DETAILED ACTION
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
This Office action is in response to the communication filed 12-7-22.
Claims 1-13, 16, 19-21 are pending in the instant application.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1-13, 16, 19-21 are rejected under 35 U.S.C. 112, first paragraph, because the specification, while being enabling for the design and optimization of siRNAs comprising the particular targets, mutations and modifications claimed, and the testing of in vitro silencing of mutant and wild type k-ras, does not reasonably enable methods for performing RNA interference to any target mutant allele of any gene in any cell in vitro or in vivo, comprising introducing any chimeric nucleic acid molecule comprising an RNA molecule satisfying the following: (1) the molecule has a nucleotide sequence complementary to a nucleotide sequence of a coding region of the mutant allele except for a base specified in (2-1) below; and (2) when counted from the base at the 5'-end of a nucleotide sequence complementary to the nucleotide sequence of the mutant allele, (2-1) a base at position 5 or 6 is mismatched with a base in the mutant allele; (2-2) a base at position 10 or 11 is at the position of the point mutation and is identical to the base at the position of the point mutation in the mutant allele; (2-3) the group at the 2’-position of the pentose in the ribonucleotide at position 8 is modified with OCH3, halogen, or LNA; and (2-4) the group at the 2’-position of the pentose in the ribonucleotide at position 7 is not modified with any of OCH3, halogen, and LNA, wherein the group at the 2’- position of the pentose in the ribonucleotide at position 6, counted from the base at the 5'-end of the nucleotide sequence complementary to the nucleotide sequence of the mutant allele, is modified with OCH3, halogen, or LNA, which halogen optionally comprises fluorine, and wherein the ribonucleotide at position 7 is optionally free from modification.
The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention commensurate in scope with these claims.
The following factors have been considered in determining that the specification does not enable the skilled artisan to make and/or use the invention over the broad scope claimed.
The breadth of the claims:
The claims are drawn to methods for performing RNA interference to target any mutant allele of any gene in any cell containing a wild-type allele of the gene and the mutant allele, which mutant allele has a point mutation relative to the wild-type allele, the method comprising the step of introducing a composition comprising a chimeric NA molecule into the cell, which chimeric molecule comprises an RNA molecule that targets the mutant allele of the gene, the mutant allele having a point mutation relative to a wild-type allele of the gene, wherein the RNA molecule satisfies the following: (1) the molecule has a nucleotide sequence complementary to a nucleotide sequence of a coding region of the mutant allele except for a base specified in (2-1) below; and (2) when counted from the base at the 5'-end of a nucleotide sequence complementary to the nucleotide sequence of the mutant allele, (2-1) a base at position 5 or 6 is mismatched with a base in the mutant allele; (2-2) a base at position 10 or 11 is at the position of the point mutation and is identical to the base at the position of the point mutation in the mutant allele; (2-3) the group at the 2’-position of the pentose in the ribonucleotide at position 8 is modified with OCH3, halogen, or LNA; and (2-4) the group at the 2’-position of the pentose in the ribonucleotide at position 7 is not modified with any of OCH3, halogen, and LNA, wherein the group at the 2’- position of the pentose in the ribonucleotide at position 6, counted from the base at the 5'-end of the nucleotide sequence complementary to the nucleotide sequence of the mutant allele,is modified with OCH3, halogen, or LNA, which halogen optionally comprises fluorine, and wherein the ribonucleotide at position 7 is optionally free from modification.
Teachings in the art and in the specification.
Teachings in the art:
Roberts et al (Nature Rev., Drug Discovery, Vol. 19, pages 673-694 (2020)) teaches on page 673 that “achieving efficient oligonucleotide delivery, particularly to extrahepatic tissues, remains a major translational limitation.”
Kobelt et al (Cancer Gene Therapy in Gene Therapy of Cancer: Methods and Protocols, Methods in Molecular Biology, Vol. 2521, pages 1-15 (Springer Nature 2022)) teach that limitations to cancer gene therapy relate to limitations in gene transfer efficiency (see esp. pages 3-4).
