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 Division of U.S. Application No. 15/752,130 filed on 02/12/2018, now U.S. Patent No. 11,207,320 which is a national stage entry of PCT/US2016/046912 filed on 08/12/2016 which claims benefit of U.S. Provisional Application No. 62/204,875 filed on 08/13/2015.
Response to Amendment
Applicant’s amendment filed on January 2, 2026 amending claim 4 has been entered. Claims 5, 15 and 16 remain withdrawn. Claims 1-3, 11-13 and 17-19 are canceled. Claims 4, 6-10 and 14 are currently presented for examination.
Response to Arguments
Applicant's arguments found on pages 4-6 of Applicant’s remarks filed January 2, 2026 with respect to the rejection under 35 USC 101 have been fully considered but they are not persuasive.
It is maintained that Applicant’s arguments are found not persuasive since claim 4 as amended recites “A method of identifying and treating a subject having a cancer cell responsive to PDE3A modulation, the method comprising detecting an increase in a PDE3A and SLFN12 polypeptide or polynucleotide level in a biological sample of the subject relative to a reference, thereby identifying said subject as having a cancer responsive to PDE3A modulation, and administering a PDE3A modulator to the subject identified as having cancer responsive to PDE3A modulation, wherein the PDE3A modulator promotes binding of the PDE3A polypeptide with the SLFN12 peptide in the cancer cell.”
The claims relate in part to a process for identifying a subject with cancer that may be responsive to PDE3A modulation and thus the subject of the method as claimed is any subject with cancer. In other words, the subject of the claimed method may or may not have cancer that is responsive to PDE3A modulation. Therefore, the claims are rejected under 35 USC 101 since the claims encompass in part detecting an increase in a PDE3A and SLFN12 polypeptide or polynucleotide level in a biological sample of the subject relative to a reference and only administering a PDE3A modulator to the subject identified as having cancer responsive to PDE3A modulation. Therefore the claims encompass in part, only detecting an increase in a PDE3A and SLFN12 polypeptide or polynucleotide level in a biological sample of the subject relative to a reference, if the subject is determined to not have an increase in a PDE3A and SLFN12 polypeptide or polynucleotide level. In said subject not having the required increases in the biomarkers, the administration of a PDE3A modulator would not occur since the subject would not be identified as having cancer responsive to PDE3A modulation. The claims remain rejected under 35 USC 101 since not all subjects tested will be determined to be responsive to a PDE3A modulator and thus will not be administered the modulator. Moreover, the claims do not exclude testing subjects that do not have an increase in a PDE3A and SLFN12 polypeptide or polynucleotide level who would not be administered the PDE3A modulator as argued by Applicant.
Therefore it is maintained that the claims are drawn in part to collecting a biological sample from a patient with cancer, such as a tissue sample, and performing certain procedures on that sample, such as immunoblotting, Northern blot, or microarray analysis, to determine the natural state of the levels of PDE3A and SLFN12 polypeptide or polynucleotide levels in that sample prior to any administration of any non-naturally occurring component. The rejected claims are drawn in part to only to a method of determining if a patient is suitable for treatment with a compound that modulates PDE3A and not to treating said patient by administering a compound if that patient is not identified as suitable for treatment. Thus the claims encompass in part no administration of any modulator if the subject is not identified as having a cancer responsive to PDE3A modulation.
Thus it is maintained that even though Applicant has discovered the correlation between PDE3A and SLFN12 polypeptide or polynucleotide levels and a cancer cell that is responsive to PDE3A modulation, and thus takes a human action to trigger the manifestation of the correlation, the correlation exists in principle apart from any human action. Thus, the PDE3A and/or SLFN12 polypeptide or polynucleotide levels in a cancer cell and a cancer cell that is responsive to PDE3A modulation is a natural phenomenon or a naturally occurring correlation.
For these reasons the previous rejection under 35 USC 101 is hereby maintained and reproduced below.
Due to Applicant’s amendments to the claims, the previous rejection of claims 4, 6-10 and 14 under 35 U.S.C. 112(a) for failing to comply with the written description requirement is hereby withdrawn. Specifically, the claims have been amended to recite administration of a PDE3 modulator that promotes binding of the PDE3A polypeptide with SLFN12 peptide in the cancer cell which corresponds to the results of Figures 19 and 20 which demonstrates that only PDE3A modulators that induce an interaction between PDE3A and SLFN12 and not all PDE3A modulators, are useful in the claimed method (page 53 of specification). Applicant’s arguments with respect to said rejection have been fully considered but moot in view of the withdrawal of the rejection.
