of the RYR2 gene or peptide.
Next, Applicant argue that an ordinary artisan would not have a reasonable expectation of success in view of the cited references (page 11-15).
In support, Applicant allege that “Stanczyk's data do not establish predictability of the claimed therapeutic outcome” (pages 11-13). Applicant note that “Stanczyk did not test any mutated form of RYR2 in any system.” and allege that “Mere in vitro binding experiments on the wild-type, non-diseased state do not establish predictability of an inhibitory effect on the mutationally increased RYR2 expression” (page 11-12. bridging para). Applicant also contend that Stanczyk “is not a body of data from which a person of ordinary skill in the art could have predicted the in vivo therapeutic outcome as instantly claimed” because of the various functional parameters tested only one was affected and “Stancyzk does not provide any in vivo animal model data.” (page 12, para 1, 2). Applicant also allege that functional analysis done using HEK cells in Stancyzk “is not functional evidence that supports a finding of in vivo therapeutic predictability” (page 12, para 3).
In response, regarding the level of predictability required for obviousness analysis, see MPEP 2143.02. “Where there is a reason to modify or combine the prior art to achieve the claimed invention, the claims may be rejected as prima facie obvious provided there is also a reasonable expectation of success. The reasonable expectation of success requirement refers to "the likelihood of success" in combining or modifying prior art disclosures to meet the limitations of the claimed invention. See Elekta Ltd. v. ZAP Surgical Sys., Inc., 81 F.4th 1368, 1375, 2023 USPQ2d 1100 (Fed. Cir. 2023) and Intelligent Bio-Sys., Inc. v. Illumina Cambridge Ltd., 821 F.3d 1359, 1367, 119 USPQ2d 1171, 1176 (Fed. Cir. 2016).)”. “Conclusive proof of efficacy is not required to show a reasonable expectation of success. OSI Pharm., LLC v. Apotex Inc., 939 F.3d 1375, 1385, 2019 USPQ2d 379681 (Fed. Cir. 2019).” “Obviousness does not require absolute predictability, but at least some degree of predictability is required. Evidence showing there was no reasonable expectation of success may support a conclusion of nonobviousness.” (emphasis added).
Applicant have not established that there was no reasonable expectation of success when combining the teachings of Priori and Stanczyk along with NP_000247.2 (human) and NP_032679.2 (mouse). Applicant have not established why in vitro binding experiments on the wild-type RYR2 that shows that MYBPC and its C-terminal fragments bind and inhibit RYR2 would not suggest and motivate an ordinary artisan to use MYBPC and its C-terminal fragments bind and inhibit RYR2 in vivo, especially in diseases associated with pathologically increased RYR2 function.
Regarding the quality or quantity of Stanczyk’s body of data, this argument has been addressed in the OA dated 7/16/2024 (page 17). To reiterate, reduction in RYR2 spontaneous Ca²+ oscillations is the key parameter relevant for cardiac disorders such as CPVT wherein RYR2 spontaneous Ca²+ oscillations cause arrhythmia. Therefore, Stanczyk's results showing MYBPC3 can inhibit this key parameter that is highly relevant for cardiac pathology. This is especially the case because RYR2 inhibition is a known treatment for arrythmia (see Figure 1 in Watanabe, ref of record). Furthermore, as noted previously, an ordinary artisan recognizes the utility of evidence garnered from in vitro experiments. For example, Handhle (ref of record) showed that Casq2 binds and inhibits RyR2 spontaneous activity using the same systems as Stanczyk (Figures 1-3). Subsequently, Priori showed that Casq2 can be used to inhibit increased RyR2 activity in CPVT mouse model (Example 1).
Regarding Handhle, Applicant contend that “The success of any particular in vitro to in vivo translation turns on the particularities of the molecule and the mechanism, not on the existence of a previous successful translation involving a totally different molecule. "[H]ope that a potentially promising drug will treat a particular cancer is not enough to create a reasonable expectation of success in a highly unpredictable art." OSI Pharms., LLC v. Apotex Inc., 939 F.3d 1375, 1385 (Fed. Cir. 2019).” (page 13, para 1)
In response, indeed “success” does depend on particularities of the molecule and the mechanism. However, as noted above, obviousness analysis does not require “success”, it requires reasonable expectation of success. Handhle and its relation to Priori is thus relevant because it establishes the utility of in vitro experiments and the reasonable expectations that are derived from them when conducting in vivo experiments.
Of note, Applicants have not established that gene therapy for RYR2-based arrythmias is a “highly unpredictable art”.
