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 .
Applicant’s amendment, filed on 9/29/2025, is acknowledged.
Claims 3, 11-15, 17, 19-87, 90-95, 97-100, 104-113, and 116-164 are cancelled.
Claims 1, 2, 4-10, 16, 18, 88, 89, 96, 101-103, 114, 115, and 165 are currently pending.
Election/Restrictions
Applicants’ election without traverse of Group I, claims 1, 2, 4-10, 16, 18, 88, 89, 96, 101, 114, 115, and 165, directed to a method of generating T-cells comprising multi-specific TCRs, and the species of: i) a CMV vector expressing UL40 and US28; ii) and iii) a first and second MHC-E antigen peptide complex; iv) a human; v) a recombinant human CMV vector; vi) HIV and a different pathogen specific antigen; vii) the combination in claim 96(i); viii) IV administration; and ix) miR126, filed on 9/29/2025, is acknowledged.
Claims 9, 102, 103 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to nonelected inventions and/or species.
Claims 1, 2, 4-8, 10, 16, 18, 88, 89, 96, 101, 114, 115, and 165 are under examination.
Claim 1 is the only independent claim under examination.
Priority
Applicant’s claim for the benefit of a prior-filed U.S. Provisional Application No. 62/948,691, filed December 16, 2019, is acknowledged.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 12/13/2022, 4/12/2024, and 4/14/2025 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statements are being considered by the examiner in their entireties.
Nucleotide and/or Amino Acid Sequence Disclosures
Specific deficiency – Nucleotide and/or amino acid sequences appearing in the specification are not identified by sequence identifiers in accordance with 37 CFR 1.821(d).
The specification discloses the amino acid sequence SIINFEKL in ¶[0004] without its corresponding sequence identifier.
Required response – Applicant must provide:
A substitute specification in compliance with 37 CFR 1.52, 1.121(b)(3) and 1.125 inserting the required sequence identifiers, consisting of:
A copy of the previously-submitted specification, with deletions shown with strikethrough or brackets and insertions shown with underlining (marked-up version);
A copy of the amended specification without markings (clean version); and
A statement that the substitute specification contains no new matter.
Claim Objections
Claims 114 and 115 are objected to because the claim recites the acronym "MRE", which is not a readily recognized acronym in the art, such as “DNA” for 5’-deoxyribonucleic acid. Please define the acronym "MRE" when it is first used in the claims.
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.
Claims 114 and 115 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.
Claim 114 and 115 recites the limitation "…wherein the MRE…". These claims depend on claim 1, which makes no mention of a MRE. There is insufficient antecedent basis for this limitation in the claim.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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.
Claims 1, 2, 4-8, 10, 16, 18, 88, 89, 96, 101, 114, 115, and 165 are rejected under 35 U.S.C. 103 as being unpatentable over Picker et al. (U.S. PGPub 20180133321) in view of Schneck et al. (U.S. PGPub 20020127231), as evidenced by Santis et al. (Eur J Immunol. 1992 May;22(5):1253-9. doi: 10.1002/eji.1830220521).
Claim 1 recites:
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To summarize, claim 1 recites a method of generating a population of T-cells expressing a multi-specific TCR (i.e., one TCR that recognizes two different antigens), followed by screening of the generated TCRs for one that binds a specific peptide of interest with high avidity.