Upon further consideration and in view of Applicant’s remarks, the previous rejection of claims 4, 6-10 and 14 under 35 U.S.C. 112(b) is hereby withdrawn. The subject as claimed in claim 4 is given its broadest reasonable interpretation as any subject having cancer. Thus the claims are interpreted as identifying a subject having cancer that would be response to PDE3A modulation and treating said subject if said subject is determined to have an increase in PDE3A and SLFN12 levels.
Applicant’s arguments with respect to the double patenting rejections have been fully considered but are found not persuasive.
Applicant argues that the patents do not recite any detection step as claimed.
These arguments are found not persuasive since each of the patents teach a selection step which necessarily encompasses a detection step as claimed in the instant claims.
Claims 1-10 of ‘320 claim wherein the cell was selected as having an increase in the level of a PDE3A and a SLFN12 polypeptide or polynucleotide relative to a reference; claims 1-8 of ‘986 claim wherein the cell was selected as responsive when the cell has an increased level of a PDE3A and Schlafen 12 (SLFN12) polypeptide or polynucleotide, relative to a reference; the cited claims of ‘522 claim the cell was selected as having an increase in the level of a PDE3A and/or PDE3B or Schlafen 12 (SLFN12) polypeptide or polynucleotide, or combination thereof, relative to a reference, thereby reducing the survival of the cancer cell; and the subject is pre-selected by detecting an increase in the level of a PDE3A and/or PDE3B and Schlafen 12 (SLFN12) polypeptide or polynucleotide, or combination thereof, in a cell from the subject's cancer relative to a reference; and claims 1-13 of ‘880 claim wherein said cell is selected as responsive to said PDE3 modulator when said cell: has increased expression of PDE3A and/or PDE3B polypeptides or polynucleotides relative to a reference, and (iii) has increased expression of SLFN12 polypeptides or polynucleotides relative to the reference, and detecting the expression of phosphodiesterase 3A (PDE3A) polypeptides or polynucleotides or the expression of phosphodiesterase 3B (PDE3B) polypeptides or polynucleotides in the cell relative to a reference, and the expression of Schlafen family member 12 (SLFN12) polypeptides or polynucleotides in the cell relative to the reference. Thus each of the cited patents teach selection based on levels of PDE3A and SLFN12 levels and necessarily encompass detecting the levels of said proteins as claimed in the instant claims. Moreover, patents ‘880 and ‘522 specifically recite a detecting step contrary to Applicant’s arguments. Thus the previous double patenting rejections are hereby maintained and reproduced below.
This action is final.
Claim Rejections - 35 USC § 101
35 U.S.C. 101 reads as follows:
Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title.
Claims 4, 6-10 and 14 are rejected under 35 U.S.C. 101 because the claimed invention is directed to the judicial exception of a natural phenomenon or an abstract idea without significantly more.
The cited claims recite a method of identifying and treating a subject having a cancer cell responsive to PDE3A modulation, the method comprising detecting an increase in a PDE3A and SLFN12 polypeptide or polynucleotide level in a biological sample of the subject relative to a reference, thereby identifying said subject as having a cancer responsive to PDE3A modulation, and administering a PDE3A modulator to the subject identified as having cancer responsive to PDE3A modulation.
The claims are rejected under 35 USC 101 since the claims encompass in part detecting an increase in a PDE3A and SLFN12 polypeptide or polynucleotide level in a biological sample of the subject relative to a reference and only administering a PDE3A modulator to the subject identified as having cancer responsive to PDE3A modulation. Therefore the claims encompass in part, only detecting an increase in a PDE3A and SLFN12 polypeptide or polynucleotide level in a biological sample of the subject relative to a reference, if the subject is determined to not have an increase in a PDE3A and SLFN12 polypeptide or polynucleotide level. In said subject not having the required increases, the administration of a PDE3A modulator would not occur since the subject would not be identified as having cancer responsive to PDE3A modulation. The claims are rejected since not all subjects tested will be determined to be responsive to a PDE3A modulator and thus will not be administered the modulator. Moreover, the claims do not exclude testing subjects that do not have an increase in a PDE3A and SLFN12 polypeptide or polynucleotide level who would not be administered the PDE3A modulator.
