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 .
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.
Status of Claims
Claims 6 and 14-16 are pending and under examination. Claims 1-5 and 7-13 are canceled. Claims 14-16 are new.
Withdrawn Rejections
In light of the amendments, the objection is hereby withdrawn.
In light of the amendments, the 35 U.S.C. 101 rejection is hereby withdrawn.
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.
Claims 6 and 15 are rejected under 35 U.S.C. 103 as being unpatentable over Andorsky et al. (“Programmed Death Ligand 1 Is Expressed by Non–Hodgkin Lymphomas and Inhibits the Activity of Tumor-Associated T Cells”, Human Cancer Biology, Clinical Cancer Research, vol. 17(13), pgs. 4232-4244, published 07/01/2011) in view of Brahmer et al. (“Safety and Activity of Anti–PD-L1 Antibody in Patients with Advanced Cancer”, N. Engl. J. Med., vol. 366(26), 2455-2465, cited passages pgs. 1-16, published 06/28/2012).
With respect to claims 6 and 15, Andorsky teaches programmed death ligand 1 (PD-L1) is expressed on antigen-presenting cells and inhibits activation of T cells through its receptor PD-1 and PD-L1 is aberrantly expressed on some epithelial malignancies (see abstract). Andorsky teaches peripheral blood mononuclear cells (PBMC) were obtained from a patient (RS-27) (see pg. 4234, right col., para. 2). Andorsky further teaches to show that PD-L1 can also be immunologically active when expressed by B-cell lymphomas, analogous experiments were conducted using a tumor sample from patient with an aggressive DLBCL (RS-27) and circulating tumor cells strongly coexpressed PD-L1 and CD20, as measured by flow cytometry and PBMCs containing approximately 75% tumor cells and 20% CD3+ T cells were cultured with PHA in the presence or absence of anti-PD-L1 (see pg. 4238, right col., para. 4; and Fig. 4A). Note that Andorsky’s PBMCs containing tumor cells would read on the claimed CTC. Andosky teaches targeting PD-1/PD-L1 pathway using antagonistic mAbs may thus be an attractive approach to lymphoma immunotherapy (see pg. 4343, left col., para. 1). Andosky teaches PD-L1 is aberrantly expressed on some epithelial malignancies and Hodgkin lymphomas (see abstract), which would read on a subject having a solid tumor.
Even though Andosky teaches using anti-PD-L1 for detection and discloses mAbs may be an attractive approach for immunotherapy, the reference does not explicitly teach a subject having a solid tumor and administering an immunotherapy that inhibits the activity of PD-L1.
Brahmer teaches programmed death 1 (PD-1) protein, a T-cell coinhibitory receptor, and one of its ligands, PD-L1, play a pivotal role in the ability of tumor cells and blockade of interactions between PD-1 and PD-L1 enhances immune function in vitro and mediates antitumor activity in preclinical models (see abstract). Brahmer teaches the multicenter phase 1 trial by administering intravenously an anti-PD-L1 antibody to patients with selected advanced cancers (see abstract under methods). Brahmer teaches anti-PD-L1 therapy has the durability of response across multiple tumor types (see pg. 7, middle of para. 2). Brahmer teaches that peripheral-blood T cells express PD-L1, it is possible to assess in vivo receptor occupancy by anti-PD-L1 antibody as a pharmacodynamic measure (see pg. 7, para. 3). Brahmer teaches PD-L1 is the primary PD-1 ligand that is up-regulated in solid tumors and these properties make PD-L1 a potentially promising target for cancer immunotherapy (see pg. 2, para. 4 of Conclusions).
It would have been obvious to a person of ordinary skill in the art before the effective filing date of the claimed invention to have used the method of screening for PD-L1 expression in circulating tumor cells as taught by Andosky with the immunotherapy as taught by Brahmer because Andosky recognizes targeting PD-1/PD-L1 pathway using mAbs antibody may be an attractive approach for immunotherapy and Brahmer teaches that blockade of interactions between PD-1 and PD-L1 enhances immune function and anti-PD-L1 therapy has the durability of response across multiple tumor types. Additionally, it would have been obvious to have used a subject with epithelial malignancies and lymphomas because PD-L1 is also expressed on epithelial malignancies, as taught by Andosky.