In addition, Osborn et al (Nucleic Acid Therapeutics, Vol. 28, No. 3, pages 128-136 (2018)) state the following about challenges to siRNA delivery on page 128:
…The primary challenge facing the clinical development of small interfering RNAs (siRNA) has been overcoming barriers that impede in vivo delivery. siRNAs are large, polyanionic macromolecules with intrinsically poor pharmacological properties. Unmodified siRNAs have a half-life of less than 5 min in circulation, and they do not permeate intact cellular membranes…
Damase et al (Frontiers in Bioengineering and Biotechnology, Vol. 9, Article 628137, pages 1-24 (2021)) on page 13 also address the challenges of using RNA-based drugs:
Targeted delivery is a major hurdle for effective RNA therapeutics, a hurdle that must be overcome to broaden the application of clinical translation of this type of therapeutic. …There is a need for novel delivery vehicles that will deliver the RNA drug to the site of therapeutic action facilitating the entry of the RNA drug into the cytoplasm where it may exert its effect…
Bost et al (ACS Nano, Vol. 15, pages 13993-14021 (2021)) on page 13993 also address the current challenges of oligonucleotide therapeutics:
…Historically, the largest hindrance to the widespread usage of ON therapeutics has been their inability to effectively internalize into cells and escape from endosomes to reach their molecular targets in the cytosol or nucleus…
Emphases added][Citations omitted].
Teachings in the specification:
The specification teaches the design and in vitro testing of various siRNA molecules targeting the K-ras gene (Figures 1-6). Table 1 teaches examples of causative genes responsible for genetic diseases. Table 2 teaches the causative gene names, positions of mutations, and SEQ ID Nos. targeting the mutations and further comprising particularly placed mismatches and particularly placed 2’ pentose modifications. Examples in the specification set forth these siRNA constructs:
…[D]ouble-stranded RNAs with the following sequences were chemically synthesized for siRNAs. The positions 9, 10, and 11 in siRNAs, K(35)9A, K(35)10A, and K(35)11A, respectively, correspond to the position of the point mutation in the A-mutant allele of the K-ras gene (c. 35G>A). In the following sequences, base pairs in the position corresponding to the position of the point mutation are enclosed in rectangles.
Fig. 1 shows gene silencing effects of the siRNAs. K(35)9A had a strong silencing effect on both A-mutant and wild-type alleles. K(35)10A and K(35)11A strongly suppressed the expression of the A- mutant allele more than that of the wild-type allele although their silencing effects
(Example 1-2) This example shows that the silencing abilities of the RNA molecule to the A-mutant allele become stronger and its specificities become much higher by, in addition to matching position 11 of an siRNA with the position of the point mutation in the A-mutant allele, changing the base at the 5'-end of the siRNA’s guide strand from guanine to uracil and changing the base at the 5'-end of the passenger strand from uracil to guanine.
The wild-type and A-mutant K reporters were used as reporters for examining gene silencing effects. A double-stranded RNA with the following sequences was chemically synthesized for an siRNA, and K(35)11A was used as a control. In the following sequences, a base pair in the position corresponding to the position of the point mutation, and the pairs of the modified bases at the 5'-ends of the guide and passenger strands are enclosed in rectangles.
Fig. 2 shows gene silencing effects of the siRNAs. K(35)11A strongly suppressed the expression of the A-mutant allele more than that of the wild-type allele, whereas K(35)11Arev exerted a stronger silencing effect on both, with a stronger suppression of the expression of the A-mutant allele than that of the wild-type allele.
(Example 1-3) This example shows that silencing abilities of the RNA molecules to the A- mutant allele become stronger and their specificities become much higher by, in addition to matching position 11 of each siRNA with the position of the point mutation in the A-mutant allele, changing the base at the 5'-end of the siRNA’s guide strand from guanine to uracil, and changing the base at the 5'-end of the passenger strand from uracil to guanine, replacing the group at 2'-position of the pentose in each of ribonucleotides at positions 6-8 of the guide strand by OCH3.
The wild-type and A-mutant K reporters were used as reporters for 5 examining gene silencing effects. Double-stranded RNAs with the following sequences were chemically synthesized for siRNAs, and K(35)11Arev was used as a control. In the following sequences, the base pairs in the position corresponding to the position of the point mutation, and the pairs of the modified bases at the 5'- ends of the guide and passenger strands are enclosed in rectangles. The nucleotides in which the group at the 2'-position of the pentose was replaced by OCH3 are hatched.
