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 .
Continued Examination Under 37 CFR 1.114
1. A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on April 7, 2026 has been entered.
Claims 26-30 and 35-39 are pending and being examined. Claims 26 and 35 are amended.
Priority Reiterated
2. It is noted that the instant application claims priority to provisional application 62/635620, filed 2/27/2018. Application 62/635620 contemplates measuring levels of progastrin in patient blood samples, including melanoma patients, in order to select patients for treating with immune checkpoint inhibitor therapy when their progastrin level is below a threshold. Slide XIII of the specification of application 62/635620 on page 18 states:
PNG
media_image1.png
372
752
media_image1.png
Greyscale
Application 62/635620 does not identify any threshold, and does not support the instant claims’ threshold of less than 3 pm as recited in claims 26 and 35.
Additionally, Application 62/635620 does not disclose several of the immune checkpoint inhibitors listed in claims 27 and 28. Application 62/635620 discloses slide XIV in the specification on page 19 listing only the following immune checkpoint inhibitors:
PNG
media_image2.png
544
794
media_image2.png
Greyscale
Application 62/635620 does not identify several drugs listed in instant claims 27 and 28, therefore does not fully support the material recited in instant claims 27 and 28.
Therefore, the effective priority date of the instant claims is considered to be February 27, 2019, the filing date of PCT/EP2019/054878 that discloses and supports the instantly claimed limitations.
New Rejections
(necessitated by amendments)
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.
3. Claims 26-30 and 35-39 are rejected under 35 U.S.C. 101 because the claimed invention is directed to a judicial exception (i.e., a law of nature/ a natural phenomenon) without significantly more. The amended claim(s) recite(s):
A method for treating cancer in a patient in need thereof comprising:
a) determining whether a patient is responsive to immune checkpoint inhibitors, wherein the determination comprises the steps of
i) contacting a biological sample from the patient with a first progastrin-binding molecule, and
ii) detecting the binding of the first progastrin-binding molecule to progastrin in the biological sample, and
iii) determining that the concentration of progastrin in the biological sample is less than 3 pM; and
b) administering an immune checkpoint inhibitor to the patient when the patient is responsive to immune checkpoint inhibitors according to the determination of step a); or
c) administering an anticancer therapy to the patient when the patient is not responsive to immune checkpoint inhibitors according to the determination of step a), wherein said anticancer therapy is not an immune checkpoint inhibitor, wherein the cancer is skin melanoma and wherein the biological sample is selected from the group consisting of: blood, serum, and plasma.
The claimed method has two possible outcomes: (1) “b) administering an immune checkpoint inhibitor to the patient when the patient is responsive to immune checkpoint inhibitors according to the determination of step a)”; and (2) “c) administering an anticancer therapy to the patient when the patient is not responsive to immune checkpoint inhibitors according to the determination of step a), wherein said anticancer therapy is not an immune checkpoint inhibitor”. Thus, the claims are directed to the judicial exception of naturally occurring levels of progastrin in serum, plasma, or blood associated with response to immune checkpoint inhibitors.