The person would have a reasonable expectation of success in screening PD-L1 expression in circulating tumor cells and administering immunotherapy because it has been well understood by Andosky and Brahmer teach a relationship between PD-L1 and PD-1 and Brahmer further recognizes blockade of interactions between PD-1 and PD-L1 enhances immune function.
Claims 6 and 14-16 are rejected under 35 U.S.C. 103 as being unpatentable over Andorsky et al. (“Programmed Death Ligand 1 Is Expressed by Non–Hodgkin Lymphomas and Inhibits the Activity of Tumor-Associated T Cells”, Human Cancer Biology, Clinical Cancer Research, vol. 17(13), pgs. 4232-4244, published 07/01/2011) in view of Brahmer et al. (“Safety and Activity of Anti–PD-L1 Antibody in Patients with Advanced Cancer”, N. Engl. J. Med., vol. 366(26), 2455-2465, cited passages pgs. 1-16, published 06/28/2012) and Adams et al. (WO2013/181532A1, published 12/05/2013, IDS submitted 12/21/2020, cite no. BA).
Andorsky and Brahmer have been discussed in the above rejection. However, the references do not teach cancer associated macrophage-like cells (CAMLs) (claims 6, 14 and 16).
Adams teaches a new sensitive cell biomarker of solid tumors is identified in blood (see abstract). Adams teaches CAMLs are detected in the biological sample, the subject is identified as having a carcinoma or solid tumor. Adams further teaches detecting circulating tumor cells (CTCs) in the biological sample (see para. [0008]). Adams teaches CAMLs and CTCs are simultaneously detected using a microfilter (see para. [0013]). Adams teaches CTCs and CAMLs express biomarkers (see paras. [0071]-[0078]). Adams teaches CAMLs may be used together with CTCs and other biomarkers in the body fluids to provide a more complete understanding of the patient’s disease (see para. [0007]).
Thus, it would have been obvious to the person to have similarly expressed PD-L1 on CAMLs and reasonably expected success because Adams teaches CAMLs are used together with CTCs and express biomarkers to provide a more complete understanding of the patient’s disease.
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 6 and 14-16 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-15 of U.S. Patent No. 10871491B2 (‘491) in view of Andorsky et al. (“Programmed Death Ligand 1 Is Expressed by Non–Hodgkin Lymphomas and Inhibits the Activity of Tumor-Associated T Cells”, Human Cancer Biology, Clinical Cancer Research, vol. 17(13), pgs. 4232-4244, published 07/01/2011) and Brahmer et al. (“Safety and Activity of Anti–PD-L1 Antibody in Patients with Advanced Cancer”, N. Engl. J. Med., vol. 366(26), 2455-2465, cited pages 1-16, published 06/28/2012) and Adams et al. (WO2013/181532A1, published 12/05/2013, IDS submitted 12/21/2020, cite no. BA).
Patent ‘491 recites a method for confirming a diagnosis of cancer in a subject diagnosed with cancer, comprising detecting Cancer Associated Macrophage-Like cells (CAMLs) in a biological sample from the subject diagnosed with cancer, wherein said detecting comprises: (a) isolating intact cells of between about 20 microns to about 300 microns from the biological sample obtained from the subject using a microfilter having pores of about 15-20 microns in size, wherein the biological sample is one or more of peripheral blood, blood, lymph nodes, bone marrow, cerebral spinal fluid, tissue, or urine; and (b) selecting cells isolated in (a) having the following characteristics: (i) multiple individual nuclei and/or large fused nucleoli having a size of about 14-64 pm diameter; (ii) morphological shape selected from the group consisting of spindle, tadpole, round, oblong, and amorphous; and (iii) expression of one or more of the following markers: cytokeratin (CK) 8, CK18, CK19, vimentin, Cluster of differentiation (CD) 45, CD11c, CD 14, CD 146, CD202b, or CD31, wherein antibodies are used to select cells expressing the one or more markers, thereby detecting CAMLs in a biological sample from a subject, wherein when CAMLs are detected in the biological sample, the diagnosis of cancer is confirmed in the subject. Claim 3 recites administering an anti-cancer therapeutic to the subject when diagnosis of cancer is confirmed in the subject. Claim 14 recites determining the identity of the cancer via staining said CAMLs for selected cancer markers. Patent ‘491 fails to recite PD-L1 expression and administering an immunotherapy that inhibits the activity of PD-L1 to the subject.
