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 .
Response to Amendment
The amendment filed March 3rd, 2026 is acknowledged. Regarding the Office Action mailed November 7th, 2025:
The Nucleotide and/or Amino Acid Sequence Disclosure requirements have been met with no errors found.
The objections to the specification are withdrawn in view of the amendments.
The rejections set forth under 35 U.S.C. 112(b) are withdrawn in view of the amendments. However, with respect to the phrase “greater than” in claims 1, 2, and 10, it is noted that the cited definitions for thresholds in the specification provided by the Applicant in the Remarks filed March 3rd, 2026 are non-limiting, particularly the definitions in paragraphs [0099] and [0101]. Other citations to determining threshold appear to rely on these non-limiting definitions. Therefore, “greater than a threshold” is given the broadest reasonable interpretation as taught in the prior art.
The rejection set forth under 35 U.S.C. 101 is withdrawn in view of the amendments.
The rejections of claims 11-13 set forth under 35 U.S.C. 103 are withdrawn given the cancellation of these claims.
The double patenting rejections of claims 11-13 set forth are withdrawn given the cancellation of these claims.
Maintained or modified rejections are set forth below, as necessitated by the amendments. New grounds of rejection are set forth below, as necessitated by the amendments. Responses to arguments, if necessary, follow their respective rejection sections.
Claim Summary
Claims 1, 2 and 10 have been amended. Claims 11-20 have been canceled. Claims 21-23 have been added. Claims 1-10 and 21-23 are pending. Claims 1-10 and 21-23 are under examination and discussed in this Office action.
Claim Rejections - 35 USC § 103 – Modified – Necessitated by Amendment
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Modified
Claims 1, 3-4, and 8 are rejected under 35 U.S.C. 103 as being unpatentable over Murugesan (WO 2024050437 A2, effectively filed August 31st, 2022; cited on the IDS filed June 17th, 2025), in view of Rocconi (Gemogenovatucel-T (Vigil) immunotherapy demonstrates clinical benefit in homologous recombination proficient (HRP) ovarian cancer, Gynecologic Oncology, June 2021, 161, 676-680; cited on the IDS filed October 7th, 2025).
Regarding instant claim 1, Murugesan teaches a method for treating a patient having a solid tumor cancer with an immunotherapy, the method comprising: determining that the patient has a clonal tumor mutation burden (cTMB) greater than a cTMB threshold (Page 5, paragraph [0019]), wherein determining that the patient has a cTMB greater than the cTMB threshold indicates that the patient is responsive to the immunotherapy (Page 5, paragraph [0020]); and administering an immunotherapy to the patient (Page 5, paragraph [0019]), wherein the immunotherapy comprises an immune checkpoint inhibitor (Page 6, paragraph [0025]), to thereby treat the solid tumor cancer (Page 5, paragraph [0019]). Murugesan further teaches that another anti-cancer therapy may be used in addition to the immunotherapy, including a cellular therapy (Page 6, paragraph [0027]).
Murugesan does not teach determining that the patient is homologous recombination proficient (HRP) in addition to determining the cTMB above a threshold, or that the additional cellular therapy is genetically modified autologous tumor cells.
Rocconi, in a reasonably pertinent field, teaches administering an immunotherapy to treat a cancer in an individual that is homologous recombination proficient (Page 677, column 1 last paragraph to column 2, first paragraph). Rocconi further teaches on determining that a patient is homologous recombination proficient (HRP) (Page 677, column 2, HRP analysis). Rocconi teaches the immunotherapy is an autologous tumor cell vaccine comprising plasmid with a human immune-stimulatory GMCSF gene and a bifunctional short-hairpin RNA construct, which specifically knocks down the proprotein convertase furin and its downstream targets TGFβ1 and TGFβ2 (Page 677, column 1, paragraph 3). This is reasonably a cellular therapy. Rocconi teaches this vaccine is an immunotherapy known as Vigil (Page 677, column 1, paragraph 3 and last paragraph). Rocconi further teaches that HRP is associated with a higher clonal neoantigen expression and clonal tumor populations, which is further associated with improved immune response targeting of Vigil (Page 679, column 2 to Page 680, column 1, paragraph 1).
It would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to have modified the method of Murugesan with determining that a patient is HRP and the genetically modified autologous tumor cells from Rocconi. Since Rocconi teaches on treating a solid cancer with immunotherapy, which is reasonably pertinent to the method of Murugesan, one of ordinary skill in the art would combine the two teachings with a reasonable expectation of success. One of ordinary skill in the art would have been motivated to make this modification because HRP is a marker associated with clonal tumor populations that is indicative of improved response to immune targeting therapy like Vigil (e.g. genetically modified autologous tumor cells) (Rocconi, Page 679, column 2 to Page 680, column 1, paragraph 1). Furthermore, using the genetically modified autologous tumor cells as additional cellular therapy in the method of Murugesan would amount to simple substitution of one known element for another to obtain predictable results (see MPEP 2141(III)).
Regarding instant claim 3, Murugesan, in view of Rocconi, teaches the method of claim 1. Rocconi further teaches wherein the patient has a wild-type BRCA1 gene and a wild-type BRCA2 gene (Page 677, column 2, HRP analysis). The 103 analysis for claim 1 also applies here.
Regarding instant claim 4, Murugesan, in view of Rocconi, teaches the method of claim 1. Murugesan further teaches wherein the clonal tumor mutation burden (cTMB) is determined by: for each of a set of mutations: determining a respective amount of tumor sequence reads that have the mutation (Pages 21-22, paragraphs [0082]-[0083]); and determining whether the mutation is a clonal mutation based on the respective amount, thereby determining clonal mutations (Pages 21-22, paragraphs [0082]-[0083]); and determining the cTMB from using the clonal mutations (Pages 21-22, paragraphs [0082]-[0083]).
