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 .
Claim Status
Claims 2, 5, 8, 11, 19, 35-36, 38-39, 45-47, and 49 are cancelled. Claims 1, 3-4,6-7, 9-10, 12-18, 20, 26, 30-34, 37, 40-44, 48, and 50 as filed on 21 July 2025 are pending. Claims 33-34, 37, and 40-44 are withdrawn. Claims 1, 3-4, 6-7, 9-10, 12-18, 20, 26, 30-32, 48, and 50 are under examination.
Rejections Withdrawn
Objection of claims 3-4, 6-7, 17, 20, and 44 is withdrawn with applicant amendment of claims correcting “SEQ ID NO:”.
Rejection of claims 3-4, 6-7, 9-10, 12-18, 20, 26, 30-32, 48, and 50 under 35 U.S.C. 112(a) is withdrawn with applicant amendment of claims.
Rejection of claims 3-4 and 6-7 under 35 U.S.C. 102 and 103 are withdrawn with applicant amendment of claims. The claims now require a combination of elements not previously required. New Rejections necessitated by these amendments have been added at the end of the Maintained but updated Rejections amended due to applicant amendment of claims 1 and 3.
To a now withdrawn rejection under 35 U.S.C. 103 applicant argues Larson did not fill the deficiencies of Champion. Please see response to arguments for the alleged deficiencies of Champion and the new rejections necessitated by applicant arguments.
Applicant noted Examiner included Larson in the first rejection under 35 U.S.C. 103 of claims 1, 3-4, 6, 17-18, 20, and 50 of the previous office action on page 11, but did not use the teachings of Larson in that rejection. Larson was not used in the teachings or rational to combine and with applicant amendment Larson is not included in the amended rejection. Claims 1, 17-18, 20, and 50 are now rejected under Champion and Satake.
Rejections Maintained – Rejection Amendments Necessitated by Applicant Amendments to Claim
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1, 9-10, 13-17, 26, and 30-32 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Champion (WO 2018/041827 A1) (IDS).
Regarding claims 1, and 30-31, Champion teaches an adenovirus vector comprising a DNA sequence of 5'ITR-B1-BA-B2-BX-BB-BY-B3-3'ITR and encodes B2 is E3, an adenovirus polypeptide, Bx is a transgene, and BB is L5, an adenovirus polypeptide (Claim 1) and further teaches the transgene is a kozak sequence or a splice acceptance sequence (page 10 in lines 5-10). Champion teaches splice acceptor sites are used with splice donor sites (page 28 in lines 30-38), further the insertion into an intron (page 30 in lines 9-13), and a stop codon (Figure 77).
Regarding claim 9, Champion teaches the vector comprising 5'ITR-B1-BA-B2-BX-BB-BY-B3-3'ITR and further teaches B1 is E1A, E1B, or E1A-E1B, B2 is E3, BX is one or more transgenes, and By is one or more transgenes (claim 1). Champion further teaches the adenovirus encodes a first and second BiTE (claim 1). Champion teaches the first and second BiTE can be encoded at the same or different locations (claims 22-23). Champion further teaches at least one BiTE is encoded in a region selection from E1, E3, Bx, or By (claim 24). Champion further teaches at least a BiTE is encoded in Bx (claim 25) and a BiTE is encoded in By (claim 26). This would then include an adenovirus vector comprising a BiTE in position E1 or B1, a splice acceptance sequence at a transgene location of Bx, and a second BiTE encoded at By. Champion teaches BiTE comprise at least two binding domains and that their BiTEs comprise binding domains to surface antigens (abstract).
Regarding claim 10, Champion teaches Bispecific T cell engager (BiTE) is a type of bispecific antibody comprising 2 scFvs wherein they bind a T cell antigen including CD3 and antigens including tumor-specific antigens. Champion further teaches the binding results in the activation of the T cells (page 17 in lines 29-40). Champion teaches BiTEs that activated T cells with EpCAM binding in Example 21. The first polypeptide would be a BiTE which binds a T cell and a tumor antigen thus it would comprise 4 antigen binding domains wherein the first and second polypeptides comprise a T cell binding domain and a tumor antigen binding domain.
Regarding claims 13-15, Champion teaches the binding of CD3 on T cells (Figure 45, example 21, and claims 3-4).
Regarding claim 16, Champion teaches the tumor antigen binding domain of EpCAM with CD3 (Example 21) and further teaches the tumor antigens of MUC1 and HER2 (Claim 10). Champion further teaches tumor antigens of interest include EGFRVIII, PSMA, and WT1 (page 40 in lines 20-31).
