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 response of 09/11/2025, including amendments to the specification, has been received and entered into the application file.
Claims 1, 88, and 90 were amended in the claim set filed 09/11/2025.
Claims 27 and 29 were cancelled in the claim set filed 09/11/2025.
Claims 1, 8, 18, 21, 30, 36, 52, 85, 88, 90, 98, 99, 126, 129, 135, 137, 141, and 146 are pending, of which claims 8, 99, 126,1 29, 135, 137, 141 and 146 were previously withdrawn.
Accordingly, claims 1, 18, 21, 30, 36, 52, 85, 88, 90, and 98 are pending and under consideration.
Election/Restrictions
Applicant previously elected without traverse Group I (claims 1, 18, 21, 27, 29, 30, 36, 52, 85, 88, 90, and 98) in the reply filed on 05/19/2025. In light of the search, the species election within the restriction requirement mailed on 03/19/2025 was withdrawn in the Action dated 06/11/2025.
Claims 8, 99, 126,1 29, 135, 137, 141 and 146 remain withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 05/19/2025.
Accordingly, claims 1, 18, 21, 30, 36, 52, 85, 88, 90, and 98 are pending and under consideration.
Status of Prior Objections/Rejections
RE: Specification
The disclosure was previously objected to because it contained an embedded hyperlink and/or other form of browser-executable code. The amendments to the specification received on 09/11/2025 have obviated the basis of the prior objection. The objection of record is hereby withdrawn.
RE: Claim Rejections - 35 USC § 112
Claims 27, 88, and 90 were previously 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.
The cancellation of claim 27 renders the rejection thereof moot.
The amendments to claim 88 have obviated the basis of the prior rejections regarding claims 88 and 90. The rejection of record is hereby withdrawn.
RE: Claim Rejections - 35 USC § 103
►Claims 1, 18, 21, 27, 29, 30, and 98 were previously rejected under 35 U.S.C. 103 as being unpatentable over WO 2017/053722 A1 (hereinafter Revenko; as cited in the IDS filed 12/07/2022) in view of WO 2018/102397 A1 (hereinafter Bolen; as cited in the IDS filed 12/07/2022).
The cancellation of claims 27 and 29 renders the rejections thereof moot.
Applicant has traversed the rejection of record, asserting that the cited art does not disclose all of the limitations of amended instant claim 1. Applicant further asserts that the antisense oligonucleotides claimed therein more efficiently knock down the expression of G12D KRAS mRNA than the wild-type KRAS mRNA, meaning these antisense oligonucleotides are capable of specifically targeting a KRAS mRNA comprising the G12D mutation.
In response, Applicant’s arguments with respect to the rejection of amended claim 1 (and claims 18, 21, 30, and 98 that depend therefrom) under 35 U.S.C. 103 have been fully considered and are persuasive. Therefore, the rejection of record has been withdrawn. However, upon further consideration and searching, new grounds of rejection necessitated by amendment are set forth in detail below.
►Claims 36, 85, 88, and 90 were previously rejected under 35 U.S.C. 103 as being unpatentable over WO 2017/053722 A1 (hereinafter Revenko; as cited in the IDS filed 12/07/2022) in view of WO 2018/102397 A1 (hereinafter Bolen; as cited in the IDS filed 12/07/2022) as applied to claim 1 above, and further in view of Haraszti et al., 2018.
Applicant has traversed the rejection of record, asserting that the cited art does not disclose all of the limitations of amended instant claim 1, from which claims 36, 85, 88, and 90 directly or indirectly depend.
In response, as set forth above, Applicant’s arguments with respect to the rejection of claims 36, 85, 88, and 90 (which directly or indirectly depend from amended instant claim 1) under 35 U.S.C. 103 have been fully considered and are persuasive. Therefore, the rejection of record has been withdrawn. However, upon further consideration and searching, new grounds of rejection necessitated by amendment are set forth in detail below.
►Claim 52 was previously rejected under 35 U.S.C. 103 as being unpatentable over WO 2017/053722 A1 (hereinafter Revenko; as cited in the IDS filed 12/07/2022) in view of WO 2018/102397 A1 (hereinafter Bolen; as cited in the IDS filed 12/07/2022) and Haraszti et al., 2018 as applied to claim 36 above, and further in view of US 10,195,290 B1 (hereinafter Dooley; as cited in the IDS filed 07/29/2024).
Applicant has traversed the rejection of record, asserting that the cited art does not disclose all of the limitations of amended instant claim 1, from which claim 52 indirectly depends.