Regarding instant claim 8, Murugesan, in view of Rocconi, teaches the method of claim 4. Murugesan further teaches wherein the respective amount of tumor sequence reads that have the mutation is an allelic fraction (Pages 21-22, paragraph [0082]). Murugesan states that variant allele frequency and variant allele fraction are interchangeable terms (Page 21, paragraph [0080]).
Response to Arguments
Applicant's arguments filed March 3rd, 2026 have been fully considered but they are not persuasive.
The Applicant first provides a summary of the Examiner’s previous rejection of claims 1, 3-4, and 8 (Page 10 of the Remarks filed March 3rd, 2026). The Applicant then provides the criteria for establishing a case of obviousness (Page 10 of the Remarks filed March 3rd, 2026). The Applicant provides a copy of claim 1 including the new amendments (Page 11 of the Remarks filed March 3rd, 2026). The Applicant argues that Murugesan does not teach determining HRP status of patients, and instead discloses treating HRD positive tumors with PARP inhibitors and/or platinum based drugs (Page 11 of the Remarks filed March 3rd, 2026). The Applicant states that HRD is the opposite of HRP, and thus Murugesan teaches that HRD is a good indicator of patient responsiveness to cancer therapy (Page 11 of the Remarks filed March 3rd, 2026). The Applicant argues that this teaches away from considering HRP as an indicator of patient responsiveness to cancer therapy (Page 11 of the Remarks filed March 3rd, 2026). The Applicant then argues that because Murugesan teaches away from considering HRP as an indicator of patient responsiveness to therapy, one of ordinary skill in the art would not have been motivated to modify the method of Murugesan with a step of determining that a patient is HRP as discussed in Rocconi as there is no expectation of success (Pages 11 and 12 of the Remarks filed March 3rd, 2026).
In response to this argument, the Examiner acknowledges that, while the teachings of Murugesan cited by the Applicant are related to HRD-positive tumor treatments, there is no direct teaching that would suggest that this excludes HRP as an indicator of patient responsiveness to therapy. The cited teachings only reference targeted therapy related to HRD-positive tumors with no further indication that this in any way would prohibit using HRP as an indicator of patient responsiveness to therapy. Without further evidence that suggests Murugesan is excluding HRP as an indicator of patient responsiveness to therapy, it cannot be concluded that Murugesan is teaching away from looking at HRP for responsiveness to therapy, and the argument is ultimately an argument of counsel. Applicant is advised that MPEP 716.01(c) makes clear that “[t]he arguments of counsel cannot take the place of evidence in the record” (In re Schulze, 346 F.2d 600, 602, 145 USPQ 716, 718 (CCPA 1965)). Thus, Applicant should not merely rely upon counsel’s arguments in place of evidence in the record. Overall, this argument is not considered persuasive.
The Applicant then presents results from the instant application (Page 12 of the Remarks filed March 3rd, 2026). The Applicant argues that based on these results, cTMB threshold identifies therapy-responsive cancer patients from therapy-non-responsive cancer patients (Page 12 of the Remarks filed March 3rd, 2026). The Applicant argues that even if Murugesan and Rocconi were combined, the combination does not render the claims obvious and also the measured metrics of cTMB and HRP provide meaningful clinical benefit to patients receiving immunotherapy (Page 12 of the Remarks filed March 3rd, 2026). The Applicant concludes that for these reasons, claims 1, 3-4 and 8 are not obvious in view of Murugesan and Rocconi (Page 13 of the Remarks filed March 3rd, 2026).
With regard to the Applicant's argument that the references fail to show certain features of the invention, it is noted that the features upon which applicant relies (i.e., Figure 12 and aspects of further survival related to administration of Vigil) are not recited in the rejected claims. Although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26 USPQ2d 1057 (Fed. Cir. 1993). In response to these arguments, the Examiner notes for the Applicant that the details cited from the specification and figures in the Applicant’s argument do not appear in the claims being addressed (claims 1, 3-4, and 8). In particular, while the Applicant concludes from these details that the cTMB threshold identifies therapy-responsive cancer patients from therapy-non-responsive cancer patients, this particular limitation is not a part of the claims. Therefore, the method having the alleged unexpected results is not commensurate in scope with the instant claims. See MPEP 716.02(d). In addition, while the Applicant focuses on determining patients above a threshold, the thresholds are broadly claimed and the cited paragraphs do not provide any limiting definition, as evidenced by the phrase “[i]n certain instances.” (see in paragraphs [0099] and [0101] in the instant specification). Thus, this argument is not considered persuasive.
Claim 2 is rejected under 35 U.S.C. 103 as being unpatentable over Murugesan (WO 2024050437 A2, effectively filed August 31st, 2022; cited on the IDS filed June 17th, 2025) and Rocconi (Gemogenovatucel-T (Vigil) immunotherapy demonstrates clinical benefit in homologous recombination proficient (HRP) ovarian cancer, Gynecologic Oncology, June 2021, 161, 676-680; cited on the IDS filed October 7th, 2025), as applied to claims 1, 3-4, and 8, and further in view of McGranahan (Clonal neoantigens elicit T cell immunoreactivity and sensitivity to immune checkpoint blockade, Science, March 2016, 351, 1463-1469; previously cited, supplementary material included for this Office Action), as evidenced by StatPearls (Pembrolizumab [online]. NCBI books, [2023] [retrieved on October 29th, 2025]. Retrieved from: https://www.ncbi.nlm.nih.gov/books/NBK546616/; previously cited).