Fig. 3 shows gene silencing effects of the siRNAs. K(35)11Arev strongly suppressed the expression of the A-mutant allele more than that of the wild-type allele, whereas K(35)11ArevOM(6-8) exerted a stronger silencing effect on both, with a stronger suppression of the expression of the A-mutant allele than that of the wild-type allele. Another control. K(35)11ArevOM(2-5) in which the group at the 2'-position of the pentose in each of ribonucleotides at positions 2-5 of the guide strand was replaced by OCH3 exerted considerably weak silencing effect on both.
(Example 1-4) 30 This example shows that silencing abilities of the RNA molecules to the wild-type allele become weaker and, as a result, their specificities for the A-mutant allele become much higher by, in addition to matching position 11 of each siRNA with the position of the point mutation in the A-mutant allele, changing the base at the 5'-end of the siRNA’s guide strand from guanine to uracil, and changing the base at the 5'-end of the passenger strand from uracil to guanine, mismatching the base at position 5 or 6 of the guide strand with that of the A-mutant allele,.
The wild-type and A-mutant K reporters were used as reporters for examining gene silencing effects. Double-stranded RNAs with the following sequences with a mismatched base at one of positions 3-7 based on K(35)11Arev were chemically synthesized for siRNAs. K(35)11Arev was used as a control. In the following sequences, the base pairs in the position corresponding to the position of the point mutation, the pairs of the modified bases at the 5'-ends of the guide and passenger strands, and base pairs with the mismatched base are enclosed in rectangles.
Fig. 4 shows gene silencing effects of the siRNAs. K(35)11Arev strongly suppressed the expression of the A-mutant allele more than that of the wild-type allele, whereas RNA molecules K(35)11ArevM5 and K(35)11ArevM6 exhibited significantly weak silencing abilities to the wild-type allele and, as a result, much higher specificities for the A-mutant allele.
This example shows that specificities of the RNA molecules for the A-mutant allele become much higher by, in addition to matching position 11 of each siRNA with the position of the point mutation in the A-mutant allele, changing the base at the 5'-end of the siRNA’s guide strand from guanine to uracil, and changing the base at the 5'-end of the passenger strand from uracil to guanine, replacing the group at the 2'-position of the pentose in each of ribonucleotides at positions 6-8 of the guide strand by OCHs, and mismatching the base at position 5 or 6 of the guide strand with that of the A-mutant allele.
The wild-type and A-mutant K reporters were used as reporters for examining gene silencing effects. Double-stranded RNAs with the following sequences with a mismatched base at one of positions 3-7 based on K(35)11Arev were chemically synthesized for siRNAs
K(35)11Arev was used as a control. In the following sequences, the base pairs in the position corresponding to the position of the point mutation, the pairs of the modified bases at the 5'-ends of the guide and passenger strands, and base pairs with the mismatched base are enclosed in rectangles. The nucleotides in which the group at the 2'-position of the pentose was replaced by OCHs are hatched.
Fig. 5 shows gene silencing effects of the siRNAs K(35)11ArevOM(6-8)M5 and K(35)11lArevOM(6-8)M6 exhibited very weak silencing abilities to the wild-type allele and, as a result, their specificities for the A-mutant allele became much higher.
(Example 1-6) This example shows that non-specific off-target effects can be reduced while silencing abilities to the wild-type allele remains weak and those to the A- mutant allele remains strong, by, in addition to matching position 11 of each siRNA with the position of the point mutation in the A-mutant allele, changing the base at the 5'-end of the siRNA’s guide strand from guanine to uracil, and changing the base at the 5'-end of the passenger strand from uracil to guanine, replacing the group at the 2'-position of the pentose in each of ribonucleotides at positions 6-8 of the guide strand by OCH: (i.e., the ribonucleotide at position 7 was not modified) and mismatching the base at position 6 of the guide strand with that of the A-mutant allele.
As reporters for examining gene silencing effects, wild-type and A-mutant K reporters and reporters for detecting off-target effects (SEQ ID NOS. 40 and 41) were used. The reporters for off-target effects were constructed by chemically synthesizing DNAs with the following reporter sequences for detecting off-target effects and inserting each of them into the 3'-UTR of the luciferase gene in an expression vector (psiCHECK), as in the cases to construct the wild-type and A- mutant K reporters were slightly reduced.
