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 .
Priority
This application is a Continuation of PCT/US2020/054607 filed on 10/07/2020 which claims the benefit of U.S. Provisional Application No. 62/912,441 filed on 10/08/2019.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1, 2, 10 and 28 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 12-15 and 31-33 of copending Application No. 17,489,022 (U.S. Publication No. 2022/0017535 A1 Provided on IDS). Although the claims at issue are not identical, they are not patentably distinct from each other because the cited claims of the instant application and the cited claims of copending ‘022 are substantially overlapping in scope.
The cited claims of the instant application claim a method of treating PMM2-CDG, and increasing PMM2 enzymatic activity in a subject with PMM2-CDG comprising administering a therapeutically effective amount of an aldose reductase inhibitor to a subject in need thereof.
The cited claims of copending ‘022 claim a method of inhibiting aldose reductase activity in a subject and treating a disorder such as phosphomannomutase 2-congenital disorder of glycosylation (PMM2-CDG) comprising the administration of a compound of formula (I) or a compound of formula (II).
Claims 1, 2, 10 and 28 of the instant application would be anticipated over the cited claims of copending ‘022 since the cited claims of copending ‘022 are drawn to a method of treating a disorder such as phosphomannomutase 2-congenital disorder of glycosylation (PMM2-CDG) comprising the administration of the aldose reductase inhibitors of a compound of formula (I) or a compound of formula (II).
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 3-5 and 20-22 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 12-15 and 31-33 of copending Application No. 17,489,022 (U.S. Publication No. 2022/0017535 A1 Provided on IDS) as applied to claims 1, 2, 10 and 28 above and further in view of Wasmuth et al. WO 2017/223179 (Provided on IDS).
The cited claims of the instant application claim a method of treating PMM2-CDG, and increasing PMM2 enzymatic activity in a subject with PMM2-CDG comprising administering a therapeutically effective amount of an aldose reductase inhibitor to a subject in need thereof, wherein the aldose reductase inhibitor is a compound of Formula (III) such as
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or a salt thereof or a compound of formula (I) or (II) such as
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The cited claims of copending ‘022 claim a method of inhibiting aldose reductase activity in a subject and treating a disorder such as phosphomannomutase 2-congenital disorder of glycosylation (PMM2-CDG) comprising the administration of a compound of formula (I) or a compound of formula (II).
The cited claims of copending ‘022 do not claim the administration of the same aldose reductase inhibitor compounds as claimed in the instant claims
Wasmuth et al. teaches that aldose reductase (AR) is a monomeric, NADPH-dependent oxidoreductase from the aldo-keto reductase family of enzymes that is present in many parts of the body and catalyzes the reduction of saturated and unsaturated aldehydes, including aldo sugars and monosaccharides, as well as a broad array of other substrates [0006]. Wasmuth et al. teaches that primarily, aldose reductase catalyzes the reduction of glucose to sorbitol, one of the steps in the sorbitol pathway that is responsible for fructose formation from glucose [0006].
Wasmuth et al. teaches compounds of formula (III) ([0009]-[0017] and [0066]-[0091]). Wasmuth et at. teaches that a preferred compound is
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([0018], [0031], [0092]-[0093], claims 10 and 23). Wasmuth et al. teaches a method of inhibiting aldose reductase activity in a human patient comprising the administration of the compounds disclosed therein [0035]-[0037]. Wasmuth et al. teaches that the compounds and/or compositions of the invention may be effective in treating, reducing, and/or suppressing complications related to aldose reductase activity [0054]. Wasmuth et al. teaches that the compounds or compositions of the invention can be useful in applications that benefit from inhibition of aldose reductase enzymes [0127]-[0128].
Wasmuth et al. teaches that the compound can be administered orally ([0139] [0152]-[0154]). Wasmuth et al. teaches that the compound can be administered once daily [0157].
Thus Wasmuth et al. teaches the same compounds as claimed in the instant claims useful for inhibiting aldose reductase activity, leading to decreases in sorbitol levels.
Accordingly, prior to the effective filing date of the instant claims it would have been obvious to a person of ordinary skill in the art to combine the teachings of the claims of copending ‘022 which specifically claim a method for treating Phosphomannomutase deficiency disease (PMM2 or PMM2-CDG) in a patient in need thereof comprising administering a therapeutically effective amount of an aldose reductase inhibitor, with the teachings of Wasmuth et al. which teaches compounds of formula (III) as claimed in the instant claims wherein a preferred compound is
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useful for inhibiting aldose reductase activity in a human patient. Thus since the compounds of Wasmuth et al. are aldose reductase inhibitors, a person of ordinary skill in the art would have been motivated to administer said compounds of Wasmuth et al. in the method of copending ‘022 with a reasonable expectation of similar success.