In outcome (2), the judicial exception is not integrated into a practical application because the claims recite the detection or observation of a naturally occurring phenomenon/law of nature, which is data gathering to observe the naturally occurring phenomenon/law of nature without applying the data to a practical application. The claim(s) does/do not include additional elements that are sufficient to amount to significantly more than the judicial exception because the claims recite use of routine laboratory procedures to detect and observe naturally occurring levels progastrin. The steps of contacting progastrin with antibodies for detection in biological samples are considered known, routine steps and are typically taken by those in the field to perform testing of a sample and are not elements that are sufficient to amount to significantly more than the judicial exception. For example, WO 2017/114973, Floch, published July 2017 teaches methods for detecting or quantifying progastrin in biological samples of cancer patients utilizing either a single antibody detection assay or a dual antibody detection assay, where the dual antibody assay comprises a capture monoclonal or polyclonal antibody that binds to the N-terminus or C-terminus of progastrin, and the detection antibody is a monoclonal or polyclonal antibody that binds to the other end of progastrin (N-terminus or C-terminus), wherein the N-terminus antibody is Mab 3, 4, 16 or 19 (comprising the same SEQ ID NOs: 4-39 instantly claimed), and/or the C-terminus antibody is Mab 14 produced by hybridoma 2H9F4B7 deposited under reference I-5158 (see prior art rejection below). US Patent Application Publication 2011/0117086, Pannequin et al, teaches methods for detecting or quantifying progastrin in biological samples of cancer patients utilizing either a single antibody detection assay or a dual antibody detection assay, where the dual antibody assay comprises a capture monoclonal or polyclonal antibody that binds to the N-terminus or C-terminus of progastrin, and the detection antibody is a monoclonal or polyclonal antibody that binds to the other end of progastrin (N-terminus or C-terminus), wherein the N-terminus antibody is Mab 3, 4, 16 or 19 (comprising the same SEQ ID NOs: 4-39 instantly claimed), and/or the C-terminus antibody is Mab 14 produced by hybridoma 2H9F4B7 deposited under reference I-5158 ([31-32]; Table 1A and 1B; [169-176]; claims 42-48). WO 2006/032980, Grimes, teach detection of progastrin in biological samples utilizing monoclonal or polyclonal antibodies that bind to the N-terminus and/or C-terminus of progastrin. Siddheshwar et al (Gut, 2001, 48:47-52) and Ciccotosto et al (Gastroenterology, 1995, 109:1142-1153) teach methods of detecting levels of progastrin in biological samples comprising utilizing N-terminus and C-terminus monoclonal or polyclonal antibodies. Prieur et al (Journal of Clinical Oncology, May 30, 2017, Vol. 35, Number 15_Suppl: abstract 11545) teaches measuring blood progastrin levels from patients having various types of cancer utilizing an ELISA comprising polyclonal antibodies and monoclonal antibodies for detection (see prior art rejection below). Routine data gathering in order to observe a natural phenomenon/ natural principle does not add a meaningful limitation to the method as it would be routinely used by those of ordinary skill in the art in order to observe the natural phenomenon/ natural principle, and it fails to narrow the scope of the claims such that others are not foreclosed from using the law of nature/natural phenomenon. Methods of detecting natural phenomenon preempt all practical uses of it as others must use/detect the natural phenomenon to apply it to any other correlations, diagnosis, prognosis, therapeutic response, monitoring, etc.
In outcome (2), this judicial exception is not integrated into a practical application because the step of “administering an anticancer therapy that is not an immune checkpoint inhibitor” is a generic instruction to apply the judicial exception and does not amount to significantly more than the judicial exception. It is a limitation that is well-understood, routine, conventional activity in the field of treating cancer and does not amount to significantly more than the judicial exception (see MPEP 2106.05(d)). Generic treatment steps are no more than appending conventional steps specified at a high level of generality, are a generic direction to “apply it,” and fail to supply inventive concept to the judicial exception. The step of “administering an anticancer therapy that is not an immune checkpoint inhibitor” does not apply or use the judicial exception to effect a particular treatment (see MPEP 2106.05(f)). The treatment step of outcome (2) fails to amount to an element significantly more than the judicial exception.
With regards to claims 27 and 28, the claims are further defining the immune checkpoint inhibitor that the anti-cancer therapy of outcome (2) is not.
