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. Election/Restrictions Applicant’s election without traverse of Group I, claims 1-13 in the reply filed on 10/24/2025 is acknowledged. Claims 14-21 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 10/24/2025. Current Status of 18/028,991 This Office action is responsive to the Response to Election /Restriction of 10/24/2025. Claims 1-13 have been examined on the merits. Priority The instant application is a national stage entry of PCT/US2021/051975, filed 09/24/2021, which claims priority to U.S. Provisional Patent Application No. 63/086,936 filed 10/02/2020. Information Disclosure Statement The information disclosure statement (IDS) submitted on 03/29/2023 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner. Drawings The drawings are objected to because the figures are small and grainy, especially the axis labels and legends . The examiner recommends replacing all figures with high resolution images that will transfer clearly . Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance. Claim Rejections - 35 USC § 112 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. Claim s 1-13 are 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 a method of treating PV through administering a composition comprising montelukast and/or a JAK 2 inhibitor (claim 9) and/or a tyrosine kinase inhibitor (claim 12) to a patient suffering from PV , does not reasonably provide enablement for the prophylactic treatment of patients at risk of having PV . 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. The factors to be considered in determining whether a disclosure meets the enablement requirements of 35 U.S.C. 112, first paragraph, have been described in In re Wands , 858 F.2d 731, 8 USPQ2d 1400 (Fed. Cir., 1988). The court in Wands states, “Enablement is not precluded by the necessity for some experimentation, such as routine screening. However, experimentation needed to practice the invention must not be undue experimentation. The key word is ‘undue’, not ‘experimentation’” ( Wands , 8 USPQ2sd 1404). Clearly, enablement of a claimed invention cannot be predicated on the basis of quantity of experimentation required to make or use the invention. “Whether undue experimentation is needed is not a single, simple factual determination, but rather is a conclusion reached by weighing many factual considerations” ( Wands , 8 USPQ2d 1404). Among these factors are: (1) the nature of the invention; (2) the breadth of the claims; (3) the state of the prior art; (4) the predictability or unpredictability of the art; (5) the relative skill of those in the art; (6) the amount of direction or guidance presented; (7) the presence or absence of working examples; and (8) the quantity of experimentation necessary. While all of these factors are considered, a sufficient amount for a prima facie case is discussed below. (1) The nature of the invention and (2) the breadth of the claims : The claims are drawn to methods of treating patients having PV or at risk of having PV. The method of claim 1 comprises administering a therapeutic composition comprising an active component consisting essentially of Montelukast . The method of claim 9 comprises administering a therapeutic composition consisting essentially of a combination of montelukast sodium and a JAK2 inhibitor. The method of claim 12 comprises administering a therapeutic composition consisting essentially of a combination of montelukast sodium and a tyrosine kinase inhibitor . Thus, the claims taken together with the specification imply that a treatment regimen s of Montelukast and/or a JAK2 or tyrosine kinase inhibitor are capable of prophylactic treatment of patients at risk of developing PV . (3) The state of the prior art and (4) the predictability or unpredictability of the art : The state of the prior art is unpredictable with respect to prophylactic treatment of patients at risk of developing PV . McKerrell et al. teaches that JAK2 V617F neoplasm develop from hematopoiesis over many years, sometimes over more than a decad e and that the genes believed responsible for the acceleration of JAK2 V61F-driven clonal expansion are highly variable. This limits the ability to forecast the likelihood of progression of JAK2 V617F hematopoiesis (pg. 969, right col. final para) . Guo et al. teaches that prophylactic treatment of persons merely “at risk” of PV would have been uncertain and unpredictable because JAK2-mutant clonal hematopoiesis is present in a portion of healthy individuals , but the vast majority of such carriers do not meet and do not go on to develop disease-defining myeloproliferative neoplasms (MPNs) (pg. 274, left col final para, Abstract , pg. 273, right col final para continuing onto pg. 274 right col ) . The