Adams, Andorsky and Brahmer have been discussed in the above rejection. It would have been obvious at the time of filing to have used the method of screening biomarkers on CAMLs as recited in the Patent with PD-L1 expression in circulating tumor cells of Andosky and immunotherapy of Brahmer because Andosky recognizes targeting PD-1/PD-L1 pathway using mAbs antibody may be an attractive approach for immunotherapy and Brahmer teaches that blockade of interactions between PD-1 and PD-L1 enhances immune function and anti-PD-L1 therapy has the durability of response across multiple tumor types. Additionally, it would have been obvious to the person to have similarly expressed PD-L1 on CAMLs and reasonably expected success because Adams teaches CAMLs are used together with CTCs and express biomarkers to provide a more complete understanding of the patient’s disease.
The person would have a reasonable expectation of success in screening PD-L1 expression on CAMLs or CTCs because the Patent recites detecting expression of biomarkers on CAMLs and administering an anti-cancer therapeutic to the subject.
Claims 6 and 14-16 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-17 of U.S. Patent No. 10247725B2 (‘725) in view of Andorsky et al. (“Programmed Death Ligand 1 Is Expressed by Non–Hodgkin Lymphomas and Inhibits the Activity of Tumor-Associated T Cells”, Human Cancer Biology, Clinical Cancer Research, vol. 17(13), pgs. 4232-4244, published 07/01/2011) and Brahmer et al. (“Safety and Activity of Anti–PD-L1 Antibody in Patients with Advanced Cancer”, N. Engl. J. Med., vol. 366(26), 2455-2465, cited pages 1-16, published 06/28/2012) and Adams et al. (WO2013/181532A1, published 12/05/2013, IDS submitted 12/21/2020, cite no. BA).
Patent ‘725 recites a method of screening a subject for cancer, comprising detecting circulating Cancer Associated Macrophage-Like cells (CAMLs) in a biological sample from a subject previously determined to be high risk for cancer, wherein said detecting comprises: (a) isolating intact cells of between 20 and 300 micron in size from a biological sample obtained from a subject using a microfilter having pores of about 7-8 micros, wherein the biological sample is peripheral blood, and (b) selecting multi-nucleated cells isolated in (a) expressing one or more of the following markers: endothelial cell markers CD146, CD202b, and CD31, and monocyte cell markers CD11c and CD14, wherein antibodies are used to select cells expressing the one or more markers, thereby detecting CAMLs in a biological sample from a subject, wherein when CAMLs are detected in the biological sample, the subject is determined to have cancer. Claim 5 recites detecting CTCs in the biological sample, wherein when CAMLs and CTCs are detected in the biological sample, the subject is diagnosed with cancer. Claim 8 recites monitoring cancer treatment.
Patent ‘725 does not explicitly recite PD-L1 expression and administering an immunotherapy that inhibits the activity of PD-L1 to the subject.
Adams, Andorsky and Brahmer have been discussed in the above rejection. It would have been obvious at the time of filing to have used the method of screening biomarkers on CAMLs as recited in the Patent with PD-L1 expression in circulating tumor cells of Andosky and immunotherapy of Brahmer because Andosky recognizes targeting PD-1/PD-L1 pathway using mAbs antibody may be an attractive approach for immunotherapy and Brahmer teaches that blockade of interactions between PD-1 and PD-L1 enhances immune function and anti-PD-L1 therapy has the durability of response across multiple tumor types. Additionally, it would have been obvious to the person to have similarly expressed PD-L1 on CAMLs and reasonably expected success because Adams teaches CAMLs are used together with CTCs and express biomarkers to provide a more complete understanding of the patient’s disease. The person would have a reasonable expectation of success in screening PD-L1 expression on CAMLs or CTCs and administering a drug because the Patent recites cancer treatment for CAML.