To obviate the rejection, there must be at least one additional element or physical step that applies, relies on, or uses the natural principle so that the claim amounts to significantly more than the judicial exception itself. The claimed method currently fails to provide a practical application of the judicial exception and fails to add any elements that amount to significantly more than the judicial exception.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
4. Claims 26-30 and 35-39 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claims 26 and 35 recite the steps of:
a) determining whether a patient is responsive to immune checkpoint inhibitors, wherein the determination comprises the steps of:
i) contacting a biological sample from the patient with a first progastrin-binding molecule, and
ii) detecting the binding of the first progastrin-binding molecule to progastrin in the biological sample, and
iii) determining that the concentration of progastrin in the biological sample is less than 3 pM; and
b) administering an immune checkpoint inhibitor to the patient when the patient is responsive to immune checkpoint inhibitors according to the determination of step a); or
c) administering an anticancer therapy to the patient when the patient is not responsive to immune checkpoint inhibitors according to the determination of step a), wherein said anticancer therapy is not an immune checkpoint inhibitor.
The claims require administering an immune checkpoint inhibitor or anticancer therapy that is not an immune checkpoint inhibitor based on identifying the patients as responsive or not responsive to immune checkpoint inhibitors “according to the determination of step a)”. It is unclear how, according to the determination step a), a patient would be identified as responsive or not responsive because there is no criteria recited that would distinguish a subject as responsive or not responsive. The claims as currently constituted require all patients to have a determined concentration of progastrin in their biological sample at less than 3 pM. Which of those patients having progastrin concentration less than 3 pM is responsive and which is not? The scope of patients receiving administration of immune checkpoint inhibitors and those receiving anticancer therapy that is not immune checkpoint inhibitor is unclear, therefore the metes and bounds of the claimed invention cannot be determined.
Maintained Rejection
(with Domingues reference added to address claim amendments)
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.
5. Claim(s) 26-30 and 35-39 remain rejected under 35 U.S.C. 103 as being unpatentable over WO 2017/114973, Floch, published July 2017; in view of Prieur et al (Journal of Clinical Oncology, May 30, 2017, Vol. 35, Number 15_Suppl: abstract 11545); Domingues et al (ImmunoTargets and Therapy, 2018; 7, p. 35-49); and Mahoney et al (Clinical Therapeutics, 2015, 37:764-782).
Floch teaches a method for detecting levels of progastrin in cancer patient blood/serum/plasma samples, the method comprising:
Contacting a blood/serum/plasma sample (p. 5; claim 13) from the cancer patient with a first progastrin-binding antibody;
Detecting binding of the first progastrin-binding antibody to progastrin in the sample by immunoassay; and
Determining the concentration of progastrin in the biological sample (p. 9-18);
wherein the cancer patient has skin melanoma (Examples, see Figure 15 below; p. 7 line 6; p. 8, line 1; claims 1-13).
Floch teaches detection of progastrin can also be accomplished using a first anti-progastrin antibody that binds to the C-terminus of progastrin, and a second antibody binding to the N-terminus of progastrin (p. 25-26, 28-29), wherein the C-terminus antibody comprises monoclonal antibody Mab14, produced by hybridoma 2H9F4B7, deposited under the Budapest Treaty at the CNCM, Institut Pasteur, 25-28 rue du Docteur Roux, 75724 Paris CEDEX 15, France, on 27 December 2016, under reference 1-5158 (p. 26, 29; claims 1-13); and wherein the N-terminus antibody comprises either a polyclonal antibody, or a monoclonal antibody selected from:
(a) mAb3 comprising CDR SEQ ID NOs:4-9 that are 100% identical to the instantly claimed CDR SEQ ID NOs:4-9;
(b) mAb4 comprising CDR SEQ ID NOs:10-15 that are 100% identical to the instantly claimed CDR SEQ ID NOs:10-15;
(c) mAb16 comprising CDR SEQ ID NOs:16-21 that are 100% identical to the instantly claimed CDR SEQ ID NOs:16-21;
(d) mAb19 comprising CDR SEQ ID NOs:22-27 that are 100% identical to the instantly claimed CDR SEQ ID NOs:22-27;
(e) mAb8 comprising CDR SEQ ID NOs:28-33 that are 100% identical to the instantly claimed CDR SEQ ID NOs:28-33; and
(f) mAb13 comprising CDR SEQ ID NOs:34-39 that are 100% identical to the instantly claimed CDR SEQ ID NOs:34-39 (p. 26, 30, claims 1-13; Tables 1-6).