Regarding claim 17, Champion teaches recombinant adenovirus vectors (claim 1, 17-21, page 21 in lines 15-18, page 37 in lines 34-35, and page 57 in lines 5-10).
Regarding claim 26, Champion teaches a 5’ ITR and a 3’ ITR (claim 1 and Figures 1B-1D).
Regarding claim 32, Champion teaches pharmaceutical formulations for the viruses of the invention that comprise pharmaceutically acceptable carriers (page 52 in particular lines 3-4 and 36; and claim 44).
Applicant Arguments
Applicant argues that Champion does not teach the elements of the claims by not teaching two polynucleotides wherein two portions of the first polypeptide and a third polynucleotide sequence encoding the second polypeptide. Applicant argues the configuration of Champion does not fall within the scope of the claims. Applicant argues the vector of Champion does not provide a vector that encodes a polypeptide in two parts.
Applicant argues the new requirements of the claim are not taught by Champion.
Response to Arguments
Applicant's arguments filed 07/21/2025 have been fully considered but they are not persuasive.
The claim does not require the first polypeptide be encoded in two parts and the vector of Champion encoding two copies of a first polypeptide would fall within the scope of the claims.
Champion teaches the new requirements of the claims as shown by the amendment to the rejection.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 1, 17-18, 20, and 50 are rejected under 35 U.S.C. 103 as being unpatentable over Champion (WO 2018/041827 A1) (IDS), and Satake et. al. Mol Med. 22:632-642 (2016) (Of Record).
Regarding claims 1 and 3, Champion teaches an adenovirus vector comprising a DNA sequence of 5'ITR-B1-BA-B2-BX-BB-BY-B3-3'ITR and encodes B2 is E3, an adenovirus polypeptide, Bx is a transgene, and BB is L5, an adenovirus polypeptide (Claim 1) and further teaches the transgene is a kozak sequence or a splice acceptance sequence (page 10 in lines 5-10). Champion teaches the vector comprising 5'ITR-B1-BA-B2-BX-BB-BY-B3-3'ITR and further teaches B1 is E1A, E1B, or E1A-E1B, B2 is E3, BX is one or more transgenes, and By is one or more transgenes (claim 1). Champion further teaches the adenovirus encodes a first and second BiTE (claim 1). Champion teaches the first and second BiTE can be encoded at the same or different locations (claims 22-23). Champion further teaches at least one BiTE is encoded in a region selection from E1, E3, Bx, or By (claim 24). Champion further teaches at least a BiTE is encoded in Bx (claim 25) and a BiTE is encoded in By (claim 26). This would then include an adenovirus vector comprising a BiTE in position E1 or B1, a splice acceptance sequence at a transgene location of Bx, and a second BiTE encoded at By. Champion teaches BiTE comprise at least two binding domains and that their BiTEs comprise binding domains to surface antigens (abstract).
Champion teaches the adenovirus further comprises transgenes encoding immunomodulators, proteins, or peptide ligands to checkpoints proteins (claims 39-43). Champion further teaches targeting the function of cells to stimulate or modulate cell activity (page 43 in lines 1-5). Champion teaches the treatment of multiple cancers including leukemia (page 17 in lines 29-40).
Champion teaches multi-specific antibody molecules which has two or more antigen binding domains including bispecific, tri-specific, or tetra-specific binding domains (page 16 in lines 1-4). Applicant defines a dimert as a protein molecule comprising two or more scFvs in which each scFv recognizes a surface polypeptide expressed on a cell and the two cells are different (applicant specification in [0127]). Champion teaches multi-specific antibody molecules that comprise non-covalent of scFv fragments which can be bi or multi-specific (page 17 in lines 4-8). Champion teaches the vector comprises at least two BiTE molecules (abstract).
Champion does not teach the use of antisense oligonucleotides.
Champion does not teach a dimert with an antisense oligonucleotide.
These deficiencies are filled by Satake.
Satake teaches an antibody conjugated to an antisense oligonucleotide that targets a transcription factor that is critical for precursor B-cell acute lymphoblastic leukemia cell survival. Satake teaches that by conjugating the transcription factor antisense oligonucleotide to an anti-CD22 antibody that targets the same cell population the treatment resulted in leukemia cell apoptosis. Satake teaches this as a novel and effective therapeutic method (abstract).
It would have been obvious at the time the application was filed to substitute the transgenes that modulate cell activity of Champion with the antisense oligonucleotide of Satake that modulates cell activity to produce an adenovirus vector comprising the dimerts of Champion that further comprises the antisense oligonucleotide of Satake. The use of antisense oligonucleotides for use in treatment of cancer including leukemia was known in the art as shown by Satake. One of ordinary skill in the art would have been motivated to identify other modulators of cell activity for use in the adenovirus of Champion for treatment of cancers including leukemia. There would have been a reasonable expectation of success as combination therapies for cancer are known method of improving patient outcomes and Champion and Satake teach effective methods of treatment.
