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 .
Claims 20-33 are pending and are under consideration.
Priority
Acknowledgment is made of applicant’s claim for foreign priority under 35 U.S.C. 119 (a)-(d). The certified copy has been filed in the presently filed application, filed on 07/10/2024.
Specification
The disclosure is objected to because of the following informalities: The specification filed 03/26/2024 is objected on page 19, line 2 for recitation of a nucleic acid sequence in the absence of a sequence identifier. See 37 CFR 1.821(c). 37 CFR 1.821(c) requires that patent applications which contain disclosures of nucleotide and/or amino acid sequences that fall within the definitions of 37 CFR 1.821(a) must contain a "Sequence Listing," as a separate part of the disclosure, which presents the nucleotide and/or amino acid sequences and associated information using the symbols and format in accordance with the requirements of 37 CFR 1.821 - 1.825.
Appropriate correction is required.
Claim Objections
Claim 29 is objected to under 37 CFR 1.75 as being a substantial duplicate of claim 30. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
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.
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.
Claim(s) 20-23, and 27-33 is/are rejected under 35 U.S.C. 103 as being unpatentable over US2018/0312604 (Throsby et al. Nov. 1, 2018) in view of Hendrikx et al. (The Oncologist, 22(10), 2017).
As to claims 20, and 28-31, Throsby et al. teach a method of treating head and neck cancer [0089] comprising administering a bispecific antibody comprising a variable region that binds an extracellular part of EGFR and a variable region that binds an extracellular part of LGR5 [00097]. For example, the variable domain can bind to ErbB-1 (which is an EGFR- see [0055]). The variable domains can comprise a VH selected from the group consisting MF3370, MF3755, MF4280 or MF4289.
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The reference further teaches [0107-0108] that the variable domain that binds an extracellular portion of LGR5 can comprise:
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11. As to the light chain, the reference teaches [0067] that further provided is a bispecific antibody according to the invention, wherein said common light chain is a germline light chain, preferably a rearranged germline human kappa light chain comprising the IgVκ1-39 gene segment, most preferably the rearranged germline human kappa light chain IgVκ1-39*01/IGJκ1*01 shown below and also in Figure 3 of the prior art:
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12. The above VL chain is 100% identical to the claimed VL chain of SEQ ID NO:122.
13. As to claim 21, Throsby et al. teach [0059] treatment of human subjects.
14. As to claim 22, Throsby et al. teach [0729, 0731] intravenous administration of the antibody.
15. As to claim 23, the invention also provides [0089] a method for the treatment of an individual that has a cancer, the method comprising administering a protein of the invention or a bispecific antibody of the invention to the individual in need thereof. The individual is preferably an individual that has cancer. The cancer is preferably an adenocarcinoma.
16. As to claim 27, Throsby et al. teach (Claim 17) wherein the cancer is characterized by expression of EGFR or LGR5 (a WNT pathway antigen).
17. As to claim 32, Throsby et al. teach [0061] that the antibody is ADCC enhanced. For instance, ADCC activity of an antibody can be improved when the antibody itself has a low ADCC activity, by slightly modifying the constant region of the antibody.
18. As to claim 33, Throsby et al. teach [0062] that a bispecific antibody of the invention can in one embodiment be afucosylated.
19. Throsby et al. do not specifically teach administering a flat dose of 1500 mg of the antibody.
20. Hendrikx reviews the advantages of fixed dosing of monoclonal antibodies in the field of oncology. Hendrikx teaches that most monoclonal antibodies in oncology are administered in body-size-based dosing schedules (e.g., body surface area (BSA, in m2) or mg/kg), which are believed to correct for variability in both drug distribution and elimination among patients (Introduction, page 1212). In oncology, monoclonal antibodies are of the immunoglobulin G (IgG) subtype and are primarily administered intravenously. Hendrikx argues that fixed dosing of monoclonal antibodies has several advantages including efficiency of compounding, reduced drug spillage, fewer medication errors, and decreased costs (e.g., Introduction, page 1213; page 1219). Hendrikx teaches that monoclonal antibodies are cleared in a linear fashion via proteolytic catabolism and intracellular degradation after target binding, the latter of which is likely not body weight-dependent (pages 1213 and 1215, text). Summarizing the results of in silico studies, Hendrikx notes that when minimal effects of body weight are observed on the volume of distribution and clearance of an antibody in plasma, fixed dose administration reduces interpatient variability compared to body weight-based dosing (pages 1215-1216). Even when strong effects of body weight are observed, Hendrikx argues that fixed dosing can still be considered for monoclonal antibodies with a wide therapeutic range for practical reasons (page 1217; Table 1). Citing the anti-EGFR antibody panitumumab as an example, Hendrikx notes that effects of body weight on antibody clearance and volume distribution were limited, which together with the wide therapeutic window of this drug suggests that a fixed dosing could successfully be employed (page 1219). Table 1 illustrates other monoclonal antibodies approved for treatment of cancer, some of which have approved therapeutic windows comprising a flat dose of 1500 mg (e.g., obinutuzumab, ofatumumab).