Therefore the claims are drawn in part to collecting a biological sample from a patient with cancer, such as a tissue sample, and performing certain procedures on that sample, such as immunoblotting, Northern blot, or microarray analysis, to determine the natural state of the levels of PDE3A and SLFN12 polypeptide or polynucleotide levels in that sample prior to any administration of any non-naturally occurring component. The rejected claims are drawn in part to only to a method of determining if a patient is suitable for treatment with a compound that modulates PDE3A and not to treating said patient by administering a compound if that patient is not identified as suitable for treatment. Thus the claims encompass in part no administration of any modulator if the subject is not identified as having a cancer responsive to PDE3A modulation.
This judicial exception is not integrated into a practical application because the claims of the instant application are directed in part to non-statutory subject matter as detailed above because it is not a patent-eligible practical application of a law of nature. The claims are directed in part to a naturally occurring correlation between PDE3A and/or SLFN12 polypeptide or polynucleotide levels and a cancer cell that is responsive to PDE3A modulation. The combination of steps recited in the claims taken as a whole, including the steps of detecting an increase in a PDE3A and/or SLFN12 polypeptide or polynucleotide level in a biological sample of the subject relative to a reference, thereby identifying said subject as having a cancer responsive to PDE3A modulation, are not sufficient to qualify as a patent-eligible practical application as the claim covers every substantial practical application of the correlation. Even though Applicant has discovered the correlation between PDE3A and/or SLFN12 polypeptide or polynucleotide levels and a cancer cell that is responsive to PDE3A modulation, and thus takes a human action to trigger the manifestation of the correlation, the correlation exists in principle apart from any human action. Thus, the PDE3A and/or SLFN12 polypeptide or polynucleotide levels in a cancer cell and a cancer cell that is responsive to PDE3A modulation is a natural phenomenon or a naturally occurring correlation.
A natural principle is the handiwork of nature and occurs without the hand of man. For example, the disinfecting property of sunlight is a natural principle. The relationship between blood glucose levels and diabetes is a natural principle. A correlation that occurs naturally when a man-made product, such as a drug, interacts with a naturally occurring substance, such as blood, is also considered a natural principle because, while it takes a human action to trigger a manifestation of the correlation, the correlation exists in principle apart from any human action. These are illustrative examples and are not intended to be limiting or exclusive.
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For this analysis, the claims focus on a natural principle since the natural principle is a limiting element or step. Thus, the claims are not directed to a practical application of the natural principle that amounts to substantially more than the natural principle itself.
Eligibility Step 2B: Whether a claim amounts to significantly more.
The claims do not include additional elements that are sufficient to amount to significantly more than the judicial exception because the claims do not include additional elements/steps or a combination of elements/steps that integrate the natural principle into the claimed invention such that the natural principle is practically applied to ensure that the claims amount to significantly more than the natural principle itself.
A claim that focuses on the use of a natural principle must also include additional elements or steps to show that the inventor has practically applied, or added something significant to, the natural principle itself. See Mayo Collaborative Servs. v. Prometheus Labs., Inc., 566 U.S. 66, 71-72, 101 USPQ2d 1961, 1966 (2012)). To show integration, the additional elements or steps must relate to the natural principle in a significant way to impose a meaningful limit on the claim scope. The analysis turns on whether the claim has added enough to show a practical application. See id. at 1968. In other words, the claim cannot cover the natural principle itself such that it is effectively standing alone. A bare statement of a naturally occurring correlation, albeit a newly discovered natural correlation or very narrowly confined correlation, is not sufficient. See id. at 1965, 1971.
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A claim with steps that add something of significance to the natural laws themselves would be eligible because it would confine its reach to particular patent-eligible applications of those laws, such as a typical patent on a new drug (including associated method claims) or a new way of using an existing drug. See id. at 1971; see also 35 U.S.C. 100(b). In other words, the claim must be limited so that it does not preempt the natural principle being recited by covering every substantial practical application of that principle. The process must have additional features that provide practical assurance that the process is more than a drafting effort designed to monopolize the law of nature itself. See id. at 1968.
