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 .
Applicants filed a Preliminary Amendment on August 4, 2023, in which Applicants canceled claims 1-40 and added new claims 41-60. Thus, claims 41-60 are pending in this application and are under examination.
Information Disclosure Statement
The Information Disclosure Statements filed February 10, 2023; April 12, 2023; May 31, 2023; October 10, 2023; January 17, 2024; March 6, 2024; July 15, 2024; April 25, 2025; August 7, 2025; and April 1, 2026 have been considered.
The listing of references in the specification is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, they have not been considered.
Specification
The disclosure is objected to because of the following informalities:
All genus and species names in the specification should be italicized.
The Tables at pages 79, 114, and 124-125 are not numbered.
The use of the terms NUCLEPORE® at paragraph [0214]; SPECTRA/POR® at paragraph [0214]; NICOMP® at paragraph [0214]; VIVAPURE® at paragraph [0214]; ZETASIZER® at paragraph [0215]; AURASENSE® at paragraph [0216]; CHELEX® at paragraph [0219]; HIGHPERFECT® at paragraph [0244]; GENEWORKS® at paragraph [0290]; and PHYTOCHROME® at paragraph [0301]; which are trade names or marks used in commerce, has been noted in this application. The terms should be accompanied by the generic terminology; furthermore the terms should be capitalized wherever they appears or, where appropriate, include a proper symbol indicating use in commerce such as ™, SM , or ® following the term.
Although the use of trade names and marks used in commerce (i.e., trademarks, service marks, certification marks, and collective marks) are permissible in patent applications, the proprietary nature of the marks should be respected and every effort made to prevent their use in any manner which might adversely affect their validity as commercial marks.
Appropriate correction is required.
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 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 set forth in Graham v. John Deere Co., 383 U.S. 1, 148 USPQ 459 (1966), that are applied 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 41-60 are rejected under 35 U.S.C. 103 as obvious over Zhang et al. (Zhang I, U.S. Patent No. 9,834,791, issued December 5, 2017, and claiming priority to U.S. Provisional Patent Application No. 61/901,215, filed November 7, 2013, and cited in the Information Disclosure Statement filed February 10, 2023), as evidenced by Cummings et al. (9(6) Human Molecular Genetics 909-916 (2000), and cited in the Information Disclosure Statement filed February 10, 2023).
Regarding claim 41, Zhang I discloses a method where a component of the composition comprises a guide sequence that hybridizes to the CRISPR-Cas gene targeting composition (i.e., a governing guide RNA), which is able to silence the targeting CRISPR-Cas composition (column 1, line 57 to column 4, line 58). Zhang I discloses that the inactivation can be via excision of CRISPR-Cas nucleotides or reduction in protein expression via a frame-shift mutation (column 1, line 57 to column 4, line 58). Zhang I discloses that the gRNA that targets the CRISPR-Cas sequences limits the effect and timing of the composition on the target sequence (column 28, line 66 to column 28, line 17). Zhang I discloses a variety of configurations of the targeting CRISPR-Cas system, as well as the governing (i.e., self-inactivating CRISPR-Cas system) (column 1, line 57 to column 27, line 43). Zhang I discloses that two, three, four, or more guide RNAs can be used (column 5, line 55 to column 6, line 16). Zhang I discloses that the vector can include a FLAG-tagged selection marker (Example 2). Zhang I discloses that the CRISPR-Cas system can be multiplexed to minimize off-target cleavage (column 1, line 64 to column 2, line 14 and Table VII-8). Zhang I discloses that the cell can be a eukaryotic cell (column 8, lines 19-28 and column 147, line 50 to column 149, line 2). Zhang I discloses that the Cas9 is stable until a linker is able to be released, which is interpreted as self-inactivating (column 221, lines 24-30). Zhang I discloses that the RNA can be chimeric RNA, and the system can include multiple chimeras (column 30, line 65 to column 31, line 23). Zhang I discloses that the components can be introduced into a cell sequentially or separately (column 3, line 64 to column 4, line 23).
Regarding claim 42, Zhang I discloses that the CRISPR-Cas system can comprise one or more nuclear localization sequences at the C-terminal or N-terminal of the sequence (column 75, lines 39-42 and Figure 6).
