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 .
Status of claim rejections
The rejections of record under 35 USC 103 are maintained and modified in view of Applicant’s remarks/amendments in the response filed 11/03/2025.
This Action is Final.
Claim Interpretation
The examiner has interpreted the limitation(s) as follows:
Claim 1 recites, inter alia, “a population of recombinant B cells comprising the following characteristics: i. at least 2 x 106 the B-cells comprising an exogenous follistatin gene operably linked to a promoter; ii. when the population is administered to a subject the population of B cells engrafts into the subject and expresses the exogenous follistatin gene; and iii. increases exogenous follistatin protein level in a subject by at least 2-fold as compared to the follistatin protein level in a subject that has not been administered the population”. As the claims are drawn to a product (i.e., a population of at least 2 x 106 B cells expressing follistatin), the limitations in (ii) and (iii) have been interpreted under broadest reasonable interpretation as inherent properties of the population of B cells expressing the exogenous follistatin because the claimed product is not required to be administered to a subject (such as in a method of treating). Where the claimed and prior art products are identical or substantially identical in structure or composition, or are produced by identical or substantially identical processes, a prima facie case of either anticipation or obviousness has been established. In re Best, 562 F.2d 1252, 1255, 195 USPQ 430, 433 (CCPA 1977) (MPEP 2112.01). In short, any population of B cells that have the recited structure in i) would inherently have the recited functional characteristics recited in ii) and iii).
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.
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.
First rejection
Claims 1 and 32 are rejected under 35 U.S.C. 103 as being unpatentable over Hung et al ((Engineering Protein-Secreting Plasma Cells by Homology-Directed Repair in Primary Human B Cells. Mol Ther. 2018 Feb 7;26(2):456-467. doi: 10.1016/j.ymthe.2017.11.012. Epub 2017 Nov 22; hereinafter “Hung”), in view of Shenton (https://medium.com/breakoutvc/q-a-with-matthew-scholz-how-dgis-technology-expands-and-enhances-the-immusoft-platform-2236140551f0 interview article, 29 March 2016, accessed 29 August 2023; prior art of record) and Goldberg et al (US 20160289637 A1, published 06 October 2016; hereinafter “Goldberg”; prior art of record).
Hung teaches engineering primary human B cells to differentiate into long-lived plasma cells and secrete a de novo protein may allow the creation of novel plasma cell therapies for protein deficiency diseases and other clinical applications (see abstract). Hung teaches differentiating and engineering B cells isolated from human peripheral blood to express and secrete factor IX or B cell activating factor (BAFF) at high levels to promote engraftment of the proteins in immunodeficient mice (a population of recombinant B cells as in claim 1) (abstract; pg. 461, Fig. 4; col 2; pg. 462 col 1-2; pg. 464, Fig. 6). Hung further teaches the creation of a population of 10 x 106 differentiated B cells expressing BAFF which were subsequently introduced into the immunodeficient mice (see pg. 465 “Materials and Methods” section, col 2) (a population of at least 2x106 as in claim 1).
The difference between Hung and the instant claim is that Hung does not teach the recombinant B cell population expressing an exogenous follistatin gene.
However, Shenton, in a Q&A interview with Matthew Scholz, teaches use of DGI’s Sleeping Beauty Transposon system in combination with Immusoft’s B cell programming platform called Immune System Programming (ISP) (title, pg. 1, paragraph 2) to program patient cells to treat disease (pg. 2, paragraph 1) via the transposon system cutting and pasting outside DNA into cell chromosomes, which then allows altered genes to be inserted back into the body (pg. 2, paragraph 3 and 4). Scholz, in response to a question posed by Shenton, suggests using this B cell platform to treat a wide range of ailments, including the production of follistatin to treat sarcopenia (pg. 3, paragraph 1). Shenton differs from claim 1 in that it fails to exemplify recombinant B cell(s) having exogenous follistatin gene. However, Shenton explicitly suggests a recombinant B cell having an exogenous follistatin gene (as in claim 1). Shenton also teaches using the Sleeping Beauty Transposon system to cut and paste outside DNA (i.e., transduce exogenous DNA) into cell chromosomes (as in claim 1). As such, Shenton provides a teaching, suggestion, or motivation to transduce B cells with a gene (such as follistatin).