reference also discloses that little is understood about why only a minority of mutated JAK2 carriers develop more severe hematological mutations, an d that acquisition of somatic mutations is largely stochastic. The study also shows that disease phenotype depends on interacting polygenic background rather than mutation status alone ( pg. 276, final para beginning on left col ). The references discussed above highlight the unpredictability in the art . The art does not provide a reliable basis for identifying which at-risk persons would actually progress to PV or would benefit from the claimed prophylactic treatment . (5) The relative skill of those in the art : The artisan would have experience in organic chemistry, medicinal chemistry, pharmaceutical sciences, or a related field. The artisan would have experience working with hematopoietic cell systems any myeloproliferative disease models and would have experience conducting in vitro and in vivo studies involving JAK2-driven signaling. The artisan would have experience in the evaluation of small-molecule inhibitors for therapeutic use. (6) The amount of direction or guidance presented and (7) the presence or absence of working examples : The specification has provided guidance for the treatment of PV in models driven by JAK2V617F mutations . The specification shows that Montelukast can inhibit growth and induce apoptosis in PV-associated cell populations . The examples further support modulation of hematopoietic stem and progenitor cell populations ex vivo (see Examples I-VIII) . However, the specification does not provide guidance for identifying patients “at risk” of developing PV. The definition provided is broad and encompasses undefined behavioral, environmental, and biochemical factors without specific diagnostic criteria or predictive biomarkers . The specification also fails to provide working examples or data demonstrating that the administration of the claimed treatment regimens prevents or delays the onset of PV in such patients. The experimental evidence of the disclosure is limited to in vitro cell lines and murine models of established disease. This data does not establish that the claimed regimens would be effective in the prevention of PV as claimed. (8) The quantity of experimentation necessary : Considering the state of the art as discussed by the references above, particularly with regards to the uncertainty in determining at-risk patient populations who may develop PV and the high unpredictability in the art as evidenced therein, and the lack of guidance provided in the specification, one of ordinary skill in the art would be burdened with undue experimentation to practice the invention commensurate in the scope of the claims. The Examiner notes that the instant disclosure appears to provide support for methods of treating PV in subjects having the disease. Accordingly, amendment of the claims to recite methods of treating PV, rather than prophylactic treatment of subjects “at risk,” would commensurate in scope with the enabling disclosure and would overcome the above rejection. 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 appl icant regards as his invention. Claim 2 is 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. Claim 2 recites the limitation " Montelukast sodium; Montelukast nitrile; and [R-(E)]-1-[[[1-[3-[2-(7-chloro-2-quinolinyl)ethenyl] phenyl]-3-[2-(1-hydroxy-1- methylethyl)phenyl]propyl]thio]methyl]-cyclopropaneacetic acid, monosodium salt " in lines 2-4 of claim 2 . There is insufficient antecedent basis for this limitation in the claim. Claim Rejections - 35 USC § 102 The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action: A person shall be entitled to a patent unless – (a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale , or otherwise available to the public before the effective filing date of the claimed invention. Claims 1, 2, 8, and 12 are rejected under 35 U.S.C. 102 (a)(1) as being anticipated by O ’ Mara (WO 2019/109147, found in IDS filed 03/29/2023) . O’Mara discloses methods of treating cancer with leukotriene receptor antagonists (Title , Abstract ) . The reference discloses a method for treating cancer in a subject comprising administering to the subject an effective amount of a leukotrien e receptor antagonist ([006]) further specifying that the cancer may be selected from a group which includes polycythemia rubera vera ([0050]). The reference teaches a method for increasing the sensitivity of a cancer to chemotherapy, the method com prising administering to a subject in need thereof an effective amount of a leukotriene receptor antagonist ([0016]), the leukotriene receptor antagonist is montelukast ([007]). The reference teaches that a second aspect of the invention provides a method for