Regarding claim 43, Zhang I discloses that the Cas9 is a Streptococcus pyogenes Cas9 or a Streptococcus thermophilus Cas9 (column 3, lines 56-57 and column 30, lines 22-38).
Regarding claim 44, Zhang I discloses that the Cas9 is a Staphylococcus aureus Cas9, and that the components used in the method are on a single vector (column 3, lines 57-58 and column 3, lines 56-57 and column 30, lines 22-38).
Regarding claim 45, Zhang I discloses that the CRISPR-Cas sequences can be codon-optimized (column 75, lines 32-38).
Regarding claim 46, Zhang I discloses that the nucleic acids can be comprised in one or more vectors, which may be a viral vector (i.e., a single vector) (column 3, line 64 to column 4, line 65).
Regarding claim 47, Zhang I discloses that vector may be a viral vector (i.e., a single vector) (column 3, line 64 to column 4, line 65).
Regarding claim 48, Zhang I discloses that the CRISPR-Cas9 system can be incorporated into one or more adeno-associated virus (AAV) vectors, which may include inverted terminal repeats (column 110, lines 41-65).
Regarding claim 49, Zhang I discloses that the composition can be administered via injection, liposome or nanoparticle (column 116, line 4 to column 120, line 7).
Regarding claims 50-51, Zhang I discloses that a repair template that can be between from 10 to 1,000 nucleotides (column 91, lines 26-31).
Regarding claim 52, Zhang I discloses that the CRISPR enzyme can be a nickase, where the sequence includes one or more mutations.
Regarding claim 53, Zhang I discloses that the mutations may be in the RuvC1 domain and that include D10A and H840A (column 87, lines 11-53).
Regarding claim 54, Zhang I discloses that the CRISPR-Cas9 system can include a functional domain (column 10, lines 25-40).
Regarding claim 55, Zhang I discloses that the functional domain can be a methylase, a transcriptional activator, a can be a
Regarding claim 56, Zhang I discloses that the multicellular organism is a mammalian organism (column )
Regarding claim 57, Zhang I discloses that the eukaryotic cell can be a brain cell or central nervous tissue cell (column 116, lines 48-53).
Regarding claims 58-60, Zhang I discloses that diseases and conditions relating to a triplet repeat disease (i.e., trinucleotide repeat diseases) can be treated by administration of a CRISPR-Cas composition that comprises a CRISPR-Cas composition that directs hybridization and cleavage of a target sequence and a second CRISPR-Cas composition that is able to hybridize to the CRISPR-Cas expression unit, thus, inactivating the composition targeting the sequences associated with the condition (column 202, lines 23-45 and Table IX-1A). Cummings discloses that a variety of diseases and conditions are related to trinucleotide repeat expansions (abstract). Cummings discloses that such conditions as Fragile X syndrome, Fragile XE syndrome, Friedreich ataxia, Myotonic Dystrophy, Spinocerebellar ataxia types 8 and 12 are caused by expansion of non-coding trinucleotide repeats (Table 1). Cummings discloses that the trinucleotide repeat may include CGG, CAG, GAA, and CTG (page 909, paragraph bridging columns 1 and 2).
Zhang I fails to explicitly disclose or suggest the exact number of guide/Cas9 complexes and targeting of a third CRISPR complex. Zhang fails to explicitly disclose or suggest how the third CRISPR complex is self-inactivated.
However, It would have been obvious to one with ordinary skill in the art before the effective filing date of the claimed invention to determine and implement the various ways that CRISPR/Cas9 complexes are self-inactivated as disclosed by Zhang I by the governing guide RNA because these are the governing guide RNA is able to inactivate the Cas9 protein if the governing guide targets the Cas9 protein or polynucleotide encoding the protein. Further, as evidenced by Cummings, the trinucleotide repeat disorders would be able to be treated by the method of Zhang I so that the defective nucleotide element of the claimed trinucleotide could be corrected, followed by inactivation of the Cas9. One of ordinary skill in the art would understand that inactivation of the Cas9 would be desired, so that once corrected, no additional CRISPR-Cas9 actions would be needed or desired. Because the level of skill in the molecular biology art is extremely high, one of ordinary skill in the art would have had the knowledge and tools to determine method of inactivating a third (or even fourth) CRISPR/Cas9 complex using the governing guide RNAs as disclosed and suggested by Zhang I.