In response, as set forth above, Applicant’s arguments with respect to the rejection of claim 52 (which indirectly depends from amended instant claim 1) under 35 U.S.C. 103 have been fully considered and are persuasive. Therefore, the rejection of record has been withdrawn. However, upon further consideration and searching, new grounds of rejection necessitated by amendment are set forth in detail below.
New/Maintained Grounds of 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.
Claims 1, 18, 21, 30, and 98 are rejected under 35 U.S.C. 103 as being unpatentable over US 8,889,642 B2 (hereinafter Shemi) in view of WO 2017/053722 A1 (hereinafter Revenko; as cited in the IDS filed 12/07/2022; of record) and WO 2018/102397 A1 (hereinafter Bolen; as cited in the IDS filed 12/07/2022; of record), as evidenced by Watts and Corey, 2011 and Lam et al., 2015.
With regard to amended claim 1, which recites “An extracellular vesicle (EV) comprising an antisense oligonucleotide (ASO) which comprises a contiguous nucleotide sequence of 10 to 30 nucleotides in length that is complementary to a nucleic acid sequence within nucleotides 5,568 to 5,606 of a KRAS G12D transcript, which is set forth in SEQ ID NO: 1, wherein the ASO comprises a nucleotide sequence selected from any one of SEQ ID NOs: 7-9, 20-23, 28, 35-39, 44, 45, 51, 59, 60, 71, 82, and 83,” Shemi discloses methods and compositions for treating mutated K-ras expressing cancers such as those in which there are gain-of-function mutations at codon 12 (K-ras G12D) (abstract; column 1, lines 26-30). The methods disclosed in Shemi comprise administration of a pharmaceutical composition comprising a duplex RNAi agent (specifically siRNA as disclosed at column 39-SEQ ID NO 40) to a patient having a tumor expressing a K-ras protein containing a G12D mutation, wherein the sense and antisense strands are SEQ ID NOs: 39 and 40, respectively (column 14, lines 41-50). SEQ ID NO: 40 of
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Shemi comprises 100% identity to instant SEQ ID NO: 8, as shown in the alignment below.
Furthermore, as shown in the alignment below, SEQ ID NO: 40 of Shemi targets nucleotides 5,577-5,595 of instant SEQ ID NO: 1, the region of which is completely encompassed by the instantly claimed complementarity to nucleotides 5,568-5,606 of a KRAS G12D transcript set forth in SEQ ID NO: 1.
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Per the instant specification, the claimed term of an “antisense oligonucleotide” (ASO) “refers to an oligomer or polymer of nucleosides…that are covalently linked to each other through internucleotide linkages…[and are] are least partially complementary to a target nucleic acid, such that the ASO hybridizes to the target nucleic acid sequence” (paragraph [0096]).
As is known to those of ordinary skill in the art, duplex RNAi agents such as siRNAs and single-stranded antisense oligonucleotides share fundamental principles of function, by which an oligonucleotide binds to a target RNA through Watson-Crick base pairing (Watts and Corey, 2011: page 365, column 2, paragraph 2). As shown in Figure 1 of Watts and Corey, 2011, while antisense oligonucleotides are delivered as a single strand and find their target alone, duplex RNAi agents such as siRNAs are delivered as a duplex, which associates with Argonaute (part of the RNA-induced silencing complex), after which the passenger strand (also known as the sense strand per Lam et al., 2015: page 2, column 1, paragraph 1) is removed, leaving the guide strand (also known as the antisense strand per Lam et al., 2015: page 2, column 1, paragraph 1) associated with Argonaute to guide the silencing complex to a complementary transcript sequence, thereby facilitating cleavage and/or repression of said transcript. Accordingly, the antisense strand of Shemi (SEQ ID NO: 40) is considered to read on the instantly claimed “antisense oligonucleotide,” as the antisense strand of Shemi meets the definition of an antisense oligonucleotide as set forth at paragraph [0096] of the instant specification.
The functionally analogous nature of single-stranded antisense oligonucleotides and duplex RNAi agents such as siRNA (comprising an antisense strand) is supported by the literature, as both species have successfully targeted KRAS transcripts, including KRAS G12D transcripts. As set forth above, Shemi discloses targeting of a K-ras protein containing a G12D mutation with siRNA (column 14, lines 41-50). As previously set forth, Revenko discloses methods, compounds, and compositions for inhibiting KRAS expression (abstract), including administration of antisense oligonucleotides targeting KRAS (page 26, line 13). Example 8 (pages 138-141) discloses antisense oligonucleotides targeting KRAS and their impact on KRAS inhibition (table 30). Thus, the disclosure of Revenko establishes that antisense oligonucleotides are also capable of targeting KRAS transcripts. As set forth above, the mechanisms of action by which the antisense strands of siRNAs and antisense oligonucleotides function are functionally indistinct. Accordingly, Shemi and Revenko collectively disclose all the limitations of amended instant claim 1, with the exception of packaging the antisense oligonucleotide into an extracellular vesicle. However, the disclosure of Bolen cures this deficiency, as set forth below.