Therefore, it would have been prima facie obvious to one of ordinary skill to modify the population of recombinant B cells as taught by Hung by creating a population of B cells expressing follistatin as taught by Shenton to arrive at the claimed invention. As Hung teaches a population of B cells recombinantly expressing an exogenous gene to produce proteins and Shenton suggests the expression of exogenous follistatin in B cells, one of ordinary skill would have been motivated to modify the B cells of Hung with exogenous follistatin as suggested by Shenton with a reasonable expectation of success. One of ordinary skill would have been motivated to make the modification because Hung teaches that immune cells such as B cells can successfully engineered to produce a population of cells harboring exogenous genes to produce proteins, and Shenton explicitly suggests that B cells can be programmed specifically to produce follistatin. As such, the combination of Hung and Shenton renders prima facie obvious claim 1.
Neither Hung nor Shenton explicitly teach having the follistatin gene operably linked to a promoter.
However, Goldberg teaches methods, compositions and methods of preparing autologous (or allogeneic) B cells that secrete a monoclonal of interest useful in immunotherapy or B cells with an altered function (abstract). Goldberg teaches that isolated human B cell can comprise one or more genetic modifications to express a defined protein of interest (see claim 1 of Goldberg). Specifically, Goldberg teaches that B cells are edited by the use of exogenous DNA (paragraph 0065, 0152), and that the expression of nucleic acids in the B cells can be done in operable combination or order, and operatively linked (i.e., operably linked) to the operational linkage of nucleic acid sequences placed in functional relationships with each other (paragraph 0185). Goldberg further teaches that an operatively linked promoter, enhancer elements, open reading frame, 5′ and 3′ UTR, and terminator sequences result in the accurate production of molecules, and operatively linked nucleic acid elements result in the transcription of an open reading frame and ultimately the production of a polypeptide (paragraph 0185).
Therefore, it would have been prima facie obvious to one of ordinary skill at the time of filing to modify the recombinant B cell population as taught by Hung and Shenton by having the exogenous gene operably linked to a promoter as taught by Goldberg to arrive at the claimed invention. As Goldberg teaches that the expression of nucleic acids in the B cells can be done in operable combination or order, and operatively linked (i.e., operably linked) to the operational linkage of nucleic acid sequences placed in functional relationships with each other, one of ordinary skill would have been motivated to modify the population of cells with a reasonable expectation of success. One of ordinary skill would have been motivated to make the modification because Goldberg explicitly teaches that an operatively linked promoters advantageously result in the accurate production of molecules, and operatively linked nucleic acid elements result in the transcription of an open reading frame and ultimately the production of a polypeptide.
Please note that the claims are drawn to a product (i.e., a population of at least 2 x 106 B cells expressing follistatin), such that the limitations in (ii) and (iii) have been interpreted under broadest reasonable interpretation as an inherent property of the population of B cells expressing the exogenous follistatin because the claimed product is not required to be administered to a subject (such as in a method of treating). The prior art (see above) teaches, in combination, the population of B cells as instantly claimed. MPEP 21102.01 states “[w]here the claimed and prior art products are identical or substantially identical in structure or composition, or are produced by identical or substantially identical processes, a prima facie case of either anticipation or obviousness has been established. In re Best, 562 F.2d 1252, 1255, 195 USPQ 430, 433 (CCPA 1977).
Regarding claim 32, Hung teaches using B cells isolated from patient peripheral blood.
Accordingly, the claimed invention was prima facie obvious to one of ordinary skill at the time of filing, especially in the absence of evidence to the contrary.
Second rejection
Claim 4 is rejected under 35 U.S.C. 103 as being unpatentable over Hung, Shenton, and Goldberg as applied to claims 1, and 32 above, and further in view of Haidet et al (Proc Natl Acad Sci USA. 2008 Mar 18;105(11):4318-43122, hereinafter “Haidet”; prior art of record).