Next, in support of lack of reasonable expectation of success, Applicant allege that they demonstrate that MYBPC3 binding does not predictably correlate with function (page 13-14). Applicant point to figure 5A that shows that fragments C6-C9 and C6-C7 reduced Fractional Shortening, an indicator of heart contractility, and are not as effective as other fragments (page 13, para 4). Applicant also point to the specification that states “C7-C8 are sufficient to bind RYR2” (page 13-14, bridging para). Applicant conclude that The Examiner cannot rely on Fig. 2B of Stancyzk to predict that C6-C8 will perform at least as well as C6-C10 without also accepting that C6-C7, which Fig. 2B of Stanczyk shows is comparable to C6-C8, should perform similarly. Applicant has demonstrated C6-C7 does not in fact perform similarly and instead causes deleterious effects in vivo..” (page 14, para 1)
In response, it is critical to note here that the claims are not limited to a vector encoding only the C-terminus or any specific domains of the C-terminus of MYBPC3. Since a full-length MYBPC3 protein comprises a C-terminus, including C6-C8 domains, the instant method embraces administering any portion of MYBPC3 protein as long as it comprises the full-length C-terminus (Claims 2, 45, 47) and/or at least the C6-C8 domains (claims 2, 44, 46).
Next, Applicant’s data is from mouse and mouse proteins while Stancyk is from human cells and proteins. Thus, some species differences is expected. Applicant’s data showing that C7 is essential for and C7-C8 are sufficient to bind RYR2 does not show that C7 or C7-C8 have the strongest binding affinity. Thus, this data does not support Applicant’s argument that “Examiner's assumption would lead to an expectation that all 4 of the above-referenced fragments would perform comparably in vivo” (page 13-14, bridging para).
Data comparing the strength of interaction is shown in Figure 11 which is largely similar to Fig. 2B of Stancyzk. Although the two data sets are generated using different in vitro techniques and using different species, both figures show that C6-C8 is the strongest binding with C6-C7 showing comparatively weaker binding. Neither data sets tested C6-C9 fragment. Some differences in efficacy of MYBPC fragments is expected when testing them using different techniques, in vitro vs in vivo or mouse vs human. However, Stancyzk’s provides sufficient data that suggests and motivates an ordinary artisan to use MyBPC or its C-terminal fragments in inhibiting pathologically increased RYR2 function. Further, Priori provides sufficient teachings regarding viral vector based treatment of arrythmia caused by RYR2 gain of function and claimed sequences taught by NP_000247.2 (human) and NP_032679.2 (mouse). Taken together, Priori and Stanczyk along with NP_000247.2 (human) and NP_032679.2 (mouse) render the instant claims prima facie obvious.
Finally, in support of lack of reasonable expectation of success, Applicant allege that “The Examiner's own findings on the record acknowledge that predictability is not established” (page 14-15). Applicant point to the enablement rejection and conclude that “Examiner has found Stanczyk does not teach the precise mechanism by which MYBPC3 inhibits RYR2, nor the binding site on RYR2, thereby characterizing the level of detail to which Stanczyk teaches the interaction between MYBPC3 and RYR2” (page 14, last para). applicant allege that “The Examiner cannot simultaneously assert that Stancyzk's teachings are insufficient to establish a state of the prior art that allows for possession of broader claim scope under§ 112(a), while also asserting that the same teachings establish predictability sufficient to render obvious the scope of the instant claims, particularly when the Examiner relies on the MYBPC3-RYR2 binding data of Stancyzk.” (page 15, para 1).
In response, indeed Stanczyk does not teach the precise mechanism by which MYBPC3 inhibits RYR2 such that the broadly claimed methods of claims 53-56 could be enabled. However, this does not suggest that Stanczyk’s teachings are not sufficient to enable the instant narrower claims.
Claims 53-56 are now cancelled but were directed to acquired arrhythmias and heart failure, that are not limited to the gain of function mutations of claim 2. These claims also were rejected under U.S.C. 112(d) for broadening the scope of the independent claim 2. Although, Stanczyk’s teachings are applicable to methods of treating diseases associated with RYR2 gain-of-function mutation, such as in instant claims, because Stanczyk teaches that MYBPC3 binds and directly inhibits RYR2, their findings do not enable a method wherein an increase in RYR2 protein or function is due to other pathologies, such as in cancelled claims. See teachings from Marx and Kistmas in the previous enablement rejection that teach diverse causal factors for acquired arrythmias. For example, Marx teaches that heart failure induces RYR2 leakiness due to chronic increase in beta-adrenergic stimulation resulting in depletion of calstabin 2 from the RYR2 channel complex (page 228, left column, para 1). Based on Stanczyk and the instant specification, it is unpredictable that MYBPC3 or its C-terminal fragment could inhibit RYR2 leakiness caused by increased beta-adrenergic stimulation seen in heart failure. Critically, it is unpredictable that RYR2 inhibition could prevent heart failure since RYR2 leakiness emerges as an downstream effect of heart failure.
Conclusion
No claim is allowed.
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 MATASHA DHAR whose telephone number is (571)272-1680. The examiner can normally be reached M-F 8am-4pm (EST).
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/MATASHA DHAR/Examiner, Art Unit 1632
/EMILY A CORDAS/Primary Examiner, Art Unit 1632
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