Claims 41-60 are rejected under 35 U.S.C. 103 as obvious over Zhang et al. (Zhang II, U.S. Patent Application Publication No. 2018/0127783, published, and claiming priority to U.S. Patent No. 9,834,791, issued December 5, 2017, and U.S. Provisional Patent Application No. 61/901,215, filed November 7, 2013, and cited in the Information Disclosure Statement filed February 10, 2023) as evidenced by Cummings et al. (9(6) Human Molecular Genetics 909-916 (2000), and cited in the Information Disclosure Statement filed February 10, 2023).
Regarding claim 41, Zhang II discloses a method where a component of the composition comprises a guide sequence that hybridizes to the CRISPR-Cas gene targeting composition (i.e., a governing guide RNA), which is able to silence the targeting CRISPR-Cas composition (paragraphs [0007]-[0051]). Zhang II discloses that the inactivation can be via excision of CRISPR-Cas nucleotides or reduction in protein expression via a frame-shift mutation (paragraphs [0007]-[0051]). Zhang II discloses that the gRNA that targets the CRISPR-Cas sequences limits the effect and timing of the composition on the target sequence (paragraph [0423]). Zhang II discloses a variety of configurations of the targeting CRISPR-Cas system, as well as the governing (i.e., self-inactivating CRISPR-Cas system) (paragraphs [0007]-[0405]). Zhang II discloses that the vector can include a FLAG-tagged selection marker (Example 2). Zhang II discloses that the CRISPR-Cas system can be multiplexed to minimize off-target cleavage (paragraph [0008] and Table VII-8). Zhang II discloses that two, three, four, or more guide RNAs can be used (paragraph [0068]). Zhang II discloses that the Cas9 is stable until a linker is able to be released within 48 hours, which is interpreted as self-inactivating within 48 hours (paragraph [1660]).
Regarding claim 42, Zhang II discloses that the CRISPR-Cas system can comprise one or more nuclear localization sequences at the C-terminal or N-terminal of the sequence (paragraph [0172] and Figure 6).
Regarding claim 43, Zhang II discloses that the Cas9 is a Streptococcus pyogenes Cas9 or a Streptococcus thermophilus Cas9 (paragraph [0815]).
Regarding claim 44, Zhang II discloses that the Cas9 is a Staphylococcus aureus Cas9, and that the components used in the method are on a single vector (paragraphs [0185] and [1225]-[1226]).
Regarding claim 45, Zhang II discloses that the CRISPR-Cas sequences can be codon-optimized (paragraph [1071).
Regarding claim 46, Zhang II discloses that the nucleic acids can be comprised in one or more vectors, which may be a viral vector (i.e., a single vector) (paragraphs [0043]-[0053]).
Regarding claim 47, Zhang II discloses that the nucleic acids can be comprised in one or more vectors, which may be a viral vector (i.e., a single vector) (paragraphs [0043]-[0053] and [1234]).
Regarding claim 48, Zhang II discloses that the CRISPR-Cas9 system can be incorporated into one or more adeno-associated virus (AAV) vectors, which may include inverted terminal repeats, which can drive expression of genes (e.g., Cas9) (paragraph [1234]).
Regarding claim 49, Zhang II discloses that the CRISPR-Cas9 system can be delivered in liposomes, exosomes, or nano particles (paragraphs [1227] and [1258]-[1289], and Table V-2).
Regarding claim 50, Zhang II discloses a repair template for homology-directed repair (paragraphs [1090]-[1092]).
Regarding claim 51, Zhang II discloses that the template can be between from 10 to 1,000 nucleotides (paragraph [1132]).
Regarding claim 52, Zhang II discloses that the CRISPR enzyme can be a nickase, where the sequence includes one or more mutations (paragraphs [1096]-[1100]).
Regarding claim 53, Zhang II discloses that the CRISPR enzyme can be a nickase, where the sequence includes one or more mutations, which may be in the RuvC1 domain, or that include D10A and H840A (paragraphs [1096]-[1100]).
Regarding claim 54, Zhang II discloses that the Cas9 may be fused with a heterologous protein domain (paragraphs [01062-[1065]).