treating a hematological cancer in a subject, comprising administering to the subject an effective amount of montelukast or a pharmaceutically acceptable salt thereof ([0013]). The term “effective amount” includes within its meaning a non-toxic but sufficient amount or dose of an agent or compound to provide the desired effect ([0033]). “Treating” and “treatment” refer to any and all uses which remedy a condition or one or more symptoms, or otherwise hinder retard, or reverse the progression of a condition or one or more symptoms thereof in any way whatsoever ([0043]). These teachings anticipate a) and b) of instant claim 1. [0043] of the reference discloses that Montelukast ((R, E)-2-(l-((l-(3-(2-(7-chloroquinolin-2-yl) vinyl)- phenyl)-3-(2- (2-hydroxypropan-2-y!) phenyl) propyl thio ) -methyl) cyclopropyl) acetic acid) is a leukotriene receptor antagonist …typically in the form of a sodium salt and that montelukast sodium, also referred to herein as montelukast . This anticipates the limitations of instant claim 2. [0035] discloses that the term “subject” refers to mammals and includes humans, anticipating the limitations of instant claim 8. [006] and [0050] teach a method for treating a cancer in a subject comprising administering to the subject and effective amount of leukotriene receptor antagonist, wherein the cancer treating includes polycythemia rubera vera. [007] and [ 0043] specify that montelukast is an embodied leukotriene receptor antagonist of the invention. The reference further discloses that the methods may be employed as an adjunct to chemotherapy [0052] and that suitable chemotherapeutic agents may be employed alone, or in any combination include kinase inhibitors such as erlotinib and gefitinib. The reference teaches that a second aspect of the invention provides a method for treating a hematological cancer in a subject, comprising administering to the subject an effective amount of montelukast or a pharmaceutically acceptable salt thereof ([0013]). The terms “effective amount” , “treating” and “treatment” are defined in [00 3 3] and [0034] (see above) . These teachings anticipated the limitations of instant claim 12. Claims 9 and 10 are rejected under 35 U.S.C. 102 (a)(1) as being anticipated by Puretech (WO 2020/176 859, found in IDS filed 03/29/2023) . Puretech discloses methods of treating a disease, disorder, or condition comprising administering to a patient in need thereof a disclosed lipid prodrug or a pharmaceutical composition thereof (Abstract). The disease, disorder, or condition is selected from a group which includes polycythemia vera ([00168]) and the method of treating a cancer in a patient in need thereof includes cancers, wherein the cancer is polycythemia vera ([00 170], claim 26). The reference teaches that the invention provides a compound of Formula I ([0027]); A is a JAK inhibitor, or a pharmaceutically acceptable salt thereof ([00100]); and the JAK inhibitor is a selective inhibitor of JAK2 ([00101]) ; A is tofacitinib or ruxulitinib ([00102]) , these teachings anticipate the limitations of instant claim 10 . The reference further teaches that in those compositions comprising an additional therapeutic agent, the additional therapeutic agent and the disclosed lipid prodrug may act synergistically wherein the amount of additional therapeutic agent in such compositions will be less than that required in a monotherapy utilizing only that therapeutic agent ([00306]) . Examples of agents that may be combined with the lipid prodrugs of the claimed invention include Singulair ([ 00307]). The disclosed lipid prodrugs are also useful as co-therapeutic compounds for us in com bination with other drugs such as anti-inflammatory substances ([00307]) wherein suitable anti-inflammatory drugs include LTD4 antagonists such as montelukast ([00372]) . The reference further teaches administering the lipid prodrug or composition results in complete response, partial response, reduced severity, or stable disease ([00244]). These teachings anticipated a) and b) of instant claim 9. Claim Rejections - 35 USC § 103 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. Claim s 1 and 3-7 are rejected under 35 U.S.C. 103 as being unpatentable over O’Mara in view of Chen ( Chen, Yaoyu , et al. "Alox5 blockade eradicates JAK2V617F-induced polycythemia vera in mice." Cancer research 77.1 (2017): 164-174. ) . The teachings of O’Mara are discussed above and are incorporated by reference into this rejection. O’Mara anticipates the methods of claims 1 and 12. The reference does not expressly disclose hematopoietic stem cells (HSCs) bearing a JAK2V617F mutation nor does it discl ose methods of isolating HSCs from a first or second sample. Chen is in the same field of treating polycythemia vera (PV). The reference