As discussed above, claims 1, and 32 were rendered prima facie obvious by the combined teachings of Hung, Shenton, and Goldberg.
The difference between Hung, Shenton, Goldberg, and the instant claim is that none of the references explicitly teach a follistatin gene that is an FST-344 splice site variant.
However, Haidet teaches the long-term enhancement of skeletal muscle mass and strength by single gene administration of myostatin inhibitors (title), where increasing size and strength of muscle is promising for therapeutics for musculoskeletal disorders (abstract). Haidet also teaches that recent data demonstrated muscle mass enhancement in muscular dystrophy mice, attributed to follistatin because it inhibits myostatin activity (pg. 4318, paragraph 1). Haidet also teaches that introduction of follistatin using a one-time postnatal intramuscular injection of recombinant AAV1 vectors encoding myostatin inhibitor proteins resulted in long-term improvement of muscle size and strength in wild-type animals, and delivery in dystrophic mdx animals reversed muscle pathology and improved strength (pg. 4318, col 2, paragraph 2; pg. 4319, col 1, Fig 1a-1d; Fig. 2a-2c; pg. 4320, Fig. 3a-3e). Haidet further teaches that the variant used in the method is the FS-344 variant (also known as the FST-344 variant as in claim 4), because it exclusively generates the serum circulating FS-315 isoform of follistatin and includes a C-terminal acidic region (pg. 4319, col 1, paragraph 1). The second variant, FS-317, produces the FS-288 isoform after peptide cleavage, which lacks the C-terminus and shows preferential localization to ovarian follicular fluid and high tissue binding affinity through heparin sulfate proteoglycans (pg. 4319, col 1, paragraph 1).
Therefore, it would have been prima facie obvious to one of ordinary skill at the time of filing to modify the population of recombinant B cells as taught by Hung, Shenton, and Goldberg by using the FS-344 variant as taught by Haidet to arrive at the claimed invention. As Haidet teaches the successful use of recombinant FS-344 splice variant to treat muscular disorders, a person of ordinary skill in the art would have been motivated to modify the cell population of Hung, Shenton, and Goldberg with the splice variant of Haidet with reasonable expectation of success. One of ordinary skill in the art would have been motivated to make the modification because the FS-344 variant advantageously produces the serum circulating FS-315 isoform of follistatin, without the preferential localization to other tissues or ovarian follicular fluid as seen in the FS-288 isoform produced by the FS-317 variant.
Accordingly, the claimed invention was prima facie obvious to one of ordinary skill at the time of filing, especially in the absence of evidence to the contrary.
Third rejection
Claim 14 is rejected under 35 U.S.C. 103 as being unpatentable over Hung, Shenton, and Goldberg as applied to claims 1 and 32 above, and further in view of Matthew Scholz (“Introduction to Immusoft” video, https://vimeo.com/132126056, 29 June 2015, accessed 23 August 2023, hereinafter “Scholz”; prior art of record).
As discussed above, claims 1 and 32 were rendered prima facie obvious by the combined teachings of Hung, Shenton, and Goldberg.
The difference between Hung, Shenton, Goldberg, and the instant claim is that none of the references explicitly teach that follistatin protein is secreted by the recombinant B cell (as in claim 14).
However, Scholz, in a video titled “Introduction to Immusoft” posted on Vimeo.com, teaches Immusoft’s Immune System Programming technology to and cure disease (title, description). The video shows that this kind of gene therapy would allow key cells in the body to make the protein needed, and further shows an animation of the proteins being secreted by the cells (as in claim 14) (minute 00:24- 00:36, shown in first screenshot below). Scholz further teaches the steps of engineering the cells including: 1) Collecting and isolating immune cells from the blood of a human patient, 2) electroporating the cells with DNA encoding a therapeutic protein, 3) expanding selected cells ex vivo, 4) differentiating the expanded cells ex vivo into plasma cells and/or plasmablasts, and 5) cells engrafting and producing the therapeutic protein and re-infusing the cells back into the patient (minute 1:25, shown in the second screenshot below). Scholz then shows that the cell to be programmed is a B cell via a novel transposon system using exogenous DNA (minute 1:30-1:40, shown in the third screenshot below).