Regarding claim 55, Zhang II discloses that the heterologous protein domain can be a methylase, a transcriptional repressor, a transcriptional activator, or a histone remodeler (paragraphs [1062]-[1065]).
Regarding claim 56, Zhang II discloses that the cell can be a mammalian cell, i.e., a cell from a multicellular organism (paragraphs [0121] and [0141]).
Regarding claim 57, Zhang II discloses that the cell can be a eukaryotic cell, including brain or central nervous system cells (paragraphs [0121]-[0123] and [1386]-[1399]).
Regarding claims 58-60, Zhang II discloses that diseases and conditions relating to a triplet repeat disease (i.e., trinucleotide repeat diseases) can be treated by administration of a CRISPR-Cas composition that comprises a CRISPR-Cas composition that directs hybridization and cleavage of a target sequence and a second CRISPR-Cas composition that is able to hybridize to the CRISPR-Cas expression unit, thus, inactivating the composition targeting the sequences associated with the condition (paragraphs [1513]-[1515] and Table IX-1A). Cummings discloses that a variety of diseases and conditions are related to trinucleotide repeat expansions (abstract). Cummings discloses that such conditions as Fragile X syndrome, Fragile XE syndrome, Friedreich ataxia, Myotonic Dystrophy, Spinocerebellar ataxia types 8 and 12 are caused by expansion of non-coding trinucleotide repeats (Table 1). Cummings discloses that the trinucleotide repeat may include CGG, CAG, GAA, and CTG (page 909, paragraph bridging columns 1 and 2).
Zhang II fails to explicitly disclose or suggest that the genome editing and/or self-inactivation.
However, It would have been obvious to one with ordinary skill in the art before the effective filing date of the claimed invention to determine and implement the various ways that CRISPR/Cas9 complexes are self-inactivated as disclosed by Zhang II by the governing guide RNA because these are the governing guide RNA is able to inactivate the Cas9 protein if the governing guide targets the Cas9 protein or polynucleotide encoding the protein. Further, as evidenced by Cummings, the trinucleotide repeat disorders would be able to be treated by the method of Zhang II so that the defective nucleotide element of the claimed trinucleotide could be corrected, followed by inactivation of the Cas9. One of ordinary skill in the art would understand that inactivation of the Cas9 would be desired, so that once corrected, no additional CRISPR-Cas9 actions would be needed or desired. Because the level of skill in the molecular biology art is extremely high, one of ordinary skill in the art would have had the knowledge and tools to determine method of inactivating a third (or even fourth) CRISPR/Cas9 complex using the governing guide RNAs as disclosed and suggested by Zhang II.
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 §§ 706.02(l)(1) - 706.02(l)(3) 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 USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The 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/process/file/efs/guidance/eTD-info-I.jsp.
Claims 41-60 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-30 of U.S. Patent No. 9,834,791.
Although the claims at issue are not identical, they are not patentably distinct from each other because the ‘791 patent claims a method of treating a subject by altering the target nucleic acid in a eukaryotic cell with a CRISPR-Cas9 composition, followed by silencing/inactivating the CRISPR-Cas9 composition with a governing guide RNA. Therefore, the claims are not patentably distinct. In addition, the instant application claims treatment of nucleotide repeat disorders.
However, the ‘791 patent does not claim that the excision of the target sequence or inactivation of the CRISPR/Cas9 system.
However, It would have been obvious to one with ordinary skill in the art before the effective filing date of the claimed invention to determine and implement the various ways that CRISPR/Cas9 complexes are self-inactivated as claimed by the ‘791 patent by the governing guide RNA because these are the governing guide RNA is able to inactivate the Cas9 protein if the governing guide targets the Cas9 protein or polynucleotide encoding the protein. One of ordinary skill in the art would understand that inactivation of the Cas9 would be desired, so that once corrected, no additional CRISPR-Cas9 actions would be needed or desired. Because the level of skill in the molecular biology art is extremely high, one of ordinary skill in the art would have had the knowledge and tools to determine method of inactivating a third (or even fourth) CRISPR/Cas9 complex using the governing guide RNAs as claimed by the ‘791 patent.
Claims 41-60 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-26 of U.S. Patent No. 10,190,137.