In the instant case, the claims are drawn in part to only the natural correlation between PDE3A and/or SLFN12 polypeptide or polynucleotide levels and a cancer cell that is responsive to PDE3A modulation; and thus the claims do not require any further steps that integrate the recited judicial exceptions into a practical application of the exception. The claims are drawn in part as detailed above to only identifying if a subject having a cancer cell is responsive to PDE3A modulation and no further limitations are present in the claims reciting the next steps when it is confirmed that the subject is not responsive. Therefore if the subject is not identified as having a cancer responsive to PDE3A modulation, no further steps are performed. Thus, said claims encompass in part no administration step of any compound, since the subject can be identified as having a cancer that is not responsive to PDE3A modulation.
For these reasons, when the claims are considered as a whole, the claims do not recite anything significantly more than a judicial exception and therefore are not directed to patent eligible subject matter.
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 §§ 706.02(l)(1) - 706.02(l)(3) 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 USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The 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/process/file/efs/guidance/eTD-info-I.jsp.
Claims 4, 6-10 and 14 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-10 of U.S. Patent No. 11,207,320 B2 (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 would be anticipated by the cited claims ‘320.
Claims 4, 6-10 and 14 of the instant application claim a method of identifying and treating a subject having a cancer cell responsive to PDE3A modulation, the method comprising detecting an increase in a PDE3A and SLFN12 polypeptide or polynucleotide level in a biological sample of the subject relative to a reference, thereby identifying said subject as having a cancer responsive to PDE3A modulation, and administering a PDE3A modulator to the subject identified as having cancer responsive to PDE3A modulation.
Claims 1-10 of ‘320 claim a method of reducing cancer cell proliferation, killing, or reducing the survival of a cancer cell selected as responsive to a phosphodiesterase 3A (PDE3A) modulator, the method comprising contacting the cell with a PDE3A modulator that induces interaction between PDE3A and Schlafen 12 (SLFN12) proteins in the cell, wherein the cell was selected as having an increase in the level of a PDE3A and a SLFN12 polypeptide or polynucleotide relative to a reference, thereby reducing cancer cell proliferation, killing, or reducing the survival of the cancer cell, wherein the PDE3A modulator is 6-(4-(diethylamino)-3-nitrophenyl)-5-methyl-4,5-dihydropyridazin-3(2H)-one (DNMDP), or a pharmaceutically acceptable salt thereof.
Thus the claims of the instant application would be anticipated over the cited claims of ‘320.
Therefore, the cited claims of the instant application are not patentably distinct over the cited claims of ‘320.
Claims 4, 6-10 and 14 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-8 of U.S. Patent No. 10,966,986 (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 would be anticipated by the cited claims ‘986.
Claims 4, 6-10 and 14 of the instant application claim a method of identifying and treating a subject having a cancer cell responsive to PDE3A modulation, the method comprising detecting an increase in a PDE3A and SLFN12 polypeptide or polynucleotide level in a biological sample of the subject relative to a reference, thereby identifying said subject as having a cancer responsive to PDE3A modulation, and administering a PDE3A modulator to the subject identified as having cancer responsive to PDE3A modulation.
Claims 1-8 of ‘986 claim a method of killing or reducing survival of a cancer cell selected as responsive to a phosphodiesterase 3A (PDE3A) modulator, the method comprising contacting the cell with a PDE3A modulator wherein the cell was selected as responsive when the cell has an increased level of a PDE3A and Schlafen 12 (SLFN12) polypeptide or polynucleotide, relative to a reference, thereby reducing the survival of the cancer cell; and a method of reducing cancer cell proliferation in a subject pre-selected as having a cancer that is responsive to a PDE3A modulator, the method comprising administering to said subject a PDE3A modulator wherein the subject is pre-selected by detecting an increased level of a PDE3A and Schlafen 12 (SLFN12) polypeptide or polynucleotide, relative to a reference, thereby reducing cancer cell proliferation in said subject. Thus the claims of the instant application would be anticipated over the cited claims of ‘986.
Therefore, the cited claims of the instant application are not patentably distinct over the cited claims of ‘986.
Claims 4, 6-10 and 14 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 3-7, 9 and 10 of U.S. Patent No. 11,142,522 B2 (of record). Although the claims at issue are not identical, they are not patentably distinct from each other because the cited claims of the instant application would be anticipated by the cited claims ‘522.