Claims 6 and 14-16 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-26 of U.S. Patent No. 11156596B2 (‘596) in view of Andorsky et al. (“Programmed Death Ligand 1 Is Expressed by Non–Hodgkin Lymphomas and Inhibits the Activity of Tumor-Associated T Cells”, Human Cancer Biology, Clinical Cancer Research, vol. 17(13), pgs. 4232-4244, published 07/01/2011) and Brahmer et al. (“Safety and Activity of Anti–PD-L1 Antibody in Patients with Advanced Cancer”, N. Engl. J. Med., vol. 366(26), 2455-2465, cited pages 1-16, published 06/28/2012) and Adams et al. (WO2013/181532A1, published 12/05/2013, IDS submitted 12/21/2020, cite no. BA).
Patent ‘596 recites a method of screening a subject for cancer, comprising detecting circulating Cancer Associated Macrophage-Like cells (CAMLs) in a biological sample from a subject, wherein said detecting comprises: (a) isolating intact cells of between 20 and 300 micron in size from a biological sample obtained from a subject using a means selected from the group consisting of size exclusion methodology, immunocapture, red blood cell lysis, white blood cell depletion, FICOLL separation, electrophoresis, dielectrophoresis, flow cytometry, magnetic levitation, microfluidic chip, and a combination thereof, and selecting multi-nucleated cells isolated in (a) expressing CD31 and one or more of the following additional markers: cytokeratin (CK) 8, CK18, CK19, epithelial cellular adhesion molecule (EpCAM), cluster of differentiation (CD)45, vimentin, CD146, CD202b, CD11c or CD14, wherein antibodies are used to select cells expressing the one or more markers, thereby detecting CAMLs in a biological sample from a subject, wherein when CAMLs are detected in the biological sample, the subject is determined to have cancer. Claim 4 recites detecting circulating tumor cells (CTCs) in the biological sample. Claim 14 recites monitoring cancer treatment.
Patent ‘596 does not explicitly recite PD-L1 expression and administering an immunotherapy that inhibits the activity of PD-L1 to the subject.
Adams, Andorsky and Brahmer have been discussed in the above rejection. It would have been obvious at the time of filing to have used the method of screening biomarkers on CAMLs as recited in the Patent with PD-L1 expression in circulating tumor cells of Andosky and immunotherapy of Brahmer because Andosky recognizes targeting PD-1/PD-L1 pathway using mAbs antibody may be an attractive approach for immunotherapy and Brahmer teaches that blockade of interactions between PD-1 and PD-L1 enhances immune function and anti-PD-L1 therapy has the durability of response across multiple tumor types. Additionally, it would have been obvious to the person to have similarly expressed PD-L1 on CAMLs and reasonably expected success because Adams teaches CAMLs are used together with CTCs and express biomarkers to provide a more complete understanding of the patient’s disease. The person would have a reasonable expectation of success in screening PD-L1 expression on CAMLs or CTCs and administering a drug because the Patent recites cancer treatment for CAML.
Claims 6 and 14-16 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-26 of copending Application No. 17509661 (reference application) in view of Andorsky et al. (“Programmed Death Ligand 1 Is Expressed by Non–Hodgkin Lymphomas and Inhibits the Activity of Tumor-Associated T Cells”, Human Cancer Biology, Clinical Cancer Research, vol. 17(13), pgs. 4232-4244, published 07/01/2011) and Brahmer et al. (“Safety and Activity of Anti–PD-L1 Antibody in Patients with Advanced Cancer”, N. Engl. J. Med., vol. 366(26), 2455-2465, cited pages 1-16, published 06/28/2012) and Adams et al. (WO2013/181532A1, published 12/05/2013, IDS submitted 12/21/2020, cite no. BA).