Applicant Arguments
Applicant argues that Champion does not teach the elements of the claims by not teaching the limitations of the claims as argued in the argument to the rejection under 35 U.S.C. 102.
Applicant argues Satake does not teach the position of the antisense required by the claims. Applicant states the substitution in the rejection would not place the antisense oligonucleotides of Satake in between two polynucleotides that together encode a polypeptide.
Response to Arguments
Applicant's arguments filed 07/21/2025 have been fully considered but they are not persuasive.
Regarding the applicant alleged deficiencies of Champion, see previous response to arguments in the 102(a)(1) rejection set forth above.
Champion teaches the vector comprising 5'ITR-B1-BA-B2-BX-BB-BY-B3-3'ITR and further teaches B1 is E1A, E1B, or E1A-E1B, B2 is E3, BX is one or more transgenes, and By is one or more transgenes (claim 1). The placement at BX in Champion would be between 2 polynucleotides encoding a polypeptide.
As stated in the response to arguments under the rejection under 35 U.S.C. 102 the claim does not require the first polypeptide be encoded in two parts and the vector of Champion encoding two copies of a first polypeptide would fall within the scope of the claims. Therefore this is not a limitation either Champion or Satake have to teach.
Claims 1, 12, and 48 are rejected under 35 U.S.C. 103 as being unpatentable over Champion (WO 2018/041827 A1) (IDS).
Regarding claim 1, Champion teaches an adenovirus vector comprising a DNA sequence of 5'ITR-B1-BA-B2-BX-BB-BY-B3-3'ITR and encodes B2 is E3, an adenovirus polypeptide, Bx is a transgene, and BB is L5, an adenovirus polypeptide (Claim 1) and further teaches the transgene is a kozak sequence or a splice acceptance sequence (page 10 in lines 5-10). Champion teaches the vector comprising 5'ITR-B1-BA-B2-BX-BB-BY-B3-3'ITR and further teaches B1 is E1A, E1B, or E1A-E1B, B2 is E3, BX is one or more transgenes, and By is one or more transgenes (claim 1). Champion further teaches the adenovirus encodes a first and second BiTE (claim 1). Champion teaches the first and second BiTE can be encoded at the same or different locations (claims 22-23). Champion further teaches at least one BiTE is encoded in a region selection from E1, E3, Bx, or By (claim 24). Champion further teaches at least a BiTE is encoded in Bx (claim 25) and a BiTE is encoded in By (claim 26). This would then include an adenovirus vector comprising a BiTE in position E1 or B1, a splice acceptance sequence at a transgene location of Bx, and a second BiTE encoded at By. Champion teaches BiTE comprise at least two binding domains and that their BiTEs comprise binding domains to surface antigens (abstract).
Champion teaches multi-specific antibody molecules which has two or more antigen binding domains including bispecific, tri-specific, or tetra-specific binding domains (page 16 in lines 1-4). Applicant defines a dimert as a protein molecule comprising two or more scFvs in which each scFv recognizes a surface polypeptide expressed on a cell and the two cells are different (applicant specification in [0127]). Champion teaches multi-specific antibody molecules that comprise non-covalent of scFv fragments which can be bi or multi-specific (page 17 in lines 4-8). Champion teaches the vector comprises at least two BiTE molecules (abstract).
Champion teaches PCR (page 96 in lines 31-48 and page 99 in lines 15-19).
Champion does not make embodiments with more than two BiTEs.
It would have been obvious to one of ordinary skill in the art that the adenovirus vector of Champion encodes more than two transgenes and that more than two BiTEs could be encoded by the vector. Champion itself teaches the encoding of two or more antigen binding molecules and further teaches the use of two or more scFvs and tri and tetra-specific binding domains. One of ordinary skill in the art would have been motivated to use combinations comprising additional antigen binding domains as combination therapy is a known method of improving immunotherapy for cancer patients. There would have been a reasonable expectation of success as the vector of Champion is already encoding more than two transgenes.
Champion does not teach a kit comprising the polynucleotide or vector of claim 1. Champion and one of ordinary skill in the art would have known that polynucleotides can be stored in a kit as shown by the use of PCR which one of skill in the art would have known that PCR includes nucleic acid sequences that had been stored in a kit. Further, a kit does not change the physical characteristics of the vector of the claims (see MPEP 2112.01). By teaching the vector of the instant claims and teaching kits comprising polynucleotides Champion teaches one of skill in the art the vector in a kit as required by claim 48.