teaches that Alox5 is a key genetic effector of JAK2V617F in driving PV and identifies this enzyme as a therapeutic target for treatment (Abstract). The reference teaches that somatic activating point mutation of JAK2 (JAK2V617F) has been found in Philadelphia chromosome-negative myeloproliferative neoplasms (MPN) in approximately 95% of patients with PV. It also teaches that JAK2V617F-positive cells outpace normal hematopoietic cells as a result of its constitutively active kinase activity and activation of growth factor signaling (pg. 164, left Col, first para.). The reference discloses a method of collecting peripheral blood from patients with PV CD34+ and isolating using a cell selection kit (pg. 165, right Col) . CD34+ cells were assayed for colony formation assay in semisolid media. CD43+ cells were plated in duplicate in tissue culture dishes, various doses of zileuton added to the medium, and then colon ies were enumerated after 14 days of incubation. Colonies were plucked and genotyped for JAK2V617F (pg. 166, left Col). Chen additionally discloses methods to study the role of Alox5 in JAK2V617F -induced PV, wherein Ba/F3 and JAK2V617F-expressing Ba/F3 cells and JA K2V617F-expressing human HEL cells were used. These cells were characterized for the activation of JAK/STAT signaling by JAK2V617F using the JAK2 inhibitor ruxolitinib and it was found that compared with Ba/F3 cells, phosphorylation of JAK2 and STAT5 was greatly increased in JAK2V617F-expressing Ba/F3 and HEL cells and that inhibition of JAK2 kinase activity by ruxolitiinib largely reduced the phosphorylation (pg. 166 right column, FIG 1A) . The reference further teaches that JAK2V617F-expressing Ba/F3 cells expression of 5-LO encoded by Alox5 was significantly increased as compared with Ba/F3 cells suggesting that Aloz5 is involved in JAK2V617F signaling ( pg 166, right Col.) Alox5 expression is upregulated by JAK2V617F and Alox5 inhibition abrogates JAK2V617F-stimulated cell growth (pg. 166, right Col., FIG 1C ) . The artisan would have experience in organic chemistry, medicinal chemistry, pharmaceutical sciences, or a related field. The artisan would have experience in the development or combination therapies for the treatment of cancer, including blood cancers. The artisan would be familiar with previously reported combination therapies and individual therapeutic agents amenable for treatment. Chen provides a framework for collecting peripheral blood from PV patients, isolating CD34+ hematopoietic stem/progenitor cells, and characterizing those cells for JAK 2V617F and Alox5 expression. Given Chen’s teaching that JAK2V617F drives Alox5 upregulation in hematopoietic cells and that PV isa stem-cell derived disease where HSCs harbor JAK2V617F , the artisan would have found it obvious that isolation of HSCs from a PV patient would inherently yield a population where a percentage of these cells would have overactive JAK2 and overexpress Alox5. Fu rther, Chen teaches that modulation of Alox5 attenuates PV cell populations. This teaching would have made it obvious to the artisan that a second isolated sample obtained at a different time point would contain a lower percentage of such cells. The artisan would have been motivated to modify the method of O’Mara to include additional steps for isolating and characterizing the samples for prevalent mutations known to promote PV. Because JAK2V617F was widely recognized as a driver mutation in PV and Chen provides a framework for isolating and characterizing patient-derived CD34+ cells, the artisan would have found it obvious to incorporate such characterization into the method of O’Mara and would have reasonably expected the isolated cells to exhibit the known molecular features of PV, including overactive JAK2 and upregulated Alox5. Claim s 9 and 11 are rejected under 35 U.S.C. 103 as being unpatentable over Puretech in view of Ohanian (WO 2020/159987 A1, found in IDS filed 03/29/2023) . The teachings of Puretech are discussed above and are incorporated by reference into this rejection. The reference teaches the method of instant claim 9. Puretech does not expressly disclose the JAK2 inhibitor as being redratinib , SAR317461, gandotinib , or CEP0701. Ohanian teaches combination therapies for the treatment of cancers, including polycythemia vera (Title, Abstract, [00 02-0006], and [00344]). The reference further teaches that anti-cancer therapeutic agents include targeted therapies, including JAK-2 inhibitors such as gandotinib ([00349]). The artisan would have experience in organic chemistry, medicinal chemistry, pharmaceutical sciences, or a related field. The artisan would have experience in the development or combination therapies for the treatment of cancer, including blood cancers. The artisan would