PNG
media_image1.png
561
640
media_image1.png
Greyscale
minute 00:24-00:36
PNG
media_image2.png
906
1184
media_image2.png
Greyscale
minute 01:25
PNG
media_image3.png
688
806
media_image3.png
Greyscale
minute 01:30-01:40
Therefore, it would have been prima facie obvious to one of ordinary skill at the time of filing to use the protocol to reprogram isolated patient B cells as taught by Scholz to produce and secrete a therapeutic protein (such as follistatin as taught by Hung, Shenton, and Goldberg) to arrive at the claimed invention. As Scholz teaches the steps necessary to create a recombinant B cell to produce a therapeutic protein for treatment from a subject, a person of ordinary skill would be motivated to use the protocol with a reasonable expectation of success. One of ordinary skill would have been motivated to use the protocol of Scholz to advantageously and successfully create a population of recombinant B cells isolated from a patient that is capable of producing and secreting a therapeutic protein, like follistatin.
Accordingly, the claimed invention was prima facie obvious to one of ordinary skill at the time of filing, especially in the absence of evidence to the contrary.
Fourth rejection
Claim 33-34 are rejected under 35 U.S.C. 103 as being unpatentable over Hung, Shenton, and Goldberg as applied to claims 1 and 32 above, and further in view of and further in view of Ramirez et al (Curr Opin Immunol. 2010 Apr;22(2):177-84, hereinafter “Ramirez”).
As discussed above, claims 1 and 32 were rendered prima facie obvious by the combined teachings of Hung, Shenton, and Goldberg.
The difference between Hung, Shenton, Goldberg and the instant claims is that none of the references explicitly teach that the recombinant B cell is derived from a B cell progenitor obtained from the subject (as in claim 33) or that the recombinant B cell is derived from a cell obtained from the subject that has been dedifferentiated into the B cell or a B cell progenitor (as in claim 34).
However, Ramirez teaches the mechanisms of lineage restriction and commitment of B cells (title) where the generation of B lymphocytes from hematopoietic progenitors requires lineage specific transcription factors that progressively direct cell fate choices (abstract). Pluripotent hematopoietic stem cells undergo successive rounds of lineage fate restrictions that result in specialized cells in the blood (pg. 177, paragraph 1). HSCs yield multipotent progenitors (MPPs) that give rise to lymphoid-primed multipotent progenitors (LMPPs) and common lymphoid progenitors (CLPs) (B cell progenitors as in claim 33 and 34) (pg. 1 paragraph 1). The transcription factors E box binding protein 2A (E2A) and Early B cell Factor-1 (EBF1) direct CLPs into the B cell developmental pathway (pg. 1 paragraph 1). Together with Paired box protein 5 (Pax5) and Ikaros, these factors initiate the progressive steps of V(D)J recombination and expression of accessory proteins required for the display of pre- and mature B cell receptors (BCRs) (pg. 1 paragraph 1). Signaling via functional BCR complexes promotes the egress of immature B cells from the bone marrow (pg. 1 paragraph 1).
Therefore, it would have been prima facie obvious to one of ordinary skill at the time of filing to make recombinant B cells from cells obtained from a patient as taught by Hung, Shenton, and Goldberg, and use B cell progenitors as obtained from the bone marrow as taught by Ramirez to arrive at the claimed invention. As Ramirez teaches that B cells are generated from hematopoietic progenitors in the bone marrow to yield B cells in the blood, a person of ordinary skill would be motivated to use B cell progenitors from a patient with a reasonable expectation of success. One of ordinary skill would be motivated to use B cell progenitors because Ramirez teaches the successful creation of B cells from B cell progenitors (such as CLPs) through lineage restriction and commitment via activation of transcription factors, which would advantageously result in B cells that are viable for use in a therapeutic, as taught by Hung, Shenton, and Goldberg.