Picker et al. teaches a method of generating CD8+ T cells comprising a TCR (¶[0104] and claims 13 and 19), comprising:
Administration of a recombinant CMV vector comprising a nucleic acid sequence encoding a first heterologous antigen to a subject to generate CD8+ T cells that recognize a first antigen-MHC complex (claim 91(1)): “administering to a first subject the CMV vector of any one of claims 1-12 or 50-57 in an amount effective to generate a set of CDS+ T cells that recognize MHC-E/peptide complexes”, wherein the vector does not comprise active UL128, UL130, UL146, and UL147 proteins (claim 1): “wherein the vector does not express an active UL12S protein or ortholog thereof; does not express an active UL130 protein or ortholog thereof; does not express an active UL146 or ortholog thereof; and does not express an active 147 protein or ortholog thereof”
Identifying a first CD8+ TCR from the first set of CD8+ T cells (claim 91(2)): “identifying a first CD8+ TCR from the set of CD8+ T cells, wherein the first CD8+ TCR recognizes a MHC-E/heterologous antigen-derived peptide complex”
Administration of a second CMV vector encoding a heterologous antigen to a subject in an amount effective to generate a second set of CD8+ T cells that recognize this antigen-MHC complex (¶[0090], claims 18 and 25): “…further comprising administering to the subject a second CMV vector comprising a nucleic acid sequence that encodes at least one heterologous antigen… further comprising identifying a CD8+ TCR from the CD8+ T cells elicited by the CMV vector, wherein the CD8+ TCR recognizes a MHC-E/heterologous antigen-derived peptide complex…”
Isolating one or more CD8+ T cells from the second set of CD8+ T cells (claim 91(3)): “…isolating one or more CD8+ T cells from a second subject…”
Transfecting a set of CD8+ T cells (i.e., “a third set”) with an expression vector comprising a nucleic acid sequence encoding a CD8+ TCR (i.e., “a third TCR”) and an operably linked promoter, wherein the TCR comprises the CDR3 regions of the first set of CD8+ T cells (claim 91(4)): “transfecting the one or more CD8+ T cells with an expression vector, wherein the expression vector comprises a nucleic acid sequence encoding a second CD8+ TCR and a promoter operably linked to the nucleic acid sequence encoding the second CD8+ TCR, wherein the second CD8+ TCR comprises CDR3α and CDR3β of the first CD8+ TCR, thereby generating one or more transfected CD8+ T cells that recognize a MHC-E/heterologous antigen-derived peptide complex”
Picker et al. additionally teaches the CMV vector expressed an active US28 and UL40 ([0144]): “…vector (which lacks the homologs of UL128, UL130, UL146, and UL147, but contains functional homologs of HCMV UL40 and US28…” (i.e., the limitations of instant claim 2), MHC-E derived peptide complexes (i.e., the limitations of instant claims 4 and 5; Picker et al., claim 91), a human subject (i.e., the limitations of instant claim 6, Picker et al. claim 23), and a human CMV vector (i.e., the limitations of instant claim 7; Picker et al. claim 12).
Picker et al. further teaches that the heterologous antigens can be HIV and pathogen specific antigens (i.e., the limitations of instant claims 8 and 10, Picker et al. claims 84 and 85), and the heterologous antigens can be different (¶[0090]): “[t]he second heterologous antigen may be any heterologous antigen, including a heterologous antigen identical to the heterologous antigen in the first CMV vector.” One with ordinary skill in the art would appreciate that if Picker et al. teaches that the heterologous antigen can be any antigen, then it can be different from the first (i.e., the limitations of instant claim 16).
Picker et al. additionally teaches the limitations of instant claim 88 (Picker et al. claim 77), the limitations of instant claim 89 (¶[0011]): “…this method may further comprise transfecting one or more T cells isolated from the first subject or a second subject…”, the limitations of instant claim 96 (Picker et al. claim 95), IV administration of the vector (claim 101), and the vector further comprising an MRE comprising miR126-3p, which is a species of miR126 (i.e. the limitations of instant claims 114, 115, and 165; Picker et al. claim 1).
Picker et al. does not specifically teach identification of a second TCR that is a multi-specific TCR (i.e., the limitations of instant claim 1(e)), followed by transfection of an expression vector encoding the multi-specific TCR into a set of T cells (i.e., the limitations of instant claim 1(f)., or selecting the TCR with the highest avidity (i.e., instant claim 1(g)). However, Picker et al. does teach identifying CD8+ TCRs from subjects administered different heterologous antigens at different times (¶[0126], claims 18, 21, and 25).