Regarding instant claim 2, Murugesan, in view of Rocconi, teaches the method of claim 1. Rocconi teaches that HRP is associated with a higher clonal neoantigen expression and clonal tumor populations, which is further associated with improved immune response targeting of Vigil (Page 679, column 2 to Page 680, column 1, paragraph 1).
Neither reference teaches wherein the patient has a clonal neoantigen load (cNEO) greater than a cNEO threshold, wherein a cNEO greater than the cNEO threshold identifies therapy-responsive cancer patients from therapy non-responsive cancer patients.
McGranahan, in a reasonably pertinent field, teaches wherein a patient has a clonal neoantigen load (cNEO) greater than a cNEO threshold (Page 1464, column 1, paragraph 3; Figure 1C), which is related to a better overall response to immunotherapy (Page 1465, column 1, second paragraph to Page 1466, column 1, first paragraph; Figure 4A). As evidenced by StatPearls, the drug pembrolizumab used in the cited passage is considered an immunotherapy for cancer (Page 1, Continuing Education Activity), and also a checkpoint inhibitor (Page 5, Enhancing Healthcare Team Outcomes). This reasonably represents circumstances wherein a cNEO greater than the cNEO threshold identifies therapy-responsive cancer patients from therapy-non-responsive patients.
It would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to have modified the method of Murugesan and Rocconi with determining a cNEO of McGranahan. Since McGranahan teaches on treating a solid tumor cancer with immunotherapy, which is reasonably pertinent to the method of Murugesan and Rocconi, one of ordinary skill in the art would combine the two teachings with a reasonable expectation of success. One of ordinary skill in the art would have been motivated to make this modification because low neoantigen subclonal fraction and high mutation burden demonstrated a durable clinical benefit with immunotherapy (McGranahan, Page 1465, column 1, second paragraph to Page 1466, column 1, first paragraph; Figure 4A). Furthermore, using pembrolizumab in the method of Murugesan would amount to simple substitution of one known element for another to obtain predictable results (see MPEP 2141(III)), especially considering Murugesan teaches pembrolizumab as an option for an immune checkpoint inhibitor (Page 6, paragraph [0026]).
Claims 5 and 6 are rejected under 35 U.S.C. 103 as being unpatentable over Murugesan (WO 2024050437 A2, effectively filed August 31st, 2022; cited on the IDS filed June 17th, 2025) and Rocconi (Gemogenovatucel-T (Vigil) immunotherapy demonstrates clinical benefit in homologous recombination proficient (HRP) ovarian cancer, Gynecologic Oncology, June 2021, 161, 676-680; cited on the IDS filed October 7th, 2025), as applied to claims 1, 3-4, and 8, and further in view of Liu (The Future of Parallel Tumor and Germline Genetic Testing: Is There a Role for All Patients With Cancer?, Journal of the National Comprehensive Cancer Network, July 2021, 19, 871-878; previously cited).
Regarding instant claim 5, Murugesan, in view of Rocconi, teaches the method of claim 4. Murugesan further teaches wherein the set of mutations is determined by: performing exome sequencing of tumor samples of a subject to obtain the tumor sequence reads (Pages 10-11, paragraph [0040]-[0041]); and comparing the tumor sequence reads to controls to determine the set of mutations that are in the tumor sample and not in the controls (Page 23, paragraph [0086]; Figure 2).
Murugesan does not directly teach performing exome sequencing of paired tumor and normal samples of a subject to obtain the tumor sequence reads and normal sequence reads. However, Murugesan does teach that the methods may comprise analyzing controls like a normal tissue sample or a normal adjacent tissue sample with their described methods (Page 55, paragraph [0162]). These described methods include exome sequencing of tumor samples, as cited above, meaning normal samples can undergo exome sequencing. Murugesan further indicates that these controls are intended to be matched samples through stating that when there is no control available, a tumor sample should be marked for analysis without a matched control (Page 55, paragraph [0162]). Therefore, it would be obvious to one of ordinary skill in the art that paired tumor and normal samples of a subject can be processed by the exome sequencing method Murugesan.
Murugesan does not teach comparing the tumor sequence reads to the normal sequence reads to determine the set of mutations that are in the tumor sample and not in the normal sample.
Liu, in a reasonably pertinent field, teaches on comparing tumor sequencing data to matched normal sequencing data to determine mutations that are in the tumor sample and not the normal sample (Page 872, column 1, paragraph 2).
It would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to have modified the method of Murugesan with comparing tumor sequencing to normal tissue sequencing to determine mutations that are in the tumor and not the normal sample. Since Liu teaches on evaluation of tumor sequencing data as it relates to cancer, which is reasonably pertinent to the method of Murugesan and Rocconi, one of ordinary skill in the art would combine the two teachings with a reasonable expectation of success. One of ordinary skill in the art would have been motivated to make this modification because, as stated in Liu, “the sequencing of tumor and matched normal tissue with the subsequent subtraction of germline alterations from somatic alterations, resulting in the identification of somatic mutations only on tumor assessment (somatic)” (Page 872, column 1, paragraph 2).
Regarding instant claim 6, Murugesan, in view of Rocconi and Liu, teaches the method of claim 5. Murugesan further teaches the method further comprising normalizing the cTMB using a size of the exome sequenced (Page 19, paragraph [0066]; Pages 28-29, paragraph [0099]).