Accordingly, the claimed invention was prima facie obvious to one of ordinary skill at the time of filing, especially in the absence of evidence to the contrary.
Response to Arguments
Applicant's arguments filed 11/03/25 have been fully considered but they are not persuasive.
On pg. 6-8 of the remarks, Applicant argues that the Office has mischaracterized the teachings of Hung, specifically that the Office failed to consider Hung as a whole. Applicant argues that Hung is devoted exclusively to site specific genome editing in human B cells using homology-directed repair facilitated by CRISPR-cas9 ribonucleoprotein complexes with single-stranded DNA oligonucleotide repair templates or AAV repair templates. Applicant also argues that Hung underscores historical difficulties in transducing B cells for long-term expression of exogenous genes to B cells on a therapeutic scale such that a PHOSITA “would appreciate that: a) the transduction of B cells is extremely difficult and inherently unpredictable; and that b) Hung makes it clear that the only possible solution to these previous failures is through the use of the site-specific, HDR-based engineering strategy.” From this, Applicant urges that “any teachings contained therein are not extendable past the HDR-based methods upon which it exclusively relies.” Furthermore, Applicant argues that in light of Hung and the fact that the claims require use of a transposon system, “the skilled artisan would readily appreciate that the transposon system required by the instant claims and the HDR-based system described by Hung are distinct and accomplish genetic engineering through different biophysical mechanisms” and a PHOSITA would not have been motivated by Hung to substitute HDR-based genetic engineering with a transposon-based engineering system.
In response, the examiner disagrees. First, Hung does not have to provide any teachings regarding use of transposon systems. Hung explicitly teaches “plasma cells engineered to produce de novo proteins have the potential to be curative therapies . . . However, the development of plasma cell therapeutics has been limited by technical challenges in the in vitro modification, culture, expansion, and differentiation of primary human B cells. B cells can be transduced at high rates by recombinant adenovirus or Epstein-Barr virus (EBV) vectors, which deliver transgenes as episomes . . . gamma retrovirus (γRV) and lentivirus (LV) randomly integrate into the host genome and can be used to introduce stably expressing transgenes. However, these vectors are inefficient at transducing primary human B cells . . . Because γRV and LV vectors do not efficiently transduce B cells, whereas transduction by non-integrating vectors results in only transient transgene expression, neither platform is currently effective for delivering long-term expression of exogenous genes to B cells on a therapeutic scale” (see pg. 456 col 2). At most, Hung disavows the use of viral vector transgene delivery systems but does not have any teachings or suggestions regarding the use of other transposon systems to introduce genes into B cells. As such, one of ordinary skill would have been motivated to look beyond the teachings of Hung for any teaching, suggestion, or motivation for B cell transduction systems.
Shenton provides this explicit teaching, suggestion, and motivation. Regarding use of the Sleeping Beauty Transposon System (see pg. 1-2), Shenton discloses:
The Sleeping Beauty Transposon System is a non-viral vector that can deliver genes into cells. It is vastly more scalable and much less expensive than a virus and will allow us to maximize the abilities of our own proprietary technology, Immune System Programming (ISP™), which we use to program patient cells to treat disease . . . [SBTS] is a genetic tool for cutting and pasting outside DNA into the chromosomes of cells. Since the transposon is just DNA — a small genetic program — itself, it is less complicated and easier to produce than a virus. Viral vectors are naturally targeted by the immune system, but the transposon doesn’t have any viral components . . . Being a non-viral vector, it’s possible to insert altered genes back into the body in a way that is generally thought to be easier, more scalable and less expensive than conventional gene therapy protocols that require injecting a virus into a patient. Adeno-associated virus (AAV) relies on injecting a virus into the patient, can typically only be done once and can be expensive. Even when the viral vectors are used outside the body, as is commonly done with lentiviral and retroviral vectors, when contrasted with a non-viral vector, they still cost far more to manufacture.