Applicant Arguments
Applicant argues that Champion does not teach the elements of the claims by not teaching the limitations of the claims as argued in the argument to the rejection under 35 U.S.C. 102.
Response to Arguments
Applicant's arguments filed 07/21/2025 have been fully considered but they are not persuasive.
Regarding the applicant alleged deficiencies of Champion, see previous response to arguments in the 102(a)(1) rejection set forth above.
New Rejections Necessitated by Applicant Amendment of Claims
Claims 1 and 3 are rejected under 35 U.S.C. 103 as being unpatentable over Champion (WO 2018/041827 A1) (IDS), Lee et. al. Nucleic Acid Therapeutics. 26(1):44-51. (2016) (Of Record), and Ungerechts et. al. 28(10):800-819 (2017) (Of Record).
The teachings of Champion from all previous rejections are incorporated here in full.
Regarding claims 1 and 3, Champion teaches an adenovirus vector comprising a DNA sequence of 5'ITR-B1-BA-B2-BX-BB-BY-B3-3'ITR and encodes B2 is E3, an adenovirus polypeptide, Bx is a transgene, and BB is L5, an adenovirus polypeptide (Claim 1) and further teaches the transgene is a kozak sequence or a splice acceptance sequence (page 10 in lines 5-10). Champion teaches splice acceptor sites are used with splice donor sites (page 28 in lines 30-38), further the insertion into an intron (page 30 in lines 9-13), and a stop codon (Figure 77).
Champion teaches Bispecific T cell engager (BiTE) is a type of bispecific antibody comprising 2 scFvs wherein they bind a T cell antigen including CD3 and antigens including tumor-specific antigens. Champion further teaches the binding results in the activation of the T cells (page 17 in lines 29-40). Champion teaches BiTEs that activated T cells with EpCAM binding in Example 21. The first polypeptide would be a BiTE which binds a T cell and a tumor antigen thus it would comprise 4 antigen binding domains wherein the first and second polypeptides comprise a T cell binding domain and a tumor antigen binding domain.
Champion does not teach a gene regulation sequence of a riboswitch.
These deficiencies are filled by Lee and Ungerechts
Lee teaches riboswitches are regulators of gene expression by sensing small-molecule metabolites and responding by regulating the expression of corresponding metabolic genes. Lee further teaches artificial riboswitches that are engineered to control different steps in bacteria and eukaryotic cells (abstract). Lee teaches a variety of riboswitches that respond to different ligands and the use of riboswitches in viruses (Table 1). Lee teaches the use of riboswitches for use in varying applications including clinical uses (page 49 in col 1 in lines 1-17).
Ungerechts teaches virotherapy as a unique modality for the treatment of cancer and the use of riboswitches with oncolytic viruses (OV) where the OVs selectively infect and lyse tumor cells, spread within tumors, and activate anti-tumor immunity (abstract). Ungerechts teaches the use of synthetic riboswitches in viruses including adenoviruses (Table 1). Ungerechts teaches riboswitches for tumor targeting and regulation of Ovs (page 815 in col 2 in bullet list).
It would have been obvious at the time the application was filed to combine the adenovirus vector comprising a cancer therapeutic of Champion with the known regulator component of a riboswitch in view of Lee and Ungerechts. One of skill in the art would have been motivated to improve targeting and control of the cancer therapeutic of Champion with the riboswitch that Lee and Ungerechts teach provide these advantages and Ungerechts teaches work with OVs including adenovirus used in cancer therapy. The use of a known regulator of adenovirus plasmids in cancer therapy with the adenovirus plasmid of Champion would have been obvious. There would have been a reasonable expectation of success as Champion and Ungerechts both teach the use of adenovirus vectors transporting chemotherapeutics.
Claims 1, 3-4, and 6 are rejected under 35 U.S.C. 103 as being unpatentable over Champion (WO 2018/041827 A1) (IDS), Lee et. al. Nucleic Acid Therapeutics. 26(1):44-51. (2016) (Of Record), Ungerechts et. al. 28(10):800-819 (2017) (Of Record), and Satake et. al. Mol Med. 22:632-642 (2016) (Of Record).
The teachings of Champion from the previous rejection are incorporated here in full.
Champion does not teach the use of antisense oligonucleotides.
Champion does not teach a gene regulation sequence of a riboswitch.
Champion does not teach a dimert with an antisense oligonucleotide.
These deficiencies are filled by Lee, Ungerechts, and Satake.
The teachings of Lee and Ungerechts from the previous rejections are incorporated here in full.