Claim 7 is rejected under 35 U.S.C. 103 as being unpatentable over Murugesan (WO 2024050437 A2, effectively filed August 31st, 2022; cited on the IDS filed June 17th, 2025) and Rocconi (Gemogenovatucel-T (Vigil) immunotherapy demonstrates clinical benefit in homologous recombination proficient (HRP) ovarian cancer, Gynecologic Oncology, June 2021, 161, 676-680; cited on the IDS filed October 7th, 2025), and Liu (The Future of Parallel Tumor and Germline Genetic Testing: Is There a Role for All Patients With Cancer?, Journal of the National Comprehensive Cancer Network, July 2021, 19, 871-878; previously cited), as applied to claims 1, 3-6, and 8, and further in view of Takara (Using Unique Molecular Identifiers (UMIs) in NGS experiments [online]. Takara, [2018] [retrieved on October 29th, 2025]. Retrieved from: https://www.takarabio.com/about/bioview-blog/tips-and-troubleshooting/using-umis-in-ngs-experiments; previously cited).
Regarding instant claim 7, Murugesan, in view of Rocconi and Liu, teaches the method of claim 5. Murugesan further teaches the method further comprising: attaching unique molecular identifiers to template nucleic acids of the paired tumor and normal samples (Pages 10-11, paragraphs [0040]-[0042]; see 103 analysis of claim 5 regarding paired samples); amplifying the template nucleic acids prior to sequencing to generate reads (Pages 10-11, paragraphs [0040]-[0042]).
None of the cited references teach on determining a consensus read from one or more reads for each of the unique molecular identifiers, thereby generating consensus reads.
Takara, in a reasonably pertinent filed, teaches determining a consensus read from one or more reads for each one of unique molecular identifiers (Page 1, How do UMIs work?; Figure 2), thereby generating consensus reads (Figure 2).
It would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to have modified the method of the cited references with the consensus read determination of Takara. Since Takara teaches on next generation sequencing, which is reasonably pertinent to Murugesan’s exome sequencing, one of ordinary skill in the art would combine the two teachings with a reasonable expectation of success. One of ordinary skill in the art would have been motivated to make this modification because generating consensus reads using UMIs detects errors, PCR artifacts, and false positives with regards to mutations, allowing for error correction and a more accurate read call (Page 1, How do UMIs work?; Figure 2).
None of the references as currently cited teach wherein the consensus reads are used for comparing the tumor sequence reads to the normal sequence reads to determine the set of mutations. However, based on the previous teachings of Liu presented for claim 5 and Takara presented above, it would be obvious to compare sequencing data from matched tumor and normal samples after determining a consensus read with UMIs. Takara teaches determining consensus sequences with the motivation of error correction in sequencing reads (Takara, Page 1, How do UMIs work?; Figure 2). Liu teaches comparing matched tumor and normal sequencing data with the motivation of identification of somatic mutations only in tumor samples (Liu, Page 872, column 1, paragraph 2). Therefore, it would be obvious to one of ordinary skill in the art to combine these aspects and use the consensus reads, with the motivation that errors have been corrected in these reads, to compare the tumor sequencing reads to the normal sequencing reads to determine a set of mutations, with the motivation that the comparison will identify mutations specific to the tumor.
Claim 9 is rejected under 35 U.S.C. 103 as being unpatentable over Murugesan (WO 2024050437 A2, effectively filed August 31st, 2022; cited on the IDS filed June 17th, 2025) and Rocconi (Gemogenovatucel-T (Vigil) immunotherapy demonstrates clinical benefit in homologous recombination proficient (HRP) ovarian cancer, Gynecologic Oncology, June 2021, 161, 676-680; cited on the IDS filed October 7th, 2025), as applied to claims 1, 3-4, and 8, as evidenced by Tarabichi (A practical guide to cancer subclonal reconstruction from DNA sequencing, Nature Methods, January 2021, 18, 144-155; previously cited).
Regarding instant claim 9, Murugesan, in view of Rocconi, teaches the method of claim 4.
Murugesan does not expressly teach wherein determining whether the mutation is a clonal mutation is further based on an allelic copy number and a tumor purity. However, Murugesan teaches on using a cancer cell fraction in the determination of clonal mutations (Pages 21-22, paragraph [0082]; Figure 2). As evidenced by Tarabichi, calculation of a cancer cell fraction can be performed using a copy number and a tumor purity (Box 1, Cancer cell fraction calculation, and other related terms). Therefore, Murugesan does teach on a clonal mutation being based on an allelic copy number and a tumor purity.
Response to Arguments
Applicant's arguments filed March 3rd, 2026 have been fully considered but they are not persuasive.
It is noted by the Examiner that the responses to arguments related to claims 2, 5-7, and 9 are combined here given that they are combined in the Applicant’s arguments.
The Applicant first summarizes the Examiner’s previous rejections of claims 2, 5-7, and 9 (Pages 13 and 14 of the Remarks filed March 3rd, 2026). The Applicant argues that, given claims 2, 5-7, and 9 depend from claim 1, they suffer the same lack of motivation to modify the method Murugesan with a step of determining that a patient is HRP as addressed for claim 1 (Page 14 of the Remarks filed March 3rd, 2026). The Applicant further argues that any further references used to reject each of claims 2, 5-7, and 9 do not rectify the deficiencies identified for Murugesan and Rocconi with respect to claim 1 (Page 14 of the Remarks filed March 3rd, 2026). The Applicant therefore argues that claims 2, 5-7, and 9 are not obvious over the cited references (Page 14 of the Remarks filed March 3rd, 2026).
In response to these arguments, it is noted that Applicant’s arguments rely on alleged deficiencies previously addressed, which are unpersuasive for the reasons discussed above. Therefore, the claims remained rejected based on the prior art citations presented in the rejections.