Schneck et al., in the same field of endeavor, teaches methods of generating CD8+ T cells comprising high-avidity multi-specific TCRs (Abstract and Fig. 1D): “To increase the avidity of soluble analogs for their cognates to biologically relevant levels, divalent peptide/MHC complexes or T cell receptors (superdimers) were constructed. Using a recombinant DNA strategy, DNA encoding either the MHC class II/peptide or TCR heterodimers was ligated to DNA coding for murine lg heavy and light chains. These constructs were subsequently expressed in a baculovirus expression system. Enzyme-linked immunosorbent assays (ELISA) specific for the Ig and polymorphic determinants of either the TCR or MHC fraction of the molecule indicated that infected insect cells secreted approximately 1 μg/ml of soluble, conformationally intact chimeric superdimers. SDS PAGE gel analysis of purified protein showed that expected molecular weight species. The results of flow cytometry demonstrated that the TCR and class II chimeras bound specifically with high avidity to cells bearing their cognate receptors”. Schneck et al. further teaches (Abstract) “These superdimers will be useful for studying TCR/MHC interactions, lymphocyte tracking, identifying new antigens, and have possible uses as specific regulators of immune responses.
It would have been obvious to one of ordinary skill in the art, before the effective filing date of the instant invention, to have modified the method taught by Picker et al. in view of Schneck et al. to generate CD8+ T cells comprising multi-specific TCRs with a reasonable expectation of success, as Picker et al. teaches methods of generating TCRs that can be used to generate cells comprising multi-specific TCRs as taught by Schneck et al. For example, the first and second TCRs taught by Picker et al. could be used to make the multi-specific TCR in view of Schneck et al. (i.e., “a third TCR”), which would increase the avidity of the TCR (i.e., “selecting for high-avidity TCRs”, or the limitations of instant claim 1(g)). This multi-specific TCR would comprise the CDR3α and CDR3β of the second TCR as well as the first TCR. One would have been motivated to make this change for the purposes of generating CD8+ T cells that express multi-specific TCRs that can be used for a variety of diagnostic and therapeutic purposes.
Regarding the functional limitations recited in instant claim 18, Santis et al. is used as an evidentiary reference that T-cell activation (i.e., activating from a naïve T-cell to a CD8+ cytotoxic T-cell) leads to expression of the CD69 receptor (also known as the activation inducer molecule or AIM; Introduction): “The activation inducer molecule (AIM) is the earliest activation antigen newly synthesized and expressed during T cell activation and it is absent from the surface of resting peripheral blood lymphocytes…”, and further teaches that CD69 signals T-cells to express and secrete TNF-α (pg. 1254, first ¶): “[o]ur results show that the AIM activation pathway significantly induces TNF-α production both at mRNA and protein levels.” Thus, activated T-cells expressing a multispecific TCR, such as the one taught by Picker et al. in view of Schneck et al., are considered to inherently express CD69 and TNFα.
Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the time the invention was made, as evidenced by the references, especially in the absence of evidence to the contrary.
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 1, 2, 4-8, 10, 16, 18, 88, 89, 96, 101, 114, 115, and 165 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1-67 of U.S. Patent No. 10,532,099 (herein Pat ‘099) in view of Schneck et al. (U.S. PGPub 20020127231, supra), as evidenced by Santis et al. (Eur J Immunol. 1992 May;22(5):1253-9. doi: 10.1002/eji.1830220521, supra). Although the claims at issue are not identical, they are not patentably distinct from each other.