Satake teaches an antibody conjugated to an antisense oligonucleotide that targets a transcription factor that is critical for precursor B-cell acute lymphoblastic leukemia cell survival. Satake teaches that by conjugating the transcription factor antisense oligonucleotide to an anti-CD22 antibody that targets the same cell population the treatment resulted in leukemia cell apoptosis. Satake teaches this as a novel and effective therapeutic method (abstract).
Regarding claim 3, it would have been obvious at the time the application was filed to combine the adenovirus vector comprising a cancer therapeutic of Champion with the known regulator component of a riboswitch in view of Lee and Ungerechts. One of skill in the art would have been motivated to improve targeting and control of the cancer therapeutic of Champion with the riboswitch that Lee and Ungerechts teach provide these advantages and Ungerechts teaches work with OVs including adenovirus used in cancer therapy. The use of a known regulator of adenovirus plasmids in cancer therapy with the adenovirus plasmid of Champion would have been obvious. There would have been a reasonable expectation of success as Champion and Ungerechts both teach the use of adenovirus vectors transporting chemotherapeutics.
It would have been obvious at the time the application was filed to substitute the transgenes that modulate cell activity of Champion with the antisense oligonucleotide of Satake that modulates cell activity to produce an adenovirus vector comprising the dimerts of Champion that further comprises the antisense oligonucleotide of Satake. The use of antisense oligonucleotides for use in treatment of cancer including leukemia was known in the art as shown by Satake. One of ordinary skill in the art would have been motivated to identify other modulators of cell activity for use in the adenovirus of Champion for treatment of cancers including leukemia. There would have been a reasonable expectation of success as combination therapies for cancer are known method of improving patient outcomes and Champion and Satake teach effective methods of treatment.
Claims 1, 3-4, and 7 are rejected under 35 U.S.C. 103 as being unpatentable over Champion (WO 2018/041827 A1) (IDS), Lee et. al. Nucleic Acid Therapeutics. 26(1):44-51. (2016) (Of Record), Ungerechts et. al. 28(10):800-819 (2017) (Of Record), and Larson (WO 2018/218240 A1) (Of Record).
The teachings of Champion from the previous rejection are incorporated here in full.
Champion does not teach the sequence of the stop codons used.
Champion does not teach a gene regulation sequence of a riboswitch.
These deficiencies are filled by Lee, Ungerechts, and Larson.
The teachings of Lee and Ungerechts from the previous rejections are incorporated here in full.
Regarding claim 7, Larson teaches a recombinant adenovirus with one or more nucleotide inserted between two viral transcription units (abstract and Figure 1). Larson teaches encoding transgenes ([0035]) and further teaches the transgenes are antibodies ([0039]) including tumor antigens of EpCAM, HER2, and EGFRvIII ([0040]). Larson teaches the use of an adenovirus stop codon of TAA (Example 1 in [00210]).
Regarding claim 3, it would have been obvious at the time the application was filed to combine the adenovirus vector comprising a cancer therapeutic of Champion with the known regulator component of a riboswitch in view of Lee and Ungerechts. One of skill in the art would have been motivated to improve targeting and control of the cancer therapeutic of Champion with the riboswitch that Lee and Ungerechts teach provide these advantages and Ungerechts teaches work with OVs including adenovirus used in cancer therapy. The use of a known regulator of adenovirus plasmids in cancer therapy with the adenovirus plasmid of Champion would have been obvious. There would have been a reasonable expectation of success as Champion and Ungerechts both teach the use of adenovirus vectors transporting chemotherapeutics.
It would have been obvious at the time the application was filed to substitute the generic stop codon in Champion in an adenovirus vector comprising two transgenes of antigen binding molecules and a stop codon with the adenovirus stop codon of TAA taught by Larson. Champion and Larson both teach adenovirus vectors that encode transgenes that are antigen binding domains comprising a stop codon. One of skill in the art would have been motivated to find a working stop codon for adenovirus vectors like the ones taught by Larson. The substitution of the generic stop codon of Champion with the TAA stop codon of Larson would be obvious as sequences with the same purpose in adenovirus vectors. There would have been a reasonable expectation of success as Larson teaches an adenovirus stop codon that functions in a vector comprising multiple transgenes encoding antigen binding domains.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to FRANCESCA EDGINGTON-GIORDANO whose telephone number is (571)272-8232. The examiner can normally be reached Mon - Fri 8:00 - 5:00.
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, Julie Wu can be reached at 571-272-5205. 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.
/F.E./Examiner, Art Unit 1643
/Meera Natarajan/Primary Examiner, Art Unit 1643