Double-stranded RNAs with the following sequences (SEQ ID NOS. 42 and 43) were chemically synthesized for siRNAs in which, based on K(35)11Arev, a base at position 6 was mismatched and the group at the 2’-position of the pentose in each of ribonucleotides at positions 6 and 8 was modified by OCH3 K(35)11ArevOM(6-8) was used as a control. In the following sequences, the base pairs in the position corresponding to the position of the point mutation, the pairs of the modified bases at the 5'-ends of the guide and passenger strands, and base pairs with the mismatched base are enclosed in rectangles. The nucleotides in which the group at the 2'-position of the pentose was replaced by OCH3 are hatched.
Fig. 6 shows gene silencing effects and off-target effects of each siRNA. The RNA molecule, K(35)11ArevOM(6-8)M6 exhibited very weak silencing abilities to the wild-type allele and strong silencing abilities to the A-mutant allele, whereas K(35)11ArevOM(6+8)M6 significantly reduced non-specific off-target effects with substantially the same effects on both of the wild- type and A-mutant alleles, compared to K(35)11ArevOM(6-8)M6.
[Emphases added][Citations omitted].
The examples provided in the instant specification, of in vitro testing of target gene inhibition using the specifically described siRNA sequences with specific modifications and specific mutations, targeting specific mutants of some known target genes, are not representative or correlative of the broad genus claimed and further whereby target gene inhibition is provided in a subject.
In light of the teachings in the art and the specification, one skilled in the art would not accept on its face the examples provided in the instant disclosure as being correlative or representative of the ability to provide treatment effects in a subject. Since the specification fails to provide the requisite guidance for the treatment in any subject, and since determination of the factors required for accomplishing this in any subject is highly unpredictable, it would require undue experimentation to practice the invention over the broad scope claimed.
For these reasons, the instant rejection for lacking enablement over the full scope claimed is proper.
Claims 1-13, 16, 19-21 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for pre-AIA the inventor(s), at the time the application was filed, had possession of the claimed invention.
The breadth of the claims
The claims are drawn to methods for performing RNA interference to target any mutant allele of any gene in any cell containing a wild-type allele of the gene and the mutant allele, which mutant allele has a point mutation relative to the wild-type allele, the method comprising the step of introducing a composition comprising a chimeric NA molecule into the cell, which chimeric molecule comprises an RNA molecule that targets the mutant allele of the gene, the mutant allele having a point mutation relative to a wild-type allele of the gene, wherein the RNA molecule satisfies the following: (1) the molecule has a nucleotide sequence complementary to a nucleotide sequence of a coding region of the mutant allele except for a base specified in (2-1) below; and (2) when counted from the base at the 5'-end of a nucleotide sequence complementary to the nucleotide sequence of the mutant allele, (2-1) a base at position 5 or 6 is mismatched with a base in the mutant allele; (2-2) a base at position 10 or 11 is at the position of the point mutation and is identical to the base at the position of the point mutation in the mutant allele; (2-3) the group at the 2’-position of the pentose in the ribonucleotide at position 8 is modified with OCH3, halogen, or LNA; and (2-4) the group at the 2’-position of the pentose in the ribonucleotide at position 7 is not modified with any of OCH3, halogen, and LNA, wherein the group at the 2’- position of the pentose in the ribonucleotide at position 6, counted from the base at the 5'-end of the nucleotide sequence complementary to the nucleotide sequence of the mutant allele,is modified with OCH3, halogen, or LNA, which halogen optionally comprises fluorine, and wherein the ribonucleotide at position 7 is optionally free from modification.
The teachings in the specification are not representative of the large genus of modulators claimed.
Teachings in the specification
The teachings in the specification are described above in the scope of enablement rejection. The specification teaches in vitro testing of specifically modified siRNAs target C-ras. The specification also disclosed specifically mutated and specifically modified siRNA sequences targeting specific mutations in some genes known to cause diseases due to the mutations.
The specification fails to provide the requisite guidance for making and using the large genus of modulatory agents instantly claimed, and further whereby mutants are silenced and treatment is provided in any cell in any subject. Since the disclosure fails to describe the common attributes and characteristics concisely identifying members of the proposed genus of modulators, and because the claimed genus is highly variant, the description provided is insufficient, one of skill in the art would reasonably conclude that the disclosure fails to provide a representative number of species to describe the broad genus of modulatory agents instantly claimed.