Claim 10 is rejected under 35 U.S.C. 103 as being unpatentable over Rocconi (Gemogenovatucel-T (Vigil) immunotherapy demonstrates clinical benefit in homologous recombination proficient (HRP) ovarian cancer, Gynecologic Oncology, June 2021, 161, 676-680; cited on the IDS filed October 7th, 2025), in view of McGranahan (Clonal neoantigens elicit T cell immunoreactivity and sensitivity to immune checkpoint blockade, Science, March 2016, 351, 1463-1469; previously cited, supplementary material included for this Office Action) and Barve (Pilot Study of Combination Gemogenovatucel-T (Vigil) and Durvalumab in Women With Relapsed BRCA-wt Triple-Negative Breast or Ovarian Cancer, August 2022, 16, 1-10), as evidenced by StatPearls (Pembrolizumab [online]. NCBI books, [2023] [retrieved on October 29th, 2025]. Retrieved from: https://www.ncbi.nlm.nih.gov/books/NBK546616/; previously cited).
Regarding instant claim 10, Rocconi teaches administering an immunotherapy to treat a cancer in an individual that is homologous recombination proficient (Page 677, column 1 last paragraph to column 2, first paragraph). Rocconi further teaches on determining that a patient is homologous recombination proficient (HRP) (Page 677, column 2, HRP analysis). Rocconi teaches the immunotherapy is an autologous tumor cell vaccine comprising plasmid with a human immune-stimulatory GMCSF gene and a bifunctional short-hairpin RNA construct, which specifically knocks down the proprotein convertase furin and its downstream targets TGFβ1 and TGFβ2 (Page 677, column 1, paragraph 3). Rocconi teaches this vaccine is an immunotherapy known as Vigil (Page 677, column 1, last paragraph). Rocconi further teaches that HRP is associated with a higher clonal neoantigen expression and clonal tumor populations, which is further associated with improved immune response targeting of Vigil (Page 679, column 2 to Page 680, column 1, paragraph 1).
Rocconi does not directly teach determining the patient is HRP and then administering an immunotherapy. However, this option is made obvious by patients that are HRP having favorable survival improvement when treated with the immunotherapy Vigil (Pages 678-679, Endpoint Analysis; Figure 1). One of ordinary skill in the art would be motivated to treat a patient identified as HRP with immunotherapy, like Vigil, given this favorable improvement.
Rocconi does not teach wherein the patient has a clonal neoantigen load (cNEO) greater than a cNEO threshold, that a cNEO greater than the cNEO threshold indicates that the patient is responsive to immunotherapy, or that both an immune checkpoint inhibitor and genetically modified autologous tumor cells may be used together to treat the solid tumor cancer.
McGranahan, in a reasonably pertinent field, teaches wherein a patient has a clonal neoantigen load (cNEO) greater than a threshold (Page 1464, column 1, paragraph 3; Figure 1C), which is related to a better overall response to immunotherapy (Page 1465, column 1, second paragraph to Page 1466, column 1, first paragraph; Figure 4A). As evidenced by StatPearls, the drug pembrolizumab used in the cited passage is considered an immunotherapy for cancer (Page 1, Continuing Education Activity) and also a checkpoint inhibitor (Page 5, Enhancing Healthcare Team Outcomes).
It would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to have modified the method of Rocconi with determining a cNEO of McGranahan. Since McGranahan teaches on treating a solid tumor cancer with immunotherapy that is an immune checkpoint inhibitor, which is reasonably pertinent to the method of Rocconi, one of ordinary skill in the art would combine the two teachings with a reasonable expectation of success. One of ordinary skill in the art would have been motivated to make this modification because low neoantigen subclonal fraction and high mutation burden demonstrated a durable clinical benefit with immunotherapy (McGranahan, Page 1465, column 1, second paragraph to Page 1466, column 1, first paragraph; Figure 4A). HRP is similarly associated with improved response to immunotherapy given higher clonal neoantigen expression (Rocconi, Page 679, column 2 to Page 680, column 1, paragraph 1).
None of the previously cited references teach that both an immune checkpoint inhibitor and genetically modified autologous tumor cells may be used together to treat the solid tumor cancer.
Barve, in a reasonably pertinent field, teaches that both an immune checkpoint inhibitor and genetically modified autologous tumor cells may be used together to treat a solid tumor cancer (Page 2, column 1: Durvalumab is considered a checkpoint inhibitor (CI); Page 9, column 1, paragraph 3).
It would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to have modified the method of Rocconi and McGranahan with the combination treatment of Barve. Since Barve teaches on treatment of cancer, which is reasonably pertinent to Rocconi and McGranahan, one of ordinary skill in the art would combine the two teachings with a reasonable expectation of success. One of ordinary skill in the art would have been motivated to make this modification because the combination of an immune checkpoint inhibitor and genetically modified autologous tumor cells is well tolerated and provides benefit to at least one population of cancer patients (Page 9, column 1, paragraph 3).
Response to Arguments
Applicant's arguments filed March 3rd, 2026 have been fully considered but they are not persuasive.
The Applicant first summarizes the Examiner’s previous rejection of claim 10 (Page 14 of the Remarks filed March 3rd, 2026). The Applicant provides a copy of claim 10 including the new amendments (Pages 14 and 15 of the Remarks filed March 3rd, 2026). The Applicant argues that claim 10 requires that the patient receiving immunotherapy is determined to be HRP and have cNEO greater than the cNEO threshold, while Rocconi focuses on only HRP and McGranahan only focuses on cNEO (Page 15 of the Remarks filed March 3rd, 2026). The Applicant argues that there is no suggestion to combine these aspects in either reference (Page 15 of the Remarks filed March 3rd, 2026).