As shown above, Shenton provides one of ordinary skill in the art the explicit teaching, suggestion, and motivation to use the non-viral vector SBTS because of its various advantages when used to deliver genes into cells, contrary to the use of viral vectors (which are disavowed in Hung). Indeed, an obviousness rejection under 35 U.S.C 103 requires one of ordinary skill to balance each individual teaching of the prior art references with the totality of the references in combination. Applicant’s arguments do not take into account the combination of teachings of the prior art references, and do not appreciate all of the evidence as a whole. Thus, the use of the Hung reference is maintained, especially in light of the disclosure of Shenton.
On pg. 8-10 of the remarks, Applicant argues Shenton and Goldberg fail to cure the deficiencies of Hung. Specifically, Applicant argues that Goldberg reference is simply cited for teaching operatively linked promoter, enhancer elements, etc. for the ultimate production of a polypeptide and is completely silent to transposon-based systems. Applicant then argues that the Shenton reference is “merely an interview with Matthew Scholz (Applicant) discussing the possibilities of a technology to produce follistatin as a “killer app” for “producing a biologic such as follistatin to treat age-related sarcopenia”. Applicant argues (in the previously filed Declaration) that “one cannot simply take a sequence, put the sequence into a B cell and then expect the protein to be expressed at therapeutic levels . . . Therefore, a person of skill in the art would glean nothing substantial listening to Mr. Scholz, as Mr. Scholz’s statement is nothing more than a mere wish.” Applicant urges that “there is no teaching in Shenton that informs the skilled artisan that the HDR- based gene editing system of Hung could be substituted with a transposon system with any reasonable expectation of success in effectively producing the claimed population of cells. In fact, based on the uncertainty of B cell genetic engineering (described above), the skilled artisan would actually conclude that such a substitution would render the methods taught by Hung inoperable.” Applicant then argues much of the same for the rejections of claims 4, 14, and 33-34.
In response, the examiner disagrees for much of the same reasons as set forth above. First, the Shenton reference does provide adequate teaching, suggestion, and motivation to one of ordinary skill to produce follistatin in a recombinant B cell by delivering exogenous genes into the B cell(s) (see rejection above). MPEP 2143 states that “when setting forth a rejection. . . Office personnel must provide a reasoned explanation as to why the invention as claimed would have been obvious to a person of ordinary skill in the art at the relevant time” by utilizing rationales to support a conclusion of obviousness including “some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to modify the prior art reference or to combine prior art reference teachings to arrive at the claimed invention” (see MPEP 2143(I)(G)). As Applicant concedes in the argument, Shenton does suggest producing a biologic such as follistatin in the B cells using the B cell programming platform. As such, the use of the Shenton reference is maintained as it relates to the amended claims.
Second, Goldberg, Haidet, Scholz, and Ramirez render the claims prima facie obvious in combination with the Hung reference because the references (respectively) teach an operatively linked promoters advantageously result in the accurate production of molecules, and operatively linked nucleic acid elements result in the transcription of an open reading frame and ultimately the production of a polypeptide (see Goldberg), the FS-344 variant advantageously produces the serum circulating FS-315 isoform of follistatin, without the preferential localization to other tissues or ovarian follicular fluid as seen in the FS-288 isoform produced by the FS-317 variant (see Haidet), the steps necessary to create a recombinant B cell to produce a therapeutic protein for treatment from a subject (see Scholz), and the successful creation of B cells from B cell progenitors (such as CLPs) through lineage restriction and commitment via activation of transcription factors (see Ramirez). Thus, the rejections are maintained as set forth above.
Conclusion
NO CLAIMS 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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to GEORGIANA C REGLAS whose telephone number is (571)270-0995. The examiner can normally be reached M-Th: 8:00am-2:00pm.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Melenie Gordon can be reached at 571-272-8037. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/G.C.R./Examiner, Art Unit 1651
/THOMAS J. VISONE/Supervisory Patent Examiner, Art Unit 1672