DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claim Status
Claims 1-8 were previously cancelled (9/2/2021). Claims 9, 11-20 and 22-28 have been amended (9/11/2025). Claims 29-33 are new (9/11/2025). No new matter has been added. Claims 9-33 are under examination.
Priority
Claims 9-33 receive the priority date of 3/13/2019, the filing date of Australian provisional application AU2019900836.
Objections Withdrawn
Specification:
The objections to the specification due to the use of a trademark or tradenames are withdrawn in view of Applicant’s amendments.
The objections to the specification due to the use of hyperlinks are withdrawn in view of Applicant’s amendments.
Claims:
The objections to write out abbreviations completely the first time used in claim 9 and to correct minor clerical issues to claims 9, 16, 19 and 28, as well, are withdrawn due to Applicant’s amendments.
Rejections Withdrawn
Claim Rejections - 35 USC § 112(b)
The rejections of claims 9-28 under 35 U.S.C. 112(b) or pre-AIA 35 U.S.C. 112, 2nd paragraph, are withdrawn in view of Applicant’s amendments of claims 9, 11-14, 18-20, 22-23, 27-28 to address and further clarify indefiniteness.
Claim Rejections - 35 USC § 101
The rejection of claims 9-28 under 35 U.S.C. 101 is withdrawn in view of Applicant’s amendments of claims 19, 11-20 and 22-28, as well as Applicant’s clarification of the intended invention. Specifically, the amended instant claims recite a specific, technically implemented method that applies empirically derived D-BP distance thresholds to transform genomic sequence data into a concrete determination of splice-site operability and variant pathogenicity. The claimed use of defined quantitative thresholds grounded in experimental data represents a practical application that provides significantly more than merely observing or describing a natural correlation. Accordingly, the claims are patent-eligible under Step 2A, and in the alternative, recite additional elements amounting to significantly more under Step 2B.
Rejections Maintained
Claim Rejections - 35 USC § 102
Claims 9-28 are rejected under 35 U.S.C. 102 (a)(1) and (a)(2) as being anticipated by Koon et al. (WO 2016/205749 A1, published 12/22/2016). Rejection has been modified to reflect Applicant’s amendments (9/11/2025).
Regarding claim 9, Koon teaches a method implementing precise genome targeting technologies to enable systematic reverse engineering of causal genetic variations by allowing selective perturbation of individual genetic elements, and advance medical applications (Paragraph 5, lines 1-5). Further, Koon teaches that these properties allow in vivo treatment to be applied to a wider range of diseases than ex vivo therapies (Paragraph 1145, lines 5-10). Koon also teaches that the nucleic acid components may comprise a putative CRISPR RNA (crRNA) sequence and that the pre-crRNA may comprise secondary structure that is sufficient for processing to yield the mature crRNA as well as crRNA loading onto the effector protein (Paragraph 38, lines 1-5), specifically, when targeting diseases within disease-causing splice-defects or splice-sites (Paragraph 692, line 1). Additionally, Koon teaches that the genetic variants or genome wide library includes an intron as a non-coding sequence, regulatory sequence or 5’ or 3’ splice-site or splice-defect (Paragraph 865, lines 1-5).
Koon also teaches that the polynucleotide is derived from genomic DNA and that the expression may include splicing of the mRNA in a eukaryotic cell and can further be linear or branched (i.e., modified amino acids, and it may be interrupted by non-amino acids) (Paragraph 786, lines 45-60). Further, Koon teaches that two or more of the elements expressed from the same or different regulatory elements, may be combined in a single vector, with one or more additional vectors or sequences providing any components of the nucleic acid-targeting system not included in the first vector (i.e., the coding sequence of one element may be located on the same or opposite strand of the coding sequence of a second element, and oriented in the same or opposite direction) (Paragraph 816, lines 5-15). Further, Koon teaches that a single promoter drives expression of a transcript encoding a nucleic acid-targeting effector protein and a guide RNA or related branch point site embedded within one or more intron sequences (i.e., each in a different intron, two or more in at least one intron, or all in a single intron) that are operably linked to and expressed to form a lariat or loop or specified configuration (Paragraph 816, lines 5-15).