In Example 1, Floch demonstrates detecting plasma levels of progastrin utilizing an ELISA with polyclonal antibodies to progastrin C-terminus for capture on the wells of an assay plate, and biotin-labeled polyclonal antibodies binding to the N-terminus of progastrin for detection.
In Example 2 (Figure 16), Floch demonstrates detecting plasma levels of progastrin utilizing an ELISA with monoclonal antibody mAb14 binding to the C-terminus for capture of progastrin (mAb 14 is produced by hybridoma 2H9F4B7, deposited under the Budapest Treaty at the CNCM, Institut Pasteur, 25-28 rue du Docteur Roux, 75724 Paris CEDEX 15, France, on 27 December 2016, under reference 1-5158), and with detectably labeled polyclonal antibodies binding to the N-terminus for detection of progastrin.
In Example 3 (Figure 16), Floch demonstrates detecting progastrin levels quantified by ELISA using two monoclonal antibodies: mAb 14 binding the C-terminus of progastrin for capture, and detectably labeled mAb 16 binding the C-terminus of progastrin for detection.
Figure 15:
PNG
media_image3.png
484
544
media_image3.png
Greyscale
PNG
media_image4.png
323
344
media_image4.png
Greyscale
Floch determined a median value of 6.45pM progastrin characteristic of melanoma patients, with a range that appears to span ~3 pM to ~12 pM in Figure 15. Floch determined that healthy controls with no cancer had 0 pM of progastrin (Figure 15).
Floch teaches measuring levels of progastrin as a biomarker for early cancer detection, and teaches early detection and diagnosis of cancer is important for the selection of patients to receive appropriate treatment that will benefit them and improve survival (p. 1-5). Floch teaches progastrin is essentially not detectable in samples of subjects who do not develop cancer (Figure 15; p. 3, lines 5-6). Increasing concentrations of progastrin in patient samples indicates worse prognosis for cancer (p. 27).
Floch teaches it is known patients diagnosed with cancer are treated with chemotherapy (p. 2, lines 9-21) and teaches using their method for early detection of cancer in order for patients to receive timely treatment with anti-cancer drugs (p. 1-4; p. 27).
Floch does not teach treating the melanoma patients with immune checkpoint inhibitor, such as anti-CTLA-4 antibody ipilimumab, anti-PD-1 antibodies pembrolizumab and nivolumab, and/or anti-PD-L1 antibody atezolizumab when detecting a level of progastrin less than 3 pM, or treating the melanoma patients with anticancer therapy that is not an immune checkpoint inhibitor when detecting a level of progastrin less than 3 pM.
Prieur teaches development of an early cancer screening test using progastrin as a biomarker, teaches it is known that the progastrin gene is activated in almost all types of cancers at the earliest stage of development, and progastrin is secreted by cancer cells. Prieur teaches the problem with detection of cancer in late stages is low survival rates, and teaches their assay can detect progastrin in the blood of persons having cancer at early stage. Prieur teaches measuring blood progastrin levels from patients having various types of cancer utilizing an ELISA comprising polyclonal antibodies for detection, and confirmed that the presence of progastrin is a biomarker for multiple types of cancers. Prieur then measured blood progastrin levels from patients having various types of cancer, including early stages of cancer, utilizing an ELISA comprising polyclonal antibodies and monoclonal antibodies for detection. Prieur determined that their ELISA detected melanoma with a sensitivity of 87%, and all stages of cancers were detected with high specificity of 97.5%. Early stage melanoma was detected at a sensitivity of 68% (Results). Prieur concludes progastrin is a reliable biomarker for early cancer screening, and their ELISA for detection is efficient and available for the clinic.