Copending Application 17509661 recites a method of screening a subject for cancer, comprising detecting circulating Cancer Associated Macrophage-Like cells (CAMLs) in blood of a subject, wherein said detecting comprises: (a) isolating intact cells of between 20 and 300 micron in size from a biological sample obtained from a subject using a means selected from the group consisting of size exclusion methodology, immunocapture, red blood cell lysis, white blood cell depletion, microfiltration assay comprising high molecular weight polysaccharide separation, electrophoresis, dielectrophoresis, flow cytometry, magnetic levitation, microfluidic chip, and a combination thereof, and (b) selecting cells isolated in (a) having (i) a large atypical polyploid nucleus of about 14-64 pm in size or multiple nuclei, and(ii) a morphological shape selected from the group consisting of spindle, tadpole, round, oblong, two legs, more than two legs, thin legs, and amorphous, thereby detecting CAMLs in a biological sample from a subject, wherein the cancer is breast, prostate, lung, pancreatic, or colorectal cancer, wherein when CAMLs are detected in the biological sample, the subject is determined to have cancer and said method further comprises administering a cancer treatment to the subject.
Copending Application 17509661 does not explicitly recite PD-L1 expression and administering an immunotherapy that inhibits the activity of PD-L1 to the subject.
Adams, Andorsky and Brahmer have been discussed in the above rejection. It would have been obvious at the time of filing to have used the method of screening biomarkers on CAMLs as recited in the copending Application with PD-L1 expression in circulating tumor cells of Andosky and immunotherapy of Brahmer because Andosky recognizes targeting PD-1/PD-L1 pathway using mAbs antibody may be an attractive approach for immunotherapy and Brahmer teaches that blockade of interactions between PD-1 and PD-L1 enhances immune function and anti-PD-L1 therapy has the durability of response across multiple tumor types. Additionally, it would have been obvious to the person to have similarly expressed PD-L1 on CAMLs and reasonably expected success because Adams teaches CAMLs are used together with CTCs and express biomarkers to provide a more complete understanding of the patient’s disease. The person would have a reasonable expectation of success in screening PD-L1 expression on CAMLs or CTCs and administering a drug because the copending Application recites cancer treatment for CAML.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Response to Arguments
Applicant's arguments filed 03/31/2026 have been fully considered but they are not persuasive under the obviousness rejection and nonstatutory double patenting rejections.
Applicant argues on page 5 that the amended claim has clarified that the circulating tumor cells CTCs of the present invention are those that are derived from solid tumors. Applicant further argues that Andosky are not CTCs from a subject having a solid tumor, e.g., tumors cells that breakaway from a solid tumor.
The arguments are not found persuasive because the claims only recite collecting CAML and/or CTCs from a biological sample from a subject having a solid tumor, which does not require CAMLs or CTCs to be derived from the solid tumor. The claims only require that the subject has solid tumors. As stated above, Andorsky teaches that PD-L1 is aberrantly expressed on some epithelial malignancies (see purpose under abstract), which would read on a subject having a solid tumor. Additionally, Brahmer teaches PD-L1 is the primary PD-1 ligand that is up-regulated in solid tumors and these properties make PD-L1 a potentially promising target for cancer immunotherapy (see pg. 2, para. 4 of Conclusions. Thus, it would have been obvious to have used a subject with epithelial malignancies and lymphomas because PD-L1 is also expressed on epithelial malignancies, as taught by Andosky.
With respect to the nonstatutory double patenting rejections, Applicant argues on pages 5-10 that the Patents and copending Applications are directed to methods of confirming a diagnosis of cancer based on the presence of CAMLs and not determining whether CAMLs and/or CTCs express PD-LI. There is nothing to teach or suggest that PD-L1 expression by CAML could be used as a companion diagnostic for a subject having cancer.
The arguments are not found persuasive because Andosky (see above) teaches the expression of PD-L1 on CTCs. Additionally, Adams teaches CAMLs and CTCs are used together to express biomarkers. Thus, it would have been obvious to the person to have similarly expressed PD-L1 on CAMLs and reasonably expected success because Adams teaches CAMLs are used together with CTCs and express biomarker to provide a more complete understanding of the patient’s disease. Thus, the rejections are maintained.
Conclusion
No claim is allowed.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to NAM P NGUYEN whose telephone number is (571)270-0287. The examiner can normally be reached Monday-Friday (8-4).
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, Gregory Emch can be reached at (571)272-8149. 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.
/N.P.N/Examiner, Art Unit 1678
/SHAFIQUL HAQ/Primary Examiner, Art Unit 1678
Prosecution Insights