Thus the cited claims of the instant application are rendered obvious in view of the cited prior art teachings of the claims of copending ‘022.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 6-8 and 23-27 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 12-15 and 31-33 of copending Application No. 17,489,022 (U.S. Publication No. 2022/0017535 A1 Provided on IDS) as applied to claims 1, 2, 10 and 28 above and further in view of Wasmuth et al. U.S. Publication No. 2013/0225592 A1 (Provided on IDS).
Claims 6-8 and 23-27 of the instant application claim a method of treating PMM2-CDG, and increasing PMM2 enzymatic activity in a subject with PMM2-CDG comprising administering a therapeutically effective amount of an aldose reductase inhibitor to a subject in need thereof, wherein the aldose reductase inhibitor is a compound of Formula (II) or (I) such as
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The cited claims of copending ‘022 claim a method of inhibiting aldose reductase activity in a subject and treating a disorder such as phosphomannomutase 2-congenital disorder of glycosylation (PMM2-CDG) comprising the administration of a compound of formula (I) or a compound of formula (II).
The cited claims of copending ‘022 do not claim the administration of the same aldose reductase inhibitor compounds as claimed in the instant claims
Wasmuth et al. teaches that aldose reductase, an enzyme present in many parts of the body, catalyzes the reduction of glucose to sorbitol, one of the steps in the sorbitol pathway that is responsible for fructose formation from glucose [0006].
Wasmuth et al. teaches compounds of formula (I) and (II) ([0007]-[0019, [0047]-[0129]). Wasmuth et at. teaches that preferred compounds are
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and
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([0130]-[0131], [0197], claims 10-13). Wasmuth et al. teaches a method of inhibiting aldose reductase activity in a human patient comprising the administration of the compounds disclosed therein (claims 15 and 17). Wasmuth et al. teaches that the compounds and/or compositions of the invention may be effective in treating, reducing, and/or suppressing complications related to aldose reductase activity [0029]. Wasmuth et al. teaches that the compounds or compositions of the invention can be useful in applications that benefit from inhibition of aldose reductase enzymes [0166].
Thus Wasmuth et al. teaches the same compounds as claimed in the instant claims useful for inhibiting aldose reductase activity, leading to decreases in sorbitol levels.
Accordingly, prior to the effective filing date of the instant claims it would have been obvious to a person of ordinary skill in the art to combine the teachings of the claims of copending ‘022 which specifically claims a method for treating Phosphomannomutase deficiency disease (PMM2 or PMM2-CDG) in a patient in need thereof comprising administering a therapeutically effective amount of an aldose reductase inhibitor, with the teachings of Wasmuth et al. which teaches compounds of formula (I) and (II) as claimed in the instant claims wherein preferred compounds are
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and
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useful for inhibiting aldose reductase activity in a human patient. Thus since the compounds of Wasmuth et al. are aldose reductase inhibitors, a person of ordinary skill in the art would have been motivated to administer said compounds of Wasmuth et al. in the method of the claims of copending ‘022 with a reasonable expectation of similar success.
Thus the cited claims of the instant application are rendered obvious in view of the cited claims of copending ‘022.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claim Rejections - 35 USC § 102
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 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)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1, 2, 10 and 28 are rejected under 35 U.S.C. 102(a)(2) as being anticipated by Perlstein et al. WO 2020/040831 A1 ((Provided on IDS).
Claims 1, 2, 10 and 28 of the instant application claim a method of treating PMM2-CDG, and increasing PMM2 enzymatic activity in a subject with PMM2-CDG comprising administering a therapeutically effective amount of an aldose reductase inhibitor to a subject in need thereof.
Perlstein et al. teaches that congenital disorders of glycosylation (CDG) include more than 130 inborn errors of metabolism that affects N-linked, O-linked protein and lipid-linked glycosylation wherein Phosphomannomutase deficiency disease (PMM2 or PMM2-CDG) is the most common disorder of glycosylation with more than 800 patients reported worldwide [0003]. Perlstein et al. teaches that PMM2 is a rare congenital disorder of glycosylation with no cure that is an autosomal recessive disorder arising from a dysfunctional phosphomannomutase-2 gene [0004] and [0099]. Perlstein et al. teaches that the phosphomannomutase-2 enzyme is responsible for transforming mannose 6-phosphate into mannose 1-phosphate, which in turn leads to the synthesis of GDP-mannose and insufficient levels of GDP-mannose leads to under-glycosylated glycoproteins, lysosomal enzymes and serum proteins and this in turn is associated with increased proteasomal and oxidative stress [0004] and [0099]. Perlstein et al. teaches that resolving the glycosylation defect, decreasing proteasomal stress, and decreasing oxidative stress may all or singly contribute to a therapeutic effect in the disease [0004] and [0099]. Perlstein et al. teaches that PMM2-CDG patients suffer from neuromuscular abnormalities, developmental delays, failure to thrive and multiple organ system involvement from liver to kidneys [0005] and [0099].