In response to this argument, the Examiner notes that the Applicant is essentially arguing that there is no motivation to combine the Rocconi and McGranahan references. Given this, it is recognized that obviousness may be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so found either in the references themselves or in the knowledge generally available to one of ordinary skill in the art. See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007). In this case, as cited above, Rocconi teaches that HRP is associated with a higher clonal neoantigen expression and clonal tumor populations, which is further associated with improved immune response targeting of Vigil (Page 679, column 2 to Page 680, column 1, paragraph 1), while McGranahan teaches that low neoantigen subclonal fraction and high mutation burden demonstrated a durable clinical benefit with immunotherapy (Page 1465, column 1, second paragraph to Page 1466, column 1, first paragraph; Figure 4A). This provides sufficient motivation for both HRP and cNEO to be contemplated for immunotherapy, particular given the Rocconi states that HRP is associated with higher cNEO expression. With no further information provided regarding the deficiency of the two references, this argument is not considered persuasive.
The Applicant then notes that given what is known about HRP and HRD, one of ordinary skill in the art would presume that HRP patients generally would have fewer neoantigens and HRP patients that also have high cNEO is rare and unexpected (Page 15 of the Remarks filed March 3rd, 2026). The Applicant argues that Rocconi and McGranahan, either alone or in combination, do not provide basis for one of ordinary skill in the art to seek and characterize HRP patients that have high cNEO, and there would be no reason to combine HRP with high cNEO as selection criteria for immunotherapy based on these references (Pages 15 and 16 of the Remarks filed March 3rd, 2026). The Applicant then provides information and citations from the instant disclosure regarding combining HRP with high cNEO with regards to immunotherapy (Pages 16-18 of the Remarks filed March 3rd, 2026).
In response to this argument, the Examiner would like to note that the prior art of Rocconi (cited above) states that, “Relationship of BRCA-wt, HRP expression in malignant tissue is associated with higher clonal neoantigen expression as opposed to BRCA-m, HRD tumors which contain higher proportion of subclonal neoantigen subpopulations” (Rocconi, Page 679, column 2 to Page 680, column 1, paragraph 1). This statement indicates that HRP is associated with a higher clonal neoantigen expression, where HRD is associated with higher subclonal neoantigen expression. One of ordinary skill in the art would presume, based on this description, that HRP patients are fully capable of having a high cNEO, and that HRP could be combined with high cNEO as selection criteria for immunotherapy. Much of the remaining arguments are directed to support from the specification regarding correlation of HRP with high cNEO. However, it is noted that the features upon which applicant relies (i.e., see paragraph 2 of Page 16 to paragraph 1 of Page 19 of the Remarks filed March 3rd, 2026) are not recited in the rejected claim. Although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26 USPQ2d 1057 (Fed. Cir. 1993). The Applicant has claimed determining HRP, determining cNEO greater than a threshold, wherein these determinations indicate responsiveness to immunotherapy, and then administering an immunotherapy. No other aspects are claimed, and given that the art sufficiently teaches these aspects, this argument is not considered persuasive.
New
Claim 21 is rejected under 35 U.S.C. 103 as being unpatentable over Rocconi (Gemogenovatucel-T (Vigil) immunotherapy demonstrates clinical benefit in homologous recombination proficient (HRP) ovarian cancer, Gynecologic Oncology, June 2021, 161, 676-680; cited on the IDS filed October 7th, 2025), McGranahan (Clonal neoantigens elicit T cell immunoreactivity and sensitivity to immune checkpoint blockade, Science, March 2016, 351, 1463-1469; previously cited, supplementary material included for this Office Action), and Barve (Pilot Study of Combination Gemogenovatucel-T (Vigil) and Durvalumab in Women With Relapsed BRCA-wt Triple-Negative Breast or Ovarian Cancer, August 2022, 16, 1-10), as applied to claim 10, and further in view of Murugesan (WO 2024050437 A2, effectively filed August 31st, 2022; cited on the IDS filed June 17th, 2025).
Regarding instant claim 21, Rocconi, in view of McGranahan and Barve, teaches the method of claim 10. Rocconi further teaches that HRP is associated with a higher clonal neoantigen expression and clonal tumor populations, which is further associated with improved immune response targeting of Vigil (Page 679, column 2 to Page 680, column 1, paragraph 1).
Rocconi does not teach wherein the patient has a clonal tumor mutation burden (cTMB) greater than a cTMB threshold, and wherein the patient with a cTMB greater than the cTMB threshold is responsive to an immunotherapy.
Murugesan, in a reasonably pertinent field, teaches determining that the patient has a clonal tumor mutation burden (cTMB) greater than a cTMB threshold (Page 5, paragraph [0019]) and wherein the patient with a cTMB greater than the cTMB threshold is responsive to an immunotherapy (Page 5, paragraph [0020]).
It would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to have modified the method of Rocconi with determining cTMB above a threshold of Murugesan. Since Murugesan teaches on treating a solid tumor cancer with immunotherapy, which is reasonably pertinent to the method of Rocconi, one of ordinary skill in the art would combine the two teachings with a reasonable expectation of success. One of ordinary skill in the art would have been motivated to make this modification because it is known that both cTMB and HRP are associated with improved response to immunotherapy (Murugesan, Page 17, paragraph [0062]; Rocconi, Page 679, column 2 to Page 680, column 1, paragraph 1).