be familiar with previously reported combination therapies and individual therapeutic agents amenable for treatment. Puretech teaches a method of treating polycythemia vera comprising administering a combination of montelukast sodium and a JAK2 inhibitor, but does not specify the JAK2 inhibitor as being one of those listed in instant claim 11. Ohanian teaches the use of the JAK2 inhibitor gandotinib as part of a combination therapy for the treatment of polycythemia vera. It would have been obvious to modify the method of Puretech to include other JAK2 inhibitors known to be effective in combination therapies for the treatment of polycythemia vera, such as gandotinib . Such a substitution represents the use of a known alternative JAK2 inhibitor to achieve the same therapeutic effect and would have been expected to yield predictable results. The substitution of one known JAK2 inhibitor for another known JAK2 inhibitor in the treatment of the same disease constitutes the predictable substitution of one known equivalent for another to obtain the same results. Claim s 12 and 13 are rejected under 35 U.S.C. 103 as being unpatentable over O’Mara in view of Gaikwad ( Gaikwad, Amos, and Josef T Prchal. “Study of two tyrosine kinase inhibitors on growth and signal transduction in polycythemia vera.” Experimental hematology vol. 35,11 (2007): 1647-56. doi:10.1016/j.exphem.2007.08.018 ) . The teachings of O’Mara are discussed above and are incorporated by reference into this rejection. The reference teaches claim 12. O’Mara does not explicitly disclose the tyrosine kinase inhibitor as being selected from a Bcr-Abl tyrosine kinase inhibitor, AMN107, and AEE788. Gaikwad teaches t h e efficacy of AEE788 and AMN107 in vitro on cells bearing the JAK2V617F mutation (Objective). The reference teaches that AEE788 showed a time- and dose-dependent growth inhibitory effect that was greater in FDCP cells expressing JAK2V617F and HEL cells than in cells expressing wild-type JAK2. AEE788 caused dephosphorylation of Akt (S243) and signal transducer and activator of transcription 5 (Y694) proteins, increase in Annexin-V binding and caspase-3 cleavage, suggesting induction of apoptosis. We also observed AEE788-mediated decrease in heat shock protein 70 and 90 antiapoptotic proteins. Similarly, native PV erythroid progenitors showed more sensitivity to AEE788 than normal erythroid progenitors. AEE788 also exerted dose-dependent inhibition of PV-specific erythroid colonies (Results). The reference also teaches that AEE788 has potential in the treatment of PV and other JAK2V617F positive hematological malignancies (Conclusion). The artisan would have experience in organic chemistry, medicinal chemistry, pharmaceutical sciences, or a related field. The artisan would have experience in the development or combination therapies for the treatment of cancer, including blood cancers. The artisan would be familiar with previously reported combination therapies and individual therapeutic agents amenable for treatment. The artisan would have been motivated to incorporate specific tyrosine kinase inhibitors (TKI) that have previously been shown as being effective in the treatment of PV . AEE788 is a known TKI that has been identified as a potential treatment of PV including PV bearing JAK2V617F mutations. Substituting AEE788 for another TKI in a method that generically requires a TKI represents the use of a known alternative within a class of functionally similar agents. Because AEE788 was known to inhibit tyrosine kinase signaling pathways relevant to PV pathogenesis, its incorporation would have been expected to achieve the same therapeutic outcome. Such a substitution represents the predictable use of one known equivalent for another within a recognized class of therapeutic agents. As a general principle it is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose, the idea of combining them flows logically from their having been individually taught in the prior art. See In re Kerkhoven , 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) MPEP 2144.06. Conclusion No claims are allowed. Any inquiry concerning this communication or earlier communications from the examiner should be directed to FILLIN "Examiner name" \* MERGEFORMAT CONNOR KENNEDY ENGLISH whose telephone number is FILLIN "Phone number" \* MERGEFORMAT (571)270-0813 . The examiner can normally be reached FILLIN "Work Schedule?" \* MERGEFORMAT Monday Friday, 8 a.m. 5 p.m. ET. . 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, FILLIN "SPE Name?" \* MERGEFORMAT Andrew Kosar can be reached at FILLIN "SPE Phone?" \* MERGEFORMAT (571)272-0913 . 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. /C.K.E./ Examiner, Art Unit 1625 /Andrew D Kosar/ Supervisory Patent Examiner, Art Unit 1625