21. It would have been obvious to one of ordinary skill in the art, before the filing date of the instantly claimed invention, to include administering a flat dose of 1500 mg of the bispecific antibody (which specifically binds to the extracellular parts of EGFR and LGR5) of Throsby et al, through the process of routine optimization and because of the teachings of Hendrikx. The skilled artisan would have been motivated to use a flat dose because Hendrikx teaches that fixed dosage schedules are justified based on pharmacokinetics and furthermore have several advantages, including lower healthcare costs, drug spillage, and medication errors.
22. Also, Thorsby et al. teach [0729] that IV administration of up to 25 mg/kg was safe in cynomolgous monkeys. Based on this information, and taking into account an average weight of about 70 kg for human beings to be treated, the dose of 1500 mg would be well within the realm of routine optimization. MPEP § 2144.05(II)(A) states, "[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation." In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955). Moreover, it is well settled that "discovery of an optimum value of a result effective variable in a known process is ordinarily within the skill of the art." In re Boesch, 617 F.2d 272,276, 205 USPQ 215, 219 (CCPA 1980). See also Merck & Co. v. Biocraft Labs. Inc., 874 F.2d 804,809, 10 USPQ2d 1843, 1847-48 (Fed. Cir. 1989). Optimal drug dosages are an art-recognized result-effective variable that is routinely determined and optimized in the pharmaceutical art, and it is conventional and within the skill of those in the art to identify the optimal dosages and treatment intervals necessary to achieve desired working concentrations and therapeutic efficacy. Accordingly, it would have been obvious to one of ordinary skill in the art at the time Applicants' invention was made to determine all operable and optimal therapeutic doses, and one of ordinary skill in the art would have arrived at the dosage of 1500 mg of the bispecific antibody through the process of routine optimization.
Claim(s) 24-26 is/are further rejected under 35 U.S.C. 103 as being unpatentable over US2018/0312604 (Throsby et al. Nov. 1, 2018) in view of Hendrix (The Oncologist, 22(10), 2017) in further view of NIH, NCI’s Head and Neck Cancers Website (Wayback Machine, at least 2015)
Throsby et al. and Hendrix et al. teach as set forth above.
Throsby et al. and Hendrix et al. do not specifically teach:
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26. The National Cancer Institute (NIH/NCI) states that cancers that are known collectively as head and neck cancers usually begin in the squamous cells that line the mucosal surfaces of the head and neck (for example, those inside the mouth, throat, and voice box). Cancers of the head and neck can form in the oral cavity. They can form in the throat (pharynx) which is a hollow tube about 5 inches long that starts behind the nose and leads to the esophagus. It has three parts: the nasopharynx (the upper part of the pharynx, behind the nose); the oropharynx (the middle part of the pharynx, including the soft palate (the back of the mouth), the base of the tongue, and the tonsils); the hypopharynx (the lower part of the pharynx). The reference further teaches that these head and neck cancers are inclusive of cancers in the larynx, the nasal cavity, and paranasal sinuses, and salivary glands.
27. One of ordinary skill in the art at the time of filing would consider it prima facie obvious to include the other “head and neck” cancers (e.g., cancers of the nasal cavity, paranasal sinus cancer, oral cancer, etc.) because these types of cancers were collectively known as head and neck cancers. Further, it would have been obvious to include squamous cell cancers of the head and neck because it was well known that these types of cancers usually begin in the squamous cells. One would have been motivated to do so because all of the claimed elements were known in the prior art and one skilled in the art could have combined the elements as claimed by known methods with no change in their respective functions, and the combination yielded nothing more than predictable results to one of ordinary skill in the art. KSR, 550 U.S. at 416, 82 USPQ2d at 1395.
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 20-33 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-2, and 6-30 of U.S. Patent No. 11939394 in view of Hendrix (The Oncologist, 22(10), 2017).
US Patent 11939394 claims bispecific antibodies that bind to EGFR and LRG3. These encompass the same bispecific antibodies of the pending claims for the treatment of head and neck cancers. For example, Claim 1 of 11939394 is drawn to a bispecific antibody that comprises a variable domain that binds an extracellular part of EGFR and a variable domain that binds an extracellular part of LGR5, wherein the VH chain of the variable domain that binds EGFR comprises the CDR1, CDR2 and CDR3 amino acid sequences NYAMN (SEQ ID NO:188), WINANTGDPTYAQGFTG (SEQ ID NO: 215), and ERFLEWLHFDY (SEQ ID NO: 242); and the VH chain of the variable domain that binds LGR5 comprises the CDR1, CDR2 and CDR3 amino acid sequences SSSSYWG (SEQ ID NO: 192), SFYYSGNTYYNPSLKS (SEQ ID NO: 220), and TYSSSWDGVLYYFDY (SEQ ID NO:247); and wherein the first and second variable domains further comprise the light chain variable domain comprising a CDR1 sequence QSISSY (SEQ ID NO: 299), a CDR2 sequence AAS, and a CDR3 sequence QQSYSTPPT (SEQ ID NO: 300).