Bolen discloses that exosomes (used interchangeably with “extracellular vesicle[s]” per paragraph [0041]) are effective delivery vehicles for therapeutic agents such as antisense oligonucleotides (abstract; paragraph [0009]).
With regard to claim 18, which recites “(a) the ASO [of the extracellular vesicle of claim 1] is a gapmer, a mixmer, or a totalmer; (b) the ASO comprises one or more nucleoside analogs; (c) the ASO comprises one or more 5’-methyl cytosine nucleobases; (d) the ASO is from 14 to 20 nucleotides in length; or (e) any combination of (a) to (d),” as set forth above, Revenko discloses antisense oligonucleotides targeting KRAS to inhibit its expression (abstract; page 26, line 13). Revenko further discloses that these antisense oligonucleotides may be gapmers (page 57, lines 18-30), they may comprise constrained ethyl nucleosides (page 15, lines 17-28), they may comprise at least one 5-methylcytosine (page 14, lines 32-33), and they may be 14 to 20 subunits in length (page 38, line 15). Per paragraph [0018] of the instant disclosure, constrained ethyl nucleosides are considered nucleoside analogs. Thus, Revenko is considered to disclose each and every limitation of instant claim 18 regarding the antisense oligonucleotide.
With regard to claim 21, which recites “one or more of the nucleoside analogs [of the extracellular vesicle of claim 18] are a sugar modified nucleoside,” as set forth above, Revenko discloses antisense oligonucleotides targeting KRAS to inhibit its expression (abstract; page 26, line 13). Revenko further discloses that the antisense oligonucleotides taught therein may comprise at least one modified sugar, such as a sugar comprising a 2’-O-methoxyethyl group, or a bicyclic sugar (page 14, lines 24-29). Thus, Revenko is considered to disclose each and every limitation of instant claim 21 regarding the antisense oligonucleotide.
With regard to claim 30, which recites “the extracellular vesicle of claim 1, wherein the ASO has a design selected from LLLDnLLL, LLLLDnLLLL, LLLLLDnLLLLL, LLLMMDnMMLLL, LLLMDnMLLL, LLLLMMDnMMLLLL, LLLLMDnMLLLL, LLLLLLMMDnMMLLLLL, LLLLLLMDnMLLLLL, or combinations thereof, wherein L is a nucleoside analog, D is DNA, M is 2'-MOE, and n can be any integer between 4 and 24,” as set forth above, Revenko discloses antisense oligonucleotides targeting KRAS to inhibit its expression (abstract; page 26, line 13). Revenko further discloses that the antisense oligonucleotides taught therein may be structured as gapmers, which comprise an internal “gap” region flanked on both the 5’ and 3’ ends with “wings” such that the gap and wing nucleosides are chemically distinct (page 7, lines 12-16). Revenko specifically discloses that regarding the gapmers taught therein, each nucleoside of each wing segment comprises a modified sugar (page 34, lines 10-11) and comprises 3-5 nucleosides (page 57, lines 32-33). Per paragraph [0018] of the instant disclosure, sugar modified nucleosides are considered to be nucleoside analogs, as instantly claimed. Further regarding the gapmers disclosed in Revenko, they further disclose that the gap region of the gapmer may comprise 7-10 nucleosides (page 58, line 1), which is entirely encompassed by the instantly claimed 4 and 24 nucleosides. Thus, Revenko is considered to disclose the instantly claimed antisense oligonucleotide designs of LLLDnLLL, LLLLDnLLLL, and LLLLLDnLLLLL, as in instant claim 30.
With regard to claim 98, which recites “the extracellular vesicle [of claim 1] is an exosome,” as set forth above, Bolen discloses that exosomes (used interchangeably with “extracellular vesicle[s]” per paragraph [0041]) are effective delivery vehicles for therapeutic agents such as antisense oligonucleotides (abstract; paragraph [0009]).