Also, Koon teaches that a guide sequence is any polynucleotide sequence having sufficient complementarity with a target polynucleotide sequence to hybridize with the target sequence or 5’ splice site and direct sequence-specific binding or related branch point of a nucleic acid-targeting complex to the target sequence via degree of complementarity or number of nucleotides between a guide sequence and its corresponding target sequence, when optimally aligned using a suitable alignment algorithm, is about or more than about 50%, 60%, 75%, 80%, 85%, 90%, 95%, 97.5%, 99%, or more (Paragraph 817, lines 1-5). Koon teaches that a guide sequence or pre-mRNA splice site is about or more than about 5, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 35, 40, 45, 50, 75, or more nucleotides in length (Paragraph 817, lines 5-15).
Specifically, Koon teaches that homology or likelihood comparisons may be conducted by eye, or more usually, with the aid of readily available sequence comparison programs via calculating percent (%) homology or likelihood (i.e., high or low) between two or more sequences and may also calculate the sequence identity shared by two or more amino acid or nucleic acid sequences (Paragraph 786, lines 60-70). Koon further teaches that cleavage of a target polynucleotide sequence (or a sequence in the vicinity thereof) may be evaluated in a test tube by providing the target sequence, components of a nucleic acid-targeting complex, including the guide sequence or pre-mRNA splice-site to be tested and a control guide sequence different from the test guide sequence or branch point, and comparing binding or rate of cleavage at or in the vicinity of the target sequence between the test and control guide sequence reactions in order to determine sufficiency to form the complex (Paragraph 817, lines 15-25) and further determination for applications in medicine as drug delivery agents in the treatment of different diseases including cancer and virus inhibitors, as well as contrast agents for cell labeling (Paragraph 664, lines 1-10).
Regarding claim 10, Koon teaches that the previously described methodology can be applied to variants of uncertain significance (i.e., the role of TnpB in transposons remains uncertain as it has been shown that this protein is not required for transposition) (Paragraph 1318, lines 1-4).
Regarding claim 11, Koon teaches that multiple alignments of splice-sites or related branch-point sites contain expanded branches of novel (sub)types and the resultant bootstrap support values are given as percentage points and shown only for few relevant branches or those comprises in a target sequence or genetic variant (Figures 10A, 10B; Paragraph 113, lines 1-5).
Regarding claims 12-14, Koon teaches that the previously described method of genome targeting technologies for determining the likelihood of disease via targeted sequences involves a genetic variant via double strand or single strand break in one of the strands to be sufficiently close to target positions so that correction occurs, specifically that the distance is not more than 50, 100, 200, 300, 350 or 400 nucleotides (Paragraph 544, lines 1-5) and/or a template sequence or pre-mRNA splice-site and a polynucleotide comprising a target sequence or related branch-point site are optimally aligned, the nearest nucleotide of the template polynucleotide is within about 1, 5, 10, 15, 20, 25, 50, 75, 100, 200, 300, 400, 500, 1000, 5000 from the target sequence (Paragraph 821, lines 1-15) originating from a cell that does not have altered expression or edited genome (Paragraph 100, lines 1-10).
Regarding claims 15-18, Koon teaches that the previously described method of genome targeting technologies for determining the likelihood of disease via targeted sequences including modifications involving a strand break or deletion (Paragraph 9, lines 1-10). Further, Koon teaches that a change in sequence or deletion includes 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 20, or 50 nucleotides in length (Paragraph 553, lines 1-8). Additionally, Koon teaches that the previously described methodology involves genome editing or modifying sequences associated with or at a target locus of interest, including the integration of the DNA insert is facilitated by non-homologous end joining (NHEJ)-based gene insertion mechanisms (Paragraph 14, lines 5-10). Specifically, Koon teaches that guide sequence or pre-mRNA splice site directs sequence-specific binding of a CRISPR complex to a target sequence or branch-point site is assessed to determine if the components of a CRISPR system are sufficient to form a CRISPR complex or intron loop or double-stranded DNA loop (Paragraph 211, lines 20-25; Paragraph 212, lines 1-10).
Regarding claim 19, Koon teaches that the previously described method of genome targeting technologies for determining the likelihood of disease via targeted sequences can be used to cleave a disease RNA in a cell via functional domains may include but are not limited to translational initiator, translational activator, translational repressor, nucleases, in particular ribonucleases, a spliceosome, beads, a light inducible/controllable domain or a chemically inducible/controllable domain (Paragraph 236, lines 1-5; Paragraph 244, lines 1-5). Specifically, Koon teaches that the spliceosomes can be pre-assembled ribonucleoproteins (i.e., U1/U2 dependent) (Paragraph 974, lines 1-2).