Pat ‘099 claims a method of generating CD8+ T cells comprising a TCR (claims 47 and 55), comprising:
Administration of a recombinant CMV vector comprising a nucleic acid sequence encoding a first heterologous antigen to a subject to generate CD8+ T cells that recognize a first antigen-MHC complex (claim 55(1)): “administering to a first subject the CMV vector of claim 1 in an amount effective to generate a set of CD8+ T cells that recognize MHC-E/peptide complexes”, wherein the vector does not comprise active UL128, UL130, UL146, and UL147 proteins (claim 1): “wherein the vector does not express an active UL128 protein or ortholog thereof; does not express an active UL130 protein or ortholog thereof; does not express an active UL146 or ortholog thereof; and does not express an active UL147 protein or ortholog thereof…”
Identifying a first CD8+ TCR from the first set of CD8+ T cells (claim 55(2)): “identifying a first CD8+ TCR from the set of CD8+ T cells, wherein the first CD8+ TCR recognizes a MHC-E/heterologous antigen-derived peptide complex”
Administration of a second CMV vector encoding a heterologous antigen to a subject in an amount effective to generate a second set of CD8+ T cells that recognize this antigen-MHC complex (claims 17 and 24): “…further comprising administering to the subject a second CMV vector comprising a nucleic acid sequence that encodes at least one heterologous antigen… further comprising identifying a CD8+ TCR from the CD8+ T cells elicited by the CMV vector, wherein the CD8+ TCR recognizes a MHC-E/heterologous antigen-derived peptide complex…”
Isolating one or more CD8+ T cells from the second set of CD8+ T cells (claim 55(3)): “…isolating one or more CD8+ T cells from a second subject…”
Transfecting a set of CD8+ T cells (i.e., “a third set”) with an expression vector comprising a nucleic acid sequence encoding a CD8+ TCR (i.e., “a third TCR”) and an operably linked promoter, wherein the TCR comprises the CDR3 regions of the first set of CD8+ T cells (claim 55(4)): “transfecting the one or more CD8+ T cells with an expression vector, wherein the expression vector comprises a nucleic acid sequence encoding a second CD8+ TCR and a promoter operably linked to the nucleic acid sequence encoding the second CD8+ TCR, wherein the second CD8+ TCR comprises CDR3α and CDR3β of the first CD8+ TCR, thereby generating one or more transfected CD8+ T cells that recognize a MHC-E/heterologous antigen-derived peptide complex”
Pat ‘099 does not specifically claim the CMV vectors express an active US28 and UL40, however in reviewing the scope of the claimed invention of Pat ‘099, it was found that (Col 14, 50-54): “[t]he CMV vectors comprise a nucleic acid sequence that encodes a heterologous protein antigen and lack expression of active UL128, UL130, UL146 and UL147 proteins. The vectors contain active UL40, US27 and US28 genes.” Therefore, it is interpreted that the claimed CMV vectors in Pat ‘099 all have active UL40 and US28 genes (i.e., the limitations of instant claim 2).
Pat ‘099 additionally claims MHC-E derived peptide complexes (i.e., the limitations of instant claims 4 and 5; Pat ‘099 claims 47 and 55), a human subject (i.e., the limitations of instant claim 6, Pat ‘099 claim 22), and a human CMV vector (i.e., the limitations of instant claim 7; Pat ‘099 claim 11).
Pat ‘099 does not claim the two antigens are different (i.e., the limitations of instant claim 16), however Pat ‘099 claims first and second heterologous antigens of any type, and one with ordinary skill in the art would appreciate that would mean the antigens could be the same, or could be different. Pat ‘099 further claims that the heterologous antigens can be HIV and pathogen specific antigens (i.e., the limitations of instant claims 8 and 10, Pat ‘099 claims 4 and 6).
Pat ‘099 additionally claims the limitations of instant claim 88 (Picker et al. claim 77), the limitations of instant claim 89 (claim 56), IV administration of the vector (claim 23), and the vector further comprising an MRE comprising miR126-3p, which is a species of miR126 (i.e. the limitations of instant claims 114, 115, and 165; Pat ‘099 claim 26).
Claims 88 and 96 are not specifically claimed by Pat ‘099, however (in regards to claim 88), one with ordinary skill in the art would appreciate that to transfect a TCR that one cell has into a separate cell (i.e., claim 55(4)), the simplest way to achieve this is to express the identical amino acid sequence. Additionally, in regards to claim 96, claim 55 claims two “subjects” and claim 22 claims the subjects can be humans or nonhuman primates, leading to four possible combinations. Therefore, one with ordinary skill in the art would appreciate that the limitations of 88 and 96 could be achieved through routine optimization (see MPEP § 2144.05(II)).