Given that Shemi discloses an antisense strand (SEQ ID NO: 40) satisfying the definition of the instantly claimed “antisense oligonucleotide” targeting KRAS G12D (specifically at nucleotides 5,568-5,606 of instant SEQ ID NO: 1) for use in treating patients with a tumor expressing a K-ras protein containing a G12D mutation, that Revenko discloses that single-stranded antisense oligonucleotides are known to successfully target KRAS transcripts (said antisense oligonucleotides may be gapmers and/or may comprise constrained ethyl nucleosides, 5-methylcytosine, or bicyclic sugars), and that Bolen discloses that extracellular vesicles such as exosomes are effective delivery vehicles for therapeutic agents such as antisense oligonucleotides, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to modify the antisense strand disclosed in Shemi per the teachings of Revenko and subsequently package said antisense oligonucleotides into exosomes as disclosed in Bolen to predictably effectively deliver therapeutic antisense oligonucleotides to inhibit KRAS G12D expression. One would have been motivated to make such a modification in order to receive the expected benefit of effectively delivering therapeutic antisense oligonucleotides to inhibit KRAS G12D expression.
Claims 36, 85, 88, and 90 are rejected under 35 U.S.C. 103 as being unpatentable over US 8,889,642 B2 (hereinafter Shemi) in view of WO 2017/053722 A1 (hereinafter Revenko; as cited in the IDS filed 12/07/2022; of record) and WO 2018/102397 A1 (hereinafter Bolen; as cited in the IDS filed 12/07/2022; of record), as evidenced by Watts and Corey, 2011 and Lam et al., 2015 as applied to claim 1 above, and further in view of Haraszti et al., 2018 (of record).
The combined disclosures of Revenko and Bolen are described above and applied as before. However, these disclosures do not teach the anchoring, scaffolding, or targeting moieties of instant claims 36, 85, 88, and 90.
With regard to claim 36, which recites “the extracellular vesicle of claim 1…further comprises: (i) an anchoring moiety, wherein the ASO is linked to the anchoring moiety; (ii) a scaffolding moiety; (iii) an exogenous targeting moiety; or (iv) any combination of (i) to (iii),” Haraszti et al., 2018 discloses that conjugating small interfering RNA (siRNA) molecules to hydrophobic cholesterol via TEG and C7 linkers anchors the siRNAs onto the membrane of an extracellular vesicle for delivery (page 1977, column 1, paragraph 1; page 1974, column 1, paragraph 4). Haraszti et al., 2018 further discloses that cholesterol conjugation-mediated loading of siRNAs onto extracellular vesicles is among the most reproducible and scalable loading strategies to overcome the siRNA delivery challenge, and indeed is applicable to in vivo delivery of other oligonucleotide species, such as antisense oligonucleotides, as instantly claimed (page 1973, column 1, paragraphs 1-2; page 1978, column 1, paragraph 5). Thus, Haraszti et al., 2018 discloses linking an anchoring moiety such as cholesterol to oligonucleotide species such as siRNAs and antisense oligonucleotides (as instantly claimed) in order to effectively and efficiently load the oligonucleotide species onto the membrane of the extracellular vesicle for in vivo delivery of the same.
With regard to claim 85, which recites “the anchoring moiety [of the extracellular vesicle of claim 36] comprises sterol, CM1, a lipid, a vitamin, a small molecule, a peptide, or a combination thereof,” as set forth above, Haraszti et al., 2018 discloses that conjugating siRNA molecules to hydrophobic cholesterol via TEG and C7 linkers anchors the siRNAs onto the membrane of an extracellular vesicle for delivery, and that this principle is applicable to in vivo delivery of other oligonucleotide species, such as antisense oligonucleotides, as instantly claimed (page 1977, column 1, paragraph 1; page 1974, column 1, paragraph 4; page 1978, column 1, paragraph 5). The hydrophobic cholesterol disclosed in Haraszti et al., 2018 is a sterol and thus satisfies the limitations of instant claim 85.
With regard to claims 88 and 90, which respectively recite “the ASO [of the extracellular vesicle of claim 36] is linked to the anchoring moiety by a linker,” and that “the linker [of the extracellular vesicle of claim 88]…comprises TEG,” as set forth above, Haraszti et al., 2018 discloses that conjugating siRNA molecules to hydrophobic cholesterol via TEG and C7 linkers anchors the siRNAs onto the membrane of an extracellular vesicle for delivery, and that this principle is applicable to in vivo delivery of other oligonucleotide species, such as antisense oligonucleotides, as instantly claimed (page 1977, column 1, paragraph 1; page 1974, column 1, paragraph 4; page 1978, column 1, paragraph 5). The TEG linker disclosed in Haraszti et al., 2018 reads on the instantly claimed TEG linker. Thus, the TEG linker disclosed in Haraszti et al., 2018 satisfies the limitations of instant claims 88 and 90.