Thus, Applicant was not in possession of the broadly claimed genus.
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.
Claim 1-13, 16, 19-21 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-11,14, 18-20 of copending Application No. 18/008,945 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because both sets of claims are drawn to methods for performing RNA interference to target a mutant allele of a gene in a cell containing a wild-type allele of the gene and the mutant allele, which mutant allele has a point mutation relative to the wild-type allele, the method comprising the step of introducing a composition comprising a chimeric NA molecule into the cell, which chimeric molecule comprises an RNA molecule that targets the mutant allele of the gene, the mutant allele having a point mutation relative to a wild-type allele of the gene, wherein the RNA molecule satisfies the following: (1) the molecule has a nucleotide sequence complementary to a nucleotide sequence of a coding region of the mutant allele except for a base specified in (2-1) below; and (2) when counted from the base at the 5'-end of a nucleotide sequence complementary to the nucleotide sequence of the mutant allele, (2-1) a base at position 5 or 6 is mismatched with a base in the mutant allele; (2-2) a base at position 10 or 11 is at the position of the point mutation and is identical to the base at the position of the point mutation in the mutant allele; (2-3) the group at the 2’-position of the pentose in the ribonucleotide at position 8 is modified with OCH3, halogen, or LNA; and (2-4) the group at the 2’-position of the pentose in the ribonucleotide at position 7 is not modified with any of OCH3, halogen, and LNA, wherein the group at the 2’- position of the pentose in the ribonucleotide at position 6, counted from the base at the 5'-end of the nucleotide sequence complementary to the nucleotide sequence of the mutant allele is modified with OCH3, halogen, or LNA, which halogen optionally comprises fluorine.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claim 1-13, 16, 19-21 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-14 of copending Application No. 17/626,867 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because both sets of claims are drawn to methods for performing RNA interference to target a mutant allele of a gene in a cell containing a wild-type allele of the gene and the mutant allele, which mutant allele has a point mutation relative to the wild-type allele, the method comprising the step of introducing a composition comprising a chimeric NA molecule into the cell, which chimeric molecule comprises an RNA molecule that targets the mutant allele of the gene, the mutant allele having a point mutation relative to a wild-type allele of the gene, wherein the RNA molecule satisfies the following: (1) the molecule has a nucleotide sequence complementary to a nucleotide sequence of a coding region of the mutant allele except for a base specified in (2-1) below; and (2) when counted from the base at the 5'-end of a nucleotide sequence complementary to the nucleotide sequence of the mutant allele, (2-1) a base at position 5 or 6 is mismatched with a base in the mutant allele; (2-2) a base at position 10 or 11 is at the position of the point mutation and is identical to the base at the position of the point mutation in the mutant allele; (2-3) the group at the 2’-position of the pentose in the ribonucleotide at position 8 is modified with OCH3, halogen, or LNA; and (2-4) the group at the 2’-position of the pentose in the ribonucleotide at position 7 is not modified with any of OCH3, halogen, and LNA, wherein the group at the 2’- position of the pentose in the ribonucleotide at position 6, counted from the base at the 5'-end of the nucleotide sequence complementary to the nucleotide sequence of the mutant allele is modified with OCH3, halogen, or LNA.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
Certain papers related to this application may be submitted to Art Unit 1637 by facsimile transmission. The faxing of such papers must conform with the notices published in the Official Gazette, 1156 OG 61 (November 16, 1993) and 1157 OG 94 (December 28, 1993) (see 37 C.F.R. ' 1.6(d)). The official fax telephone number for the Group is 571-273-8300. NOTE: If Applicant does submit a paper by fax, the original signed copy should be retained by applicant or applicant's representative. NO DUPLICATE COPIES SHOULD BE SUBMITTED so as to avoid the processing of duplicate papers in the Office.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Jane Zara whose telephone number is (571) 272-0765. The examiner’s office hours are generally Monday-Friday, 10:30am - 7pm. If attempts to reach the examiner by telephone are unsuccessful, the examiner's supervisor, Jennifer Dunston, can be reached on (571)-272-2916. Any inquiry of a general nature or relating to the status of this application should be directed to the Group receptionist whose telephone number is (703) 308-0196.
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Jane Zara
1-7-26
/JANE J ZARA/Primary Examiner, Art Unit 1637