Pat ‘099 does not specifically claim identification of a second TCR that is a multi-specific TCR (i.e., the limitations of instant claim 1(e)), followed by transfection of an expression vector encoding the multi-specific TCR into a set of T cells (i.e., the limitations of instant claim 1(f)), or selecting the TCR with the highest avidity (i.e., instant claim 1(g)). However, Pat ‘099 does claim identifying CD8+ TCRs from subjects administered different heterologous antigens at different times (claims 40 and 43).
Schneck et al., in the same field of endeavor, teaches methods of generating CD8+ T cells comprising high-avidity multi-specific TCRs (Abstract and Fig. 1D): “To increase the avidity of soluble analogs for their cognates to biologically relevant levels, divalent peptide/MHC complexes or T cell receptors (superdimers) were constructed. Using a recombinant DNA strategy, DNA encoding either the MHC class II/peptide or TCR heterodimers was ligated to DNA coding for murine lg heavy and light chains. These constructs were subsequently expressed in a baculovirus expression system. Enzyme-linked immunosorbent assays (ELISA) specific for the Ig and polymorphic determinants of either the TCR or MHC fraction of the molecule indicated that infected insect cells secreted approximately 1 μg/ml of soluble, conformationally intact chimeric superdimers. SDS PAGE gel analysis of purified protein showed that expected molecular weight species. The results of flow cytometry demonstrated that the TCR and class II chimeras bound specifically with high avidity to cells bearing their cognate receptors”. Schneck et al. further teaches (Abstract) “These superdimers will be useful for studying TCR/MHC interactions, lymphocyte tracking, identifying new antigens, and have possible uses as specific regulators of immune responses.
It would have been obvious to one of ordinary skill in the art, before the effective filing date of the instant invention, to have modified the method claimed by Pat ‘099 in view of Schneck et al. to generate CD8+ T cells comprising multi-specific TCRs with a reasonable expectation of success, as Pat ‘099 claims methods of generating TCRs that can be used to generate cells comprising multi-specific TCRs as taught by Schneck et al. For example, the first and second TCRs claimed by Pat ‘099 could be used to make the multi-specific TCR in view of Schneck et al. (i.e., a third TCR), which would increase the avidity of the TCR (i.e., “selecting for high-avidity TCRs”, or the limitations recited in instant claim 1(g)). This multi-specific TCR would comprise the CDR3α and CDR3β of the second TCR. One would have been motivated to make this change for the purposes of generating CD8+ T cells that express multi-specific TCRs that can be used for a variety of diagnostic and therapeutic purposes.
Regarding the functional limitations recited in instant claim 18, Santis et al. is used as an evidentiary reference that T-cell activation (i.e., activating from a naïve T-cell to a CD8+ cytotoxic T-cell) leads to expression of the CD69 receptor (also known as the activation inducer molecule or AIM; Introduction): “The activation inducer molecule (AIM) is the earliest activation antigen newly synthesized and expressed during T cell activation and it is absent from the surface of resting peripheral blood lymphocytes…”, and further teaches that CD69 signals T-cells to express and secrete TNF-α (pg. 1254, first ¶): “[o]ur results show that the AIM activation pathway significantly induces TNF-α production both at mRNA and protein levels.” Thus, activated T-cells expressing a multispecific TCR, such as the one encompassed by Pat ‘099 in view of Schneck et al., are considered to inherently express CD69 and TNFα.
Therefore, the invention encompassed by the instant claims was a prima facie obvious variant of the invention claimed by Pat’ 099 in view of Schneck et al., especially in absence of evidence to the contrary.
Conclusion
No claim is allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to ALEC JON PETERS whose telephone number is (703)756-5794. The examiner can normally be reached Monday-Friday 8:30am - 6:00pm EST.
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/ALEC JON PETERS/Examiner, Art Unit 1641
/MISOOK YU/Supervisory Patent Examiner, Art Unit 1641