The pending claims use the same VH CDRs that bind EGFR (CDRs of MF3755) and LRG5 (CDRs of MF5803) (See Figure 3b for CDRs) as well as the identical light chain (See Figure 4 and claimed as SEQ ID NO:122). Similarly, the VH domain of MF3755 is identical to SEQ ID NO:20 of the patented claims, and the VH domain of MF5803 is identical to SEQ ID NO:44.
The patent further teaches that the bispecific antibodies can be used to treat head and neck cancers. The portion of the specification of the reference that describes subject matter that falls within the scope of a reference claim may be relied upon to properly construe the scope of that claim. In particular, when ascertaining the scope of the reference’s claim(s) to a compound, the examiner should consider the reference’s specification, including all of the compound’s uses that are disclosed. See Sun Pharm. Indus., 611 F.3d at 1386-88, 95 USPQ2d at 1801-02.
That patent does not teach administering a flat dose of 1500 mg of the antibody.
Hendrikx reviews the advantages of fixed dosing of monoclonal antibodies in the field of oncology. Hendrikx teaches that most monoclonal antibodies in oncology are administered in body-size-based dosing schedules (e.g., body surface area (BSA, in m2) or mg/kg), which are believed to correct for variability in both drug distribution and elimination among patients (Introduction, page 1212). In oncology, monoclonal antibodies are of the immunoglobulin G (IgG) subtype and are primarily administered intravenously. Hendrikx argues that fixed dosing of monoclonal antibodies has several advantages including efficiency of compounding, reduced drug spillage, fewer medication errors, and decreased costs (e.g., Introduction, page 1213; page 1219). Hendrikx teaches that monoclonal antibodies are cleared in a linear fashion via proteolytic catabolism and intracellular degradation after target binding, the latter of which is likely not body weight-dependent (pages 1213 and 1215, text). Summarizing the results of in silico studies, Hendrikx notes that when minimal effects of body weight are observed on the volume of distribution and clearance of an antibody in plasma, fixed dose administration reduces interpatient variability compared to body weight-based dosing (pages 1215-1216). Even when strong effects of body weight are observed, Hendrikx argues that fixed dosing can still be considered for monoclonal antibodies with a wide therapeutic range for practical reasons (page 1217; Table 1). Citing the anti-EGFR antibody panitumumab as an example, Hendrikx notes that effects of body weight on antibody clearance and volume distribution were limited, which together with the wide therapeutic window of this drug suggests that a fixed dosing could successfully be employed (page 1219). Table 1 illustrates other monoclonal antibodies approved for treatment of cancer, some of which have approved therapeutic windows comprising a flat dose of 1500 mg (e.g., obinutuzumab, ofatumumab).
It would have been obvious to one of ordinary skill in the art, before the filing date of the instantly claimed invention, to include administering a flat dose of 1500 mg of the bispecific antibody (which specifically binds to the extracellular parts of EGFR and LGR5) of Throsby et al, through the process of routine optimization and because of the teachings of Hendrikx. The skilled artisan would have been motivated to use a flat dose because Hendrikx teaches that fixed dosage schedules are justified based on pharmacokinetics and furthermore have several advantages, including lower healthcare costs, drug spillage, and medication errors.
Claims 20-33 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim 31, 34, 37-41, 43-44, and 47 of copending Application No. 17921042 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the species of treating head and neck cancers in the pending claims anticipates the genus of cancers recited in 17921042.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Copending Application No. 17921042 encompasses treating all cancers to a human with a flat dose of 1500 mg of a bispecific antibody that binds to EGFR and LGR5. The VH chains are inclusive of the same regions as currently claimed (MF3755 and MF5816). Note, the amendment of 12/22/2025 in Claim 31 states, “wherein the bispecific antibody comprises the CDR1, CDR2, and CDR3 sequences of common light chain comprising SEQ ID NO:133”. In order to promote compact prosecution, it is assumed for examination purposes that recitation of SEQ ID NO:133 of Claim 31 is a typographical error because SEQ ID NO:133 is a hinge region and that applicant’s intended to claim the common light chain of SEQ ID NO:122 (which is the same as the pending application). Clarification is requested.