Regarding claim 20, Koon teaches methodology including additional engineered receptors for immunoresponsive cells, for example to improve targeting of a T-cell attack and/or minimize side effects or development of cancer (Paragraph 1269, lines 10-15) involving the therapeutic method of treatment may comprise gene or genome editing, or gene therapy (Paragraph 56, lines 1-3). Specifically, Koon teaches that the disease model can be used to study the effects of mutations on the animal or cell and development and/or progression of the disease using measures commonly used in the study of the disease or for studying the effect of a pharmaceutically active compound on the treatment of disease (Paragraph 835, lines 1-3). Further, Koon teaches that these properties allow in vivo treatment to be applied to a wider range of diseases than ex vivo therapies (Paragraph 1145, lines 5-10). Koon also teaches that the nucleic acid components may comprise a putative CRISPR RNA (crRNA) sequence and that the pre-crRNA may comprise secondary structure that is sufficient for processing to yield the mature crRNA as well as crRNA loading onto the effector protein (Paragraph 38, lines 1-5), specifically, when targeting diseases within disease-causing splice-defects or splice-sites (Paragraph 692, line 1). Additionally, Koon teaches that the genetic variants or genome wide library includes an intron as a non-coding sequence, regulatory sequence or 5’ or 3’ splice-site or splice-defect (Paragraph 865, lines 1-5).
Koon also teaches that the polynucleotide is derived from genomic DNA and that the expression may include splicing of the mRNA in a eukaryotic cell and can further be linear or branched (i.e., modified amino acids, and it may be interrupted by non-amino acids) (Paragraph 786, lines 45-60). Further, Koon teaches that two or more of the elements expressed from the same or different regulatory elements, may be combined in a single vector, with one or more additional vectors or sequences providing any components of the nucleic acid-targeting system not included in the first vector (i.e., the coding sequence of one element may be located on the same or opposite strand of the coding sequence of a second element, and oriented in the same or opposite direction) (Paragraph 816, lines 5-15). Further, Koon teaches that a single promoter drives expression of a transcript encoding a nucleic acid-targeting effector protein and a guide RNA or related branch point site embedded within one or more intron sequences (i.e., each in a different intron, two or more in at least one intron, or all in a single intron) that are operably linked to and expressed to form a lariat or loop or specified configuration (Paragraph 816, lines 5-15).
Also, Koon teaches that a guide sequence is any polynucleotide sequence having sufficient complementarity with a target polynucleotide sequence to hybridize with the target sequence or 5’ splice site and direct sequence-specific binding or related branch point of a nucleic acid-targeting complex to the target sequence via degree of complementarity or number of nucleotides between a guide sequence and its corresponding target sequence, when optimally aligned using a suitable alignment algorithm, is about or more than about 50%, 60%, 75%, 80%, 85%, 90%, 95%, 97.5%, 99%, or more (Paragraph 817, lines 1-5). Koon teaches that a guide sequence or pre-mRNA splice site is about or more than about 5, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 35, 40, 45, 50, 75, or more nucleotides in length (Paragraph 817, lines 5-15).
Regarding claim 21, Koon teaches that the previously described treatment methodology for minimization of disease involving target sequences can be applied to variants of uncertain significance (i.e., the role of TnpB in transposons remains uncertain as it has been shown that this protein is not required for transposition) (Paragraph 1318, lines 1-4).
Regarding claim 22, Koon teaches that the previously described treatment methodology for minimization of disease involving target sequences involves multiple alignments of splice-sites or related branch-point sites contain expanded branches of novel (sub)types and the resultant bootstrap support values are given as percentage points and shown only for few relevant branches or those comprises in a target sequence or genetic variant (Figures 10A, 10B; Paragraph 113, lines 1-5).
Regarding claim 23, Koon teaches that the previously described treatment methodology for minimization of disease involving target sequences involves a genetic variant via double strand or single strand break in one of the strands to be sufficiently close to target positions so that correction occurs, specifically that the distance is not more than 50, 100, 200, 300, 350 or 400 nucleotides (Paragraph 544, lines 1-5) and/or a template sequence or pre-mRNA splice-site and a polynucleotide comprising a target sequence or related branch-point site are optimally aligned, the nearest nucleotide of the template polynucleotide is within about 1, 5, 10, 15, 20, 25, 50, 75, 100, 200, 300, 400, 500, 1000, 5000 from the target sequence (Paragraph 821, lines 1-15) originating from a cell that does not have altered expression or edited genome (Paragraph 100, lines 1-10).