Perlstein et al. teaches methods for increasing glycosylation in a patient in need thereof comprising administering a therapeutically effective amount of an aldose reductase inhibitor [0009]. Perlstein et al. further teaches methods for treating a condition or disorder mediated, at least in part, by phosphomannomutase-2 enzyme in a patient in need thereof comprising administering a therapeutically effective amount of an aldose reductase inhibitor [0017] and [0021]. Perlstein et al. further teaches methods for treating phosphomannomutase deficiency in a patient in need thereof comprising administering a pharmaceutical composition comprising a pharmaceutically acceptable carrier and a therapeutically effective amount of an aldose reductase inhibitor [0037].
Perlstein et al. teaches an aldose reductase inhibitor is a compound that can inhibit the activity of the enzyme, aldose reductase wherein aldose reductase inhibitors may reduce the flux of glucose through the polyol pathway, which can lead to inhibition of tissue accumulation of sorbitol and fructose and prevention of reduction of redox potentials [0082]. Non-limiting examples of an aldose reductase inhibitor include but are not limited to alrestatin, epalrestat, fidarestat, imirestat, lidorestat, minalrestat, ponalrestat, ranirestat, salfredin B11, sorbinil, tolrestat, zenarestat, and zopolrestat [0082] and [0084]-[0085].
Perlstein et al. teaches the treatment of a congenital disorder of glycosylation (CDG) which is associated with deficient or defective glycosylation of various tissue proteins or lipids. Individuals with a CDG are missing an enzyme required for glycosylation [0098]. Perlstein et al. teaches the treatment of Phosphomannomutase deficiency disease (PMM2 or PMM2-CDG, and also previously known as CDG-Ia) a rare congenital disorder of glycosylation with no cure [0099].
Claims 34-43 of Perlstein et al. claim a method for increasing glycosylation in a patient in need thereof comprising administering a therapeutically effective amount of an aldose reductase inhibitor; a method for treating a condition or disorder mediated, at least in part, by phosphomannomutase-2 enzyme in a patient in need thereof comprising administering a therapeutically effective amount of an aldose reductase inhibitor; method for treating a congenital disorder of glycosylation in a patient in need thereof comprising administering a therapeutically effective amount of an aldose reductase inhibitor; a method for treating phosphomannomutase deficiency in a patient in need thereof comprising administering a therapeutically effective amount of an aldose reductase inhibitor.
Claims 1 and 2 of the instant application are anticipated since Perlstein et al. specifically teaches and claims a method for treating Phosphomannomutase deficiency disease (PMM2 or PMM2-CDG) in a patient in need thereof comprising administering a therapeutically effective amount of an aldose reductase inhibitor. Therefore since Perlstein specifically teaches treating a subject with PMM2-CDG with an effective amount of an aldose reductase inhibitor said treatment will inherently increase PMM2 enzymatic activity as claimed in claim 2 of the instant application.
Thus the cited claims of the instant application are rejected in view of the prior art teachings.
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.
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.
Claims 3-5, 20-22 are rejected under 35 U.S.C. 103 as being unpatentable over Perlstein et al. WO 2020/040831 A1 (Provided on IDS) as applied to claims 1, 2, 10 and 28 above and further in view of Wasmuth et al. WO 2017/223179 (Provided on IDS).
Claims 3-5 and 20-22 of the instant application claim a method of treating PMM2-CDG, and increasing PMM2 enzymatic activity in a subject with PMM2-CDG comprising administering a therapeutically effective amount of an aldose reductase inhibitor to a subject in need thereof, wherein the aldose reductase inhibitor is a compound of Formula (III) such as
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or a salt thereof.
Perlstein et al. is as set forth above.
Perlstein et al. does not teach the claimed compounds of formula (III).
Wasmuth et al. teaches that aldose reductase (AR) is a monomeric, NADPH-dependent oxidoreductase from the aldo-keto reductase family of enzymes that is present in many parts of the body and catalyzes the reduction of saturated and unsaturated aldehydes, including aldo sugars and monosaccharides, as well as a broad array of other substrates [0006]. Wasmuth et al. teaches that primarily, aldose reductase catalyzes the reduction of glucose to sorbitol, one of the steps in the sorbitol pathway that is responsible for fructose formation from glucose [0006].