Given that Shemi, Revenko, and Bolen collectively disclose the extracellular vesicle comprising an antisense oligonucleotide of instant claim 1 (as set forth above) and that Haraszti et al., 2018 discloses that conjugating oligonucleotide species such as siRNAs and antisense oligonucleotides to hydrophobic cholesterol via TEG linkers anchors the oligonucleotides to the membrane of an extracellular vesicle for effective in vivo delivery, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to conjugate the antisense oligonucleotide of claim 1 to hydrophobic cholesterol via linkers such as TEG to predictably anchor the oligonucleotide to the membrane of the extracellular vesicle for effective in vivo delivery. One would have been motivated to make such a modification in order to receive the expected benefit of effectively mediating in vivo delivery of therapeutic oligonucleotides packaged into and anchored to extracellular vesicles.
Claim 52 is rejected under 35 U.S.C. 103 as being unpatentable over US 8,889,642 B2 (hereinafter Shemi) in view of WO 2017/053722 A1 (hereinafter Revenko; as cited in the IDS filed 12/07/2022; of record), WO 2018/102397 A1 (hereinafter Bolen; as cited in the IDS filed 12/07/2022; of record), and Haraszti et al., 2018 (of record), as evidenced by Watts and Corey, 2011 and Lam et al., 2015 as applied to claim 36 above, and further in view of US 10,195,290 B1 (hereinafter Dooley; as cited in the IDS filed 07/29/2024; of record).
The combined disclosures of Shemi, Revenko, Bolen, and Haraszti et al., 2018 are described above and applied as before. However, these disclosures do not teach Scaffold X or Scaffold Y of instant claim 52.
With regard to claim 52, which recites “the scaffold moiety [of the extracellular vesicle of claim 36] comprises a Scaffold X, Scaffold Y, or both Scaffold X and Scaffold Y,” the instant specification discloses that Scaffold X anchors a moiety or a payload to the exterior surface of the extracellular vesicle or exosome and may be PTGFRN, BSG, IGSF2, IGSF3, IGSF8, ITGB1, ITGA4, SLC3A2, ATP1A1, ATP1A2, ATP1A3, ATP1A4, ATP1B3, ATP2B1, ATP2B2, ATP2B3, or ATP2B (either in whole or in part) (paragraph [0132]). Dooley discloses methods of preparing therapeutic exosomes using a protein newly-identified to be enriched on the surface of exosomes (abstract), such as PTGFRN, BSG, IGSF2, IGSF3, IGSF8, ITGB1, ITGA4, SLC3A2, ATP1A1, ATP1A2, ATP1A3, ATP1A4, ATP1B3, ATP2B1, ATP2B2, ATP2B3, ATP2B4-all of which are disclosed as possible species of the instantly claimed Scaffold X (column 1, line 60-column 2, line 25). Dooley discloses that these exosome proteins are better at producing surface engineered exosomes than other known exosome scaffold proteins, such as tetraspannins (column 2, lines 15-25), thereby facilitating presentation of a targeting moiety or a therapeutically relevant protein on the surface of said exosome (column 2, lines 42-49). Thus, Dooley discloses that proteins newly-identified to be enriched on the surface of exosomes are better at producing surface engineered exosomes for presentation of a targeting moiety or a therapeutically relevant protein on the surface of said exosome.
Given that Shemi, Revenko, Bolen, and Haraszti et al., 2018 collectively disclose the exosome comprising an antisense oligonucleotide linked to an anchoring moiety of claim 36 and that Dooley discloses that proteins newly-identified to be enriched on the surface of exosomes (such as PTGFRN) are better at producing surface engineered exosomes for presentation of a targeting moiety or a therapeutically relevant protein on the surface of said exosome, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to further engineer the exosome comprising an antisense oligonucleotide linked to an anchoring moiety to further comprise a scaffold moiety such as PTGFRN, as disclosed in Dooley, to predictably produce a surface engineered exosome that effectively and robustly presents a targeting moiety or a therapeutically relevant protein on the surface of said exosome. One would have been motivated to make such a modification in order to receive the expected benefit of producing surface engineered exosomes for presentation of a targeting moiety or a therapeutically relevant protein on the surface of said exosome.
Conclusion
No claims are allowed.
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 Sarah E Allen whose telephone number is (571)272-0408. The examiner can normally be reached M-Th 8-5, F 8-12.
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/SARAH E ALLEN/Examiner, Art Unit 1637
/J. E. ANGELL, Ph.D./Primary Examiner, Art Unit 1637