Claims 20-33 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 30, 33-34, 40-42, 44, 48, 49-53 of copending Application No. 17632181 (reference application) in further view of Cesare et al. (Clin.Can.Res., Vol 20(4), 2014). Although the claims at issue are not identical, they are not patentably distinct from each other because the species of head and neck cancers anticipates the genus of cancers recited in 17/632181.
The difference between the claims is that the pending claims are directed to a flat dose of 1500mg of bispecific antibody, which, as set forth above, would be obvious in view of Hendrikx et al. The second difference is that the reference claims include administration of a second chemotherapeutic- “a topoisomerase I inhibitor”. However, it would have been obvious to one of ordinary skill to combine the bispecific antibody for treating head and neck cancer with another common agent for treating cancer such as a topoisomerase I inhibitor as their combination could result in additive or even synergistic outcomes. For example, Cesare et al. (Clin.Can.Res., Vol 20(4), 2014) taught that the combination of cetuximab (an anti-EGFR antibody) with topoisomerase I inhibitors (namitecan or irinotecan) provided evidence of a synergistic antitumor response in squamous cell carcinoma models. Further, it is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art." In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980).
Claims 20-33 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 42-65 of copending Application No. 18/268168 (reference application) in further view of US2018/0312604 (Throsby et al. Nov. 1, 2018). Although the claims at issue are not identical, they are not patentably distinct from each other because the same pharmaceutical bispecific antibodies in the reference application are used in the methods of the pending application.
Claim 42 of copending 18/268168 is broadly drawn to a pharmaceutical composition comprising a bispecific antibody that binds to EGFR and LGR5 inclusive of a histidine and/or citrate buffer, a sugar component, and a non-ionic surfactant. Claims 55-63 are inclusive of the same VH regions as claimed in the current application.
The difference between the claims is that the co-pending claims do not include a flat dose of 1500mg of bispecific antibody, which, as set forth above, would be obvious in view of Hendrikx et al. The second difference is that the pending claims do not address the constituents of the pharmaceutical formulations such as the type of buffers as claimed in copending 18/268168. However, it would have been obvious to one of skill in the art to formulate the antibodies with a suitable buffering system including appropriate excipients. For example, US2018/0312640 (Throsby et al. Nov. 1, 2018) teach [0310] pharmaceutical formulations of a bispecific antibody that binds EGFR and LGRF that comprises a preferably pharmaceutically acceptable excipient or carrier. In a preferred embodiment the pharmaceutical composition comprises 5-50 mM Histidine, 100-300 mM Trehalose, 0.1-03 g/Lis disclosed which is formulated as a pharmaceutical composition with 25 mM Histidine, 220 mM Trehalose, 0.2 g/L PolySorbate20 or a combination thereof, with a pH set of most preferably 6. It would further be obvious to substitute sucrose for trehalose or polysorbate 20 for polysorbate 80 as both are well known antibody stabilizers. MPEP § 2144.05(II)(A) states, "[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation." In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955). Moreover, it is well settled that "discovery of an optimum value of a result effective variable in a known process is ordinarily within the skill of the art." In re Boesch, 617 F.2d 272,276, 205 USPQ 215, 219 (CCPA 1980). See also Merck & Co. v. Biocraft Labs. Inc., 874 F.2d 804,809, 10 USPQ2d 1843, 1847-48 (Fed. Cir. 1989).
Claims 20-33 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 29-59 of copending Application No. 18431642 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the same bispecific antibodies are used to treat head and neck cancers.
Claim 29 of the co-pending claims are drawn to methods of treating cancer comprising administering a bispecific antibody that binds EGFR and LGR5 wherein the cancer is inclusive of head and neck cancers (Claim 57 and 59). The pending claims use the same VH CDRs that bind EGFR (e.g., CDRs of MF3755) and LRG5 (e.g., CDRs of MF5803) as well as the identical light chain CDRs (See Figure 4 and claimed as SEQ ID NO:122) as claimed in the pending application.
The difference between the claims is that the co-pending claims do not include a flat dose of 1500mg of bispecific antibody, which, as set forth above, would be obvious in view of Hendrikx et al.
Claims 20-33 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 3, 9-13, 16, 18, 20, 23, 27, 36-42 of copending Application No. 18694252 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because both applications claim the same bispecific antibodies used to treat head and neck cancers (claim 9 of copending application). Further, both sets of claims include providing a flat dose of 1500 mg of the antibody (Claim 18 of co-pending application). For example, the pending application in claim 3 used a first variable domain comprising the CDRs of MF3755 and second variable domain of SEQ ID NO:13 which is 100% identical to MF5816 (SEQ ID NO:13 of pending application).
No claim is allowed.
11939394
Any inquiry concerning this communication or earlier communications from the examiner should be directed to GARY B NICKOL, Ph.D. whose telephone number is (571)272-0835. The examiner can normally be reached M-F 9AM-5:30PM.
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/GARY B NICKOL/Primary Examiner, Art Unit 1643