Claims 4, 6-10 and 14 of the instant application claim a method of identifying and treating a subject having a cancer cell responsive to PDE3A modulation, the method comprising detecting an increase in a PDE3A and SLFN12 polypeptide or polynucleotide level in a biological sample of the subject relative to a reference, thereby identifying said subject as having a cancer responsive to PDE3A modulation, and administering a PDE3A modulator to the subject identified as having cancer responsive to PDE3A modulation.
The cited claims of ‘522 claim a method of killing or reducing the survival of a cancer cell selected as responsive to a phosphodiesterase 3A (PDE3A) and/or (PDE3B) modulator involving contacting the cell with a compound of claim 1 where the cell was selected as having an increase in the level of a PDE3A and/or PDE3B or Schlafen 12 (SLFN12) polypeptide or polynucleotide, or combination thereof, relative to a reference, thereby reducing the survival of the cancer cell; and a method of reducing cancer cell proliferation in a subject pre-selected as having a cancer that is responsive to one or more PDE3A and/or PDE3B modulators comprising administering to the subject a compound of claim 1, where the subject is pre-selected by detecting an increase in the level of a PDE3A and/or PDE3B and Schlafen 12 (SLFN12) polypeptide or polynucleotide, or combination thereof, in a cell from the subject's cancer relative to a reference, thereby reducing cancer cell proliferation in said subject.
Thus the cited claims of the instant application would be anticipated over the cited claims of ‘522.
Therefore, the cited claims of the instant application are not patentably distinct over the cited claims of ‘522.
Claims 4, 6-10 and 14 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-13 of U.S. Patent No. 12,325,880 B2. Although the claims at issue are not identical, they are not patentably distinct from each other because the cited claims of the instant application would be anticipated by the cited claims ‘880.
Claims 4, 6-10 and 14 of the instant application claim a method of identifying and treating a subject having a cancer cell responsive to PDE3A modulation, the method comprising detecting an increase in a PDE3A and SLFN12 polypeptide or polynucleotide level in a biological sample of the subject relative to a reference, thereby identifying said subject as having a cancer responsive to PDE3A modulation, and administering a PDE3A modulator to the subject identified as having cancer responsive to PDE3A modulation.
Claims 1-13 of ‘880 claim a method of killing or reducing the survival of a cell selected as responsive to PDE3A-SLFN12 complex formation or PDE3B-SLFN12 complex formation comprising contacting said cell with a PDE3 modulator, wherein said cell is selected as responsive to said PDE3 modulator when said cell: (i) expresses AIP and/or TRRAP polypeptides or polynucleotides, (ii) has increased expression of PDE3A and/or PDE3B polypeptides or polynucleotides relative to a reference, and (iii) has increased expression of SLFN12 polypeptides or polynucleotides relative to the reference, and a method for the treatment of a hyperproliferative disease, disorder, or condition in a subject such as cancer, comprising administering to said subject a PDE3 modulator, wherein said subject is identified as having a hyperproliferative disease, disorder, or condition that is responsive to the PDE3 modulator by obtaining one or more cells of the hyperproliferative disease, disorder, or condition from the subject and detecting: (i) the expression of aryl hydrocarbon receptor interacting protein (AIP) polypeptides or polynucleotides and/or transformation/transcription domain associated protein (TRRAP) polypeptides or polynucleotides in the cell; (ii) the expression of phosphodiesterase 3A (PDE3A) polypeptides or polynucleotides or the expression of phosphodiesterase 3B (PDE3B) polypeptides or polynucleotides in the cell relative to a reference, and (iii) the expression of Schlafen family member 12 (SLFN12) polypeptides or polynucleotides in the cell relative to the reference; wherein said hyperproliferative disease, disorder, or condition is characterized as responsive to said complex formation if: (i) AIP and/or TRRAP are expressed in the cell, (ii) the expression of PDE3A and/or PDE3B is increased relative to the reference, and (iii) the expression of SLFN12 is increased relative to the reference.
Thus the cited claims of the instant application would be anticipated over the cited claims of ‘880.
Therefore, the cited claims of the instant application are not patentably distinct over the cited claims of ‘880.
Conclusion
Claims 4, 6-10 and 14 are rejected. Claims 5, 15 and 16 are withdrawn. Claims 1-3, 11-13 and 17-19 are canceled. No claims are allowed.
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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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/KARA R. MCMILLIAN/Primary Examiner, Art Unit 1623
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