Claims 22 and 23 are rejected under 35 U.S.C. 103 as being unpatentable over Rocconi (Gemogenovatucel-T (Vigil) immunotherapy demonstrates clinical benefit in homologous recombination proficient (HRP) ovarian cancer, Gynecologic Oncology, June 2021, 161, 676-680; cited on the IDS filed October 7th, 2025), McGranahan (Clonal neoantigens elicit T cell immunoreactivity and sensitivity to immune checkpoint blockade, Science, March 2016, 351, 1463-1469; previously cited, supplementary material included for this Office Action), and Barve (Pilot Study of Combination Gemogenovatucel-T (Vigil) and Durvalumab in Women With Relapsed BRCA-wt Triple-Negative Breast or Ovarian Cancer, August 2022, 16, 1-10), as applied to claim 10 and as further noted in the following rejections.
Regarding instant claim 22, Rocconi, in view of McGranahan and Barve, teaches the method of claim 10. Rocconi further teaches wherein the patient has a wild-type BRCA1 gene and a wild-type BRCA2 gene (Page 677, column 2, HRP analysis). The 103 analysis for claim 10 also applies here.
Regarding instant claim 23, Rocconi, in view of McGranahan teaches the method of claim 10. McGranahan further teaches wherein the cNEO is determined by: determining a set of clonal mutations that are non-synonymous (Supplementary Material, sections Multi-region Whole-Exome Sequencing, Clonal Architecture Analysis, and Variant Calling to Identification of Putative Neoantigens); determining an MHC haplotype of the patient using tumor sequence reads and/or normal sequence reads (Supplementary Material, sections Multi-region Whole-Exome Sequencing and HLA Typing of Patient Samples; it is also noted that, based on the instant specification, MHC is also considered an HLA (see paragraphs [0157], [0228], and [0255])); for each clonal mutation: generating a peptide corresponding to the clonal mutation at a genomic position (Supplementary Material, section Identification of Putative Neoantigens); determining a likelihood of the peptide being presented on a cell surface in complex with the MHC haplotype encoded by the patient (Supplementary Material, section Identification of Putative Neoantigens); identifying whether the peptide is a clonal neoantigen based on the likelihood (Supplementary Material, section Identification of Putative Neoantigens); and determining an amount of clonal neoantigens (Supplementary Material, section Identification of Putative Neoantigens; Figures 1A-C). The 103 analysis for claim 10 also applies here.
It is noted that given the broad nature of claim 23, particularly the limitation “determining a likelihood of the peptide being presented on a cell surface in complex with the MHC haplotype encoded by the patient”, the Examiner turned to the specification to better understand the method as claimed. Based on this review, a method that accomplishes the method as claimed in claim 23 appears in paragraphs [0381] and [0382]. It is particularly noted that “determining a likelihood of the peptide being presented on a cell surface in complex with the MHC haplotype encoded by the patient” appears to involve determining a binding affinity, which determines the likelihood that a peptide will appear on a cell surface. Therefore, this interpretation for the method has been applied for the above claim.
Double Patenting – Modified – Necessitated by Amendment
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.
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Claims 1-10 and 21-23 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-18 of U.S. Patent No. 11400170B2 in view of Murugesan (WO 2024050437 A2, effectively filed August 31st, 2022), Rocconi (Gemogenovatucel-T (Vigil) immunotherapy demonstrates clinical benefit in homologous recombination proficient (HRP) ovarian cancer, Gynecologic Oncology, June 2021, 161, 676-680), McGranahan (Clonal neoantigens elicit T cell immunoreactivity and sensitivity to immune checkpoint blockade, Science, March 2016, 351, 1463-1469), Liu (The Future of Parallel Tumor and Germline Genetic Testing: Is There a Role for All Patients With Cancer?, Journal of the National Comprehensive Cancer Network, July 2021, 19, 871-878), Takara (Using Unique Molecular Identifiers (UMIs) in NGS experiments [online]. Takara, [2018] [retrieved on October 29th, 2025]. Retrieved from: https://www.takarabio.com/about/bioview-blog/tips-and-troubleshooting/using-umis-in-ngs-experiments), Tarabichi (A practical guide to cancer subclonal reconstruction from DNA sequencing, Nature Methods, January 2021, 18, 144-155), and Barve (Pilot Study of Combination Gemogenovatucel-T (Vigil) and Durvalumab in Women With Relapsed BRCA-wt Triple-Negative Breast or Ovarian Cancer, August 2022, 16, 1-10). Although the claims at issue are not identical, they are not patentably distinct from each other because both the ‘170 patent and the instant application claim a method of treating a patient having cancer comprising the patient being homologous recombination proficient, having wild type BRCA1 and BRCA2 genes, and administering an immunotherapy to the patient, wherein the immunotherapy is genetically modified autologous cancer cells.
It should be noted here that the instant limitation of homologous recombination proficient and the reference claim of homologous recombination deficiency-negative are equivalent terms based on the disclosures of both the instant application (see instant paragraph [0110]) and the reference patent (see reference patent column 15, lines 41-53). It is also noted here that the reference patent specifically claims an expression vector comprising a first insert comprising a nucleic acid sequence encoding a Granulocyte Macrophage Colony Stimulating Factor (GM-CSF) sequence and a second insert comprising a sequence of SEQ ID NO:4, in an autologous cancer cell. SEQ ID NO:4, according to the reference specification, is bi-shRNAfurin. As evidenced by Rocconi, this type of expression vector with these components is an immunotherapy known as Vigil, which is also considered genetically modified autologous tumor cells (Page 677, column 1). Therefore, the reference patent teaches administering a specific immunotherapy of genetically modified autologous tumor cells.