Domingues reviews the known anti-cancer treatments of patients diagnosed with melanoma, including chemotherapies, kinase inhibitors, TLR agonists, peptide vaccines, and cytokine therapies that are not immune checkpoint inhibitors (p. 35-38, 40-44; Figures 1 and 3). Domingues further reviews known immune checkpoint inhibition therapy of melanoma including anti-CTLA-4 antibodies (ipilimumab, tremelimumab), anti-PD-1 antibodies (nivolumab, pembrolizumab), and anti-PD-L1 antibodies (durvalumab, avelumab, and atezolizumab) (p. 39-40).
Mahoney teaches that patients diagnosed with melanoma are successfully treated with immune checkpoint inhibitors that results in improved survival, and summarizes clinical success of anti-CTLA-4 antibody (ipilimumab), anti-PD1 antibodies (nivolumab and pembrolizumab), and anti-PD-L1 antibody (MPDL-3280A, also known as atezolizumab) in the treatment of melanoma (p. 764; p. 767-770; Tables II - V). Mahoney teaches the greatest clinical activity of anti-PD1 and anti-PD-L1 antibodies in unselected cancer patients is in melanoma patients (p. 764, col. 2). Mahoney explains the known mechanisms of how the immune checkpoint inhibitor antibodies function to treat cancer (Figures 1 and 2; p. 767, col. 2). Mahoney teaches the combination of nivolumab + ipilimumab has shown impressive duration and rates of response in melanoma (p. 775, col. 1). Mahoney notes that in one clinical study treating melanoma patients with pembrolizumab, patients with less baseline tumor burden (earlier stage) were more likely to respond to pembrolizumab (p. 769, col. 1).
Administering immune checkpoint inhibitor:
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to treat patients diagnosed with melanoma and having detectable progastrin levels in the blood, including levels less than 3 pM, by administering to the patients an immune checkpoint inhibitor therapy such as ipilimumab, nivolumab, pembrolizumab, and/or atezolizumab. One would have been motivated to, and have a reasonable expectation of success to because: (1) Floch and Prieur teach the need for early diagnosis of cancer, including melanoma, in order to provide the appropriate therapy to the cancer patient and to improve survival rates; (2) Floch and Prieur teach and successfully demonstrate that progastrin serves as a biomarker for melanoma diagnosis/detection, and successfully detects early stages of melanoma; (3) Floch established that lack of progastrin (0 pM) indicates no cancer, and presence of progastrin indicates the presence of cancer or risk of developing cancer, and Floch demonstrates successfully detecting levels of progastrin between 0 pM and 3pM in cancer patients using their immunoassay; (4) Domingues reviews several successful immune checkpoint inhibition therapies for patients diagnosed with melanoma are known including anti-CTLA-4 antibodies (ipilimumab, tremelimumab), anti-PD-1 antibodies (nivolumab, pembrolizumab), and anti-PD-L1 antibodies (durvalumab, avelumab, and atezolizumab); and (5) Mahoney teaches patients diagnosed with melanoma are successfully clinically treated by administration of immune checkpoint inhibitors, including ipilimumab, nivolumab, pembrolizumab, and/or atezolizumab, wherein melanoma patients having lower tumor burden demonstrated improved response to pembrolizumab treatment, and wherein the greatest clinical activity of anti-PD1 and anti-PD-L1 antibodies in unselected cancer patients is in melanoma patients.
Administering anti-cancer therapy that is not an immune checkpoint inhibitor:
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to treat patients diagnosed with melanoma and having detectable progastrin levels in the blood, including levels less than 3 pM, by administering to the patients an anti-cancer therapy that is not an immune checkpoint inhibitor therapy. One would have been motivated to, and have a reasonable expectation of success to because: (1) Floch and Prieur teach the need for early diagnosis of cancer, including melanoma, in order to provide the appropriate therapy to the cancer patient and to improve survival rates; (2) Floch and Prieur teach and successfully demonstrate that progastrin serves as a biomarker for melanoma diagnosis/detection, and successfully detects early stages of melanoma; (3) Floch established that lack of progastrin (0 pM) indicates no cancer, and presence of progastrin indicates the presence of cancer or risk of developing cancer, and Floch demonstrates successfully detecting levels of progastrin between 0 pM and 3pM in cancer patients using their immunoassay; (4) Domingues reviews several successful anti-cancer therapies for patients diagnosed with melanoma are known including chemotherapies, kinase inhibitors, TLR agonists, peptide vaccines, and cytokine therapies that are not immune checkpoint inhibitors.