Wasmuth et al. teaches compounds of formula (III) ([0009]-[0017] and [0066]-[0091]). Wasmuth et at. teaches that a preferred compound is
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([0018], [0031], [0092]-[0093], claims 10 and 23). Wasmuth et al. teaches a method of inhibiting aldose reductase activity in a human patient comprising the administration of the compounds disclosed therein [0035]-[0037]. Wasmuth et al. teaches that the compounds and/or compositions of the invention may be effective in treating, reducing, and/or suppressing complications related to aldose reductase activity [0054]. Wasmuth et al. teaches that the compounds or compositions of the invention can be useful in applications that benefit from inhibition of aldose reductase enzymes [0127]-[0128].
Wasmuth et al. teaches that the compound can be administered orally ([0139] [0152]-[0154]). Wasmuth et al. teaches that the compound can be administered once daily [0157].
Thus Wasmuth et al. teaches the same compounds as claimed in the instant claims useful for inhibiting aldose reductase activity, leading to decreases in sorbitol levels.
Accordingly, prior to the effective filing date of the instant claims it would have been obvious to a person of ordinary skill in the art to combine the teachings of Perlstein et al. which specifically teaches and claims a method for treating Phosphomannomutase deficiency disease (PMM2 or PMM2-CDG) in a patient in need thereof comprising administering a therapeutically effective amount of an aldose reductase inhibitor, with the teachings of Wasmuth et al. which teaches compounds of formula (III) as claimed in the instant claims wherein a preferred compound is
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useful for inhibiting aldose reductase activity in a human patient. Thus since the compounds of Wasmuth et al. are aldose reductase inhibitors, a person of ordinary skill in the art would have been motivated to administer said compounds of Wasmuth et al. in the method of Perlstein et al. with a reasonable expectation of similar success.
Thus the cited claims of the instant application are rendered obvious in view of the cited prior art teachings.
Claims 6-8 and 23-27 are rejected under 35 U.S.C. 103 as being unpatentable over Perlstein et al. WO 2020/040831 A1 (Provided on IDS) as applied to claims 1, 2, 10 and 28 above and further in view of Wasmuth et al. U.S. Publication No. 2013/0225592 A1 (Provided on IDS).
Claims 6-8 and 23-27 of the instant application claim a method of treating PMM2-CDG, and increasing PMM2 enzymatic activity in a subject with PMM2-CDG comprising administering a therapeutically effective amount of an aldose reductase inhibitor to a subject in need thereof, wherein the aldose reductase inhibitor is a compound of Formula (II) or (I) such as
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Perlstein et al. is as set forth above.
Perlstein et al. does not teach the claimed compounds of formula (I) or (II).
Wasmuth et al. teaches that aldose reductase, an enzyme present in many parts of the body, catalyzes the reduction of glucose to sorbitol, one of the steps in the sorbitol pathway that is responsible for fructose formation from glucose [0006].
Wasmuth et al. teaches compounds of formula (I) and (II) ([0007]-[0019, [0047]-[0129]). Wasmuth et at. teaches that preferred compounds are
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([0130]-[0131], [0197], claims 10-13). Wasmuth et al. teaches a method of inhibiting aldose reductase activity in a human patient comprising the administration of the compounds disclosed therein (claims 15 and 17). Wasmuth et al. teaches that the compounds and/or compositions of the invention may be effective in treating, reducing, and/or suppressing complications related to aldose reductase activity [0029]. Wasmuth et al. teaches that the compounds or compositions of the invention can be useful in applications that benefit from inhibition of aldose reductase enzymes [0166].
Thus Wasmuth et al. teaches the same compounds as claimed in the instant claims useful for inhibiting aldose reductase activity, leading to decreases in sorbitol levels.
Accordingly, prior to the effective filing date of the instant claims it would have been obvious to a person of ordinary skill in the art to combine the teachings of Perlstein et al. which specifically teaches and claims a method for treating Phosphomannomutase deficiency disease (PMM2 or PMM2-CDG) in a patient in need thereof comprising administering a therapeutically effective amount of an aldose reductase inhibitor, with the teachings of Wasmuth et al. which teaches compounds of formula (I) and (II) as claimed in the instant claims wherein preferred compounds are
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and
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useful for inhibiting aldose reductase activity in a human patient. Thus since the compounds of Wasmuth et al. are aldose reductase inhibitors, a person of ordinary skill in the art would have been motivated to administer said compounds of Wasmuth et al. in the method of Perlstein et al. with a reasonable expectation of similar success.
Thus the cited claims of the instant application are rendered obvious in view of the cited prior art teachings.
Conclusion
Claims 1-8, 10 and 20-28 are rejected. Claims 9 and 11-19 are canceled. No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to KARA R. MCMILLIAN whose telephone number is (571)270-5236. The examiner can normally be reached Tuesday-Friday 12:00 PM-6:00 PM.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Adam C. Milligan can be reached on (571)270-7674. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/KARA R. MCMILLIAN/Primary Examiner, Art Unit 1623
KRM