The ‘170 patent claims do not require determining cTMB above a threshold, wherein both HRP and cTMB higher than a threshold indicate the patient is responsive to immunotherapy, cNEO above a threshold, determining cTMB based on a set of mutations determining to be clonal from tumor sequencing reads, performing exome sequence of tumor and normal paired samples to determine the set of mutations, normalizing cTMB based on the size of the exome, attaching UMIs to template nucleic acids of the paired samples and amplifying to determine consensus reads, the tumor sequence reads with the mutation being an allelic fraction, clonal mutations being based on allelic copy number and tumor purity, wherein both HRP and cNEO higher than a threshold indicate the patient is responsive to immunotherapy, and wherein cNEO is determined by determining a set of clonal mutations that are non-synonymous; determining an MHC haplotype of the patient using tumor sequence reads and/or normal sequence reads; for each clonal mutation: generating a peptide corresponding to the clonal mutation at a genomic position; determining a likelihood of the peptide being presented on a cell surface in complex with the MHC haplotype encoded by the patient; identifying whether the peptide is a clonal neoantigen based on the likelihood; and determining an amount of clonal neoantigens. However, Murugesan, Rocconi, McGranahan, Liu, Takara, Tarabichi, and Barve in various combinations teach the claimed limitations as discussed in the above 103 rejections, obviating these variations to the claims of the ‘170 patent. Any additional limitations of the claims of U.S. Patent No. 11400170B2 are encompassed by the open claim language “comprising” found in the instant claims.
Claims 1-10 and 21-23 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4, 7, 15, 25-27, 32-33 and 39 of copending Application No. 18285214 in view of Murugesan (WO 2024050437 A2, effectively filed August 31st, 2022), Rocconi (Gemogenovatucel-T (Vigil) immunotherapy demonstrates clinical benefit in homologous recombination proficient (HRP) ovarian cancer, Gynecologic Oncology, June 2021, 161, 676-680), McGranahan (Clonal neoantigens elicit T cell immunoreactivity and sensitivity to immune checkpoint blockade, Science, March 2016, 351, 1463-1469), Liu (The Future of Parallel Tumor and Germline Genetic Testing: Is There a Role for All Patients With Cancer?, Journal of the National Comprehensive Cancer Network, July 2021, 19, 871-878), Takara (Using Unique Molecular Identifiers (UMIs) in NGS experiments [online]. Takara, [2018] [retrieved on October 29th, 2025]. Retrieved from: https://www.takarabio.com/about/bioview-blog/tips-and-troubleshooting/using-umis-in-ngs-experiments), Tarabichi (A practical guide to cancer subclonal reconstruction from DNA sequencing, Nature Methods, January 2021, 18, 144-155), and Barve (Pilot Study of Combination Gemogenovatucel-T (Vigil) and Durvalumab in Women With Relapsed BRCA-wt Triple-Negative Breast or Ovarian Cancer, August 2022, 16, 1-10). Although the claims at issue are not identical, they are not patentably distinct from each other because both the ‘214 application and the instant application claim a method of treating a patient having cancer comprising the patient being homologous recombination proficient, having wild type BRCA1 and BRCA2 genes, and administering an immunotherapy to the patient, wherein the immunotherapy is genetically modified autologous cancer cells.
It is noted here that the reference patent specifically claims an expression vector comprising a first insert comprising a nucleic acid sequence encoding a Granulocyte Macrophage Colony Stimulating Factor (GM-CSF) sequence and a second insert comprising a sequence of SEQ ID NO:2 in an autologous cancer cell. SEQ ID NO:2, according to the reference specification, is bi-shRNAfurin. As evidenced by Rocconi, this type of expression vector with these components is an immunotherapy known as Vigil, which is also considered genetically modified autologous tumor cells (Page 677, column 1). Therefore, the reference patent teaches administering a specific immunotherapy of genetically modified autologous tumor cells.
The ‘214 application claims do not require determining cTMB above a threshold, wherein both HRP and cTMB higher than a threshold indicate the patient is responsive to immunotherapy, cNEO above a threshold, determining cTMB based on a set of mutations determining to be clonal from tumor sequencing reads, performing exome sequence of tumor and normal paired samples to determine the set of mutations, normalizing cTMB based on the size of the exome, attaching UMIs to template nucleic acids of the paired samples and amplifying to determine consensus reads, the tumor sequence reads with the mutation being an allelic fraction, clonal mutations being based on allelic copy number and tumor purity, wherein both HRP and cNEO higher than a threshold indicate the patient is responsive to immunotherapy, and wherein cNEO is determined by determining a set of clonal mutations that are non-synonymous; determining an MHC haplotype of the patient using tumor sequence reads and/or normal sequence reads; for each clonal mutation: generating a peptide corresponding to the clonal mutation at a genomic position; determining a likelihood of the peptide being presented on a cell surface in complex with the MHC haplotype encoded by the patient; identifying whether the peptide is a clonal neoantigen based on the likelihood; and determining an amount of clonal neoantigens. However, Murugesan, Rocconi, McGranahan, Liu, Takara, Tarabichi, and Barve in various combinations teach the claimed limitations as discussed in the above 103 rejections, obviating these variations to the claims of the ‘214 application. Any additional limitations of the claims of copending Application No. 18285214 are encompassed by the open claim language “comprising” found in the instant claims.
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 March 3rd, 2026 have been fully considered but they are not persuasive.
The Applicant first summarizes the Examiner’s previous rejections, before arguing that, as discussed above, the combination of references presented for the 103 rejections of claims 1 and 10 are insufficient, and the further references do not resolve these deficiencies (Pages 19-22 of the Remarks filed March 3rd, 2026).
In response to these arguments, it is noted that Applicant’s arguments rely on alleged deficiencies previously addressed, which are unpersuasive for the reasons discussed above. Therefore, the claims remain as analyzed above.
Conclusion
All claims stand rejected.
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.
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/ALLISON E SCHLOOP/Examiner, Art Unit 1683
/Robert T. Crow/Primary Examiner, Art Unit 1683