Although the claims at issue are not identical, they are not patentably distinct from each other because the ‘137 patent claims a composition that can be used in a method of treating a subject or modifying a multicellular organism by altering the target nucleic acid in a eukaryotic cell with a CRISPR-Cas9 composition, followed by silencing the CRISPR-Cas9 composition with a governing guide RNA. It would have been obvious to one with ordinary skill in the art before the effective filing date of the claimed invention to use the composition of the ‘137 patent in the instantly claimed method because the compositions are claimed to be useful to do so. In addition, the instant application claims treatment of nucleotide repeat disorders.
However, the ‘137 patent does not claim that the excision of the target sequence or inactivation of the CRISPR/Cas9 system.
However, It would have been obvious to one with ordinary skill in the art before the effective filing date of the claimed invention to determine and implement the various ways that CRISPR/Cas9 complexes are self-inactivated as claimed by the ‘137 patent by the governing guide RNA because these are the governing guide RNA is able to inactivate the Cas9 protein if the governing guide targets the Cas9 protein or polynucleotide encoding the protein. One of ordinary skill in the art would understand that inactivation of the Cas9 would be desired, so that once corrected, no additional CRISPR-Cas9 actions would be needed or desired. Because the level of skill in the molecular biology art is extremely high, one of ordinary skill in the art would have had the knowledge and tools to determine method of inactivating a third (or even fourth) CRISPR/Cas9 complex using the governing guide RNAs as claimed by the ‘137 patent.
Claims 41-60 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-21 of U.S. Patent No. 10,851,357.
Although the claims at issue are not identical, they are not patentably distinct from each other because the ‘357 patent claims a method of treating a subject with a trinucleotide repeat element condition by altering the target nucleic acid in a eukaryotic cell with a CRISPR-Cas9 composition, where the CRISPR-Cas targeting system is self-inactivated, where the condition is a brain or central nervous system disease or disorder. In addition, the instant application claims treatment of nucleotide repeat disorders. Therefore, it would have been obvious to one with ordinary skill in the art before the effective filing date of the claimed invention to use the instant method to treat the brain/central nervous system condition of the ‘357 patent, since such a condition is a known trinucleotide repeat condition.
However, the ‘357 patent does not claim that the excision of the target sequence or inactivation of the CRISPR/Cas9 system within 48 hours.
However, It would have been obvious to one with ordinary skill in the art before the effective filing date of the claimed invention to determine and implement the various ways that CRISPR/Cas9 complexes are self-inactivated as claimed by the ‘357 patent by the governing guide RNA because these are the governing guide RNA is able to inactivate the Cas9 protein if the governing guide targets the Cas9 protein or polynucleotide encoding the protein. One of ordinary skill in the art would understand that inactivation of the Cas9 would be desired, so that once corrected, no additional CRISPR-Cas9 actions would be needed or desired. Because the level of skill in the molecular biology art is extremely high, one of ordinary skill in the art would have had the knowledge and tools to determine method of inactivating a third (or even fourth) CRISPR/Cas9 complex using the governing guide RNAs as claimed by the ‘357 patent.
Claims 41-60 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-35 of U.S. Patent No. 11,591,581.
Although the claims at issue are not identical, they are not patentably distinct from each other because the ‘581 patent claims a method of modifying a multicellular organism by altering the target nucleic acid in a eukaryotic cell with a CRISPR-Cas9 composition, where the CRISPR-Cas targeting system is self-inactivated. The ‘581 patent claims treatment of a trinucleotide repeat disorder, where the condition is a brain or central nervous system disease or disorder. Therefore, it would have been obvious to one with ordinary skill in the art before the effective filing date of the claimed invention to use the instant method to treat the brain/central nervous system condition of the ‘581 patent, since such a condition is a known trinucleotide repeat condition. The ‘581 patent claims inactivation of the CRISPR-Cas complexes within 48 hours.
Therefore, the claims are not deemed to be patentably distinct.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to NANCY J LEITH whose telephone number is (313)446-4874. The examiner can normally be reached Monday - Thursday 8:00 AM - 6:30 PM.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, NEIL HAMMELL can be reached at (571) 270-5919. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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NANCY J. LEITH
Primary Examiner
Art Unit 1636
/NANCY J LEITH/Primary Examiner, Art Unit 1636
Prosecution Insights