In the test of whether it is “obvious to try” there must be:
(1) a finding in the art at the time of filing of the invention that there had been a recognized problem or need in the art;
(2) a finding that there had been a finite number of identified, predictable potential solutions to the recognized need or problem;
(3) a finding that one of ordinary skill in the art could have pursued the known potential solutions with a reasonable expectation of success.
Floch and Prieur teach the need for an assay the provides early diagnosis of cancer, including melanoma, in order to provide the appropriate therapy to the cancer patient and to improve survival rates. Floch and Prieur teach the solution for early diagnosis of melanoma is detecting blood levels of progastrin, wherein increasing levels above 0 pM are indicative of cancer including melanoma, and Domingues and Mahoney teach the known solution to treating patients diagnosed with melanoma is administering known anti-cancer therapy or immune checkpoint inhibitors. Given the recognized need to provide early detection and diagnosis of melanoma in order to provide appropriate therapy and increase survival rate, given the known solution for early melanoma detection/diagnosis by detecting levels of progastrin above 0 pM, and given the known solution for treating patients diagnosed with melanoma is administering anti-cancer therapy or immune checkpoint inhibitor therapy, one of skill in the art could have pursued selecting patients diagnosed with melanoma and having detectable blood levels of progastrin between 0-3 pM indicative of cancer for treatment with anti-cancer therapy or immune checkpoint inhibitor therapy, and treated the melanoma with a reasonable expectation of success.
Response to Arguments
6. Applicants argue that none of the cited references teach distinguishing between patients who are potential responders and non-responders to immunotherapy. Applicants argue that none of the cited references teach progastrin levels below 3 pM as a biomarker of therapeutic responsiveness to immunotherapy, and progastrin levels above 3 pM as a biomarker of not responsive to immunotherapy. Applicants argue the Examiner used hindsight reasoning to arrive at the invention.
7. The arguments have been considered but are not persuasive. Applicants are arguing limitations not recited in the claims. The claims do not provide any limitation or criteria for distinguishing responders from non-responders to immune checkpoint inhibition therapy based on progastrin levels. The claims do not recite progastrin levels below 3 pM identify the patient as responsive to immune checkpoint inhibition, and progastrin levels above 3 pM identify patients as not responsive to immune checkpoint inhibition. The claims as currently constituted require detecting a concentration of progastrin in the biological sample at less than 3 pM in the patient biological sample, then administering immune checkpoint inhibitor therapy or administering anti-cancer therapy that is not an immune checkpoint inhibitor. The cited combined references render obvious these limitations for the reasons of record.
In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
In the instant case, the cited references provide both motivation and reasonable expectation of success to detect levels of progastrin below 3 pM for early detection and diagnosis of melanoma and to treat patients diagnosed with melanoma with immune checkpoint inhibitor or anti-cancer therapy that is not an immune checkpoint inhibitor, for the reasons of record. The motivation and reasonable expectation of success to arrive at the claimed invention are derived solely from the cited combined references.
8. Conclusion: No claim is allowed.
9. Any inquiry concerning this communication or earlier communications from the examiner should be directed to LAURA B GODDARD whose telephone number is (571)272-8788. The examiner can normally be reached Mon-Fri, 7am-3:30pm.
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, Samira Jean-Louis can be reached at 571-270-3503. 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.
/Laura B Goddard/Primary Examiner, Art Unit 1642
Prosecution Insights