Regarding claims 24-27, Koon teaches that the previously described treatment methodology for minimization of disease involving target sequences via targeted sequences including modifications involving a strand break or deletion (Paragraph 9, lines 1-10). Further, Koon teaches that a change in sequence or deletion includes 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 20, or 50 nucleotides in length (Paragraph 553, lines 1-8). Additionally, Koon teaches that the previously described methodology involves genome editing or modifying sequences associated with or at a target locus of interest, including the integration of the DNA insert is facilitated by non-homologous end joining (NHEJ)-based gene insertion mechanisms (Paragraph 14, lines 5-10). Specifically, Koon teaches that guide sequence or pre-mRNA splice site directs sequence-specific binding of a CRISPR complex to a target sequence or branch-point site is assessed to determine if the components of a CRISPR system are sufficient to form a CRISPR complex or intron loop or double-stranded DNA loop (Paragraph 211, lines 20-25; Paragraph 212, lines 1-10).
Regarding claim 28, Koon teaches that the previously described treatment methodology for minimization of disease involving target sequences can be used to cleave a disease RNA in a cell via functional domains may include but are not limited to translational initiator, translational activator, translational repressor, nucleases, in particular ribonucleases, a spliceosome, beads, a light inducible/controllable domain or a chemically inducible/controllable domain (Paragraph 236, lines 1-5; Paragraph 244, lines 1-5). Specifically, Koon teaches that the spliceosomes can be pre-assembled ribonucleoproteins (i.e., U1/U2 dependent) (Paragraph 974, lines 1-2).
Koon teaches each and every limitation of claims 9-28, and therefore Koon anticipates claims 9-28.
Applicant’s Response: The Applicant argues that Koon is directed to CRISPR-based genome editing and does not disclose or anticipate the claimed methods of predicting splice-site operability or variant pathogenicity based on donor-to-branch point (D-BP) distance. The references in Koon to introns, branching or sequence alignment are incidental to Cas protein classification and genome targeting, and do not teach quantifying D-BP span, interpreting splice efficiency, or assessing variants of uncertain significance. Accordingly, the Applicant contends that Koon neither discloses nor anticipates the claimed invention, and withdrawal of the 102 rejection is warranted.
Examiner’s Response to Traversal: Applicant’s arguments have been carefully and fully considered but are not found persuasive, as discussed below.
Pursuant to MPEP 2131 and 2131.01, anticipation is established when a single prior art reference discloses each and every claim limitation, either expressly or inherently, as arranged in the claim. Applicant’s amendments do not add structural or functional limitations that are not already disclosed or inherently present in Koon when the claims are given their broadest reasonable interpretation under MPEP 2111.
Firstly, the amended claims recite determining whether a donor 5’ splice-site to branch-point (D-BP) distance is sufficient or insufficient to enable formation of an intron-X lariat. Koon expressly teaches evaluating nucleotide distance, alignment length, and structural configuration between a splice site, a related branch-point site, and a guide template sequence to determine whether an intron loop or lariat-like structure is formed and whether the nucleic-acid targeting complex is functionally operative (Paragraphs 211-212, 816-817). These teachings necessarily require assessing whether the spacing between splice-related elements permits loop/lariat formation, thereby meeting the claimed “determining whether…sufficient to enable formation” limitation.
Further, the recited numerical D-BP distance thresholds do not confer novelty, as Koon teaches evaluating nucleotide spacing across overlapping and encompassing ranges when assessing alignment, cleavage or functional sufficiency relative to splice sites and related branch-point sequences (Paragraphs 544, 817, 821). Under MPEP 2131.02, optimization or selection of a value within a disclosed or overlapping range does not avoid anticipation.
Additionally, the Applicant argues that Koon does not teach “predicting splicing efficiency.” However, Koon teaches assessing whether splice sites or related branch-point sites are functional or defective, including splice-defect contexts, by evaluating sequence alignment, complementarity, and structural sufficiency to form splice-related complexes (Paragraphs 692, 786, 974). The determination of whether a splice-related structure forms or fails to form inherently constitutes a determination of splice operability, satisfying the claimed functional outcome.
Further, the amended claims recite determining the likelihood or pathogenicity of genetic variants, including VUS. Koon teaches applying its genome-targeting and assessment methodologies to genome-wide variant libraries, intronic and splice-site variants, and disease-associated splice defects (Paragraphs 865, 1318). The fact that Koon does not use the specific term “VUS” is not dispositive, as the functional evaluation of variants with uncertain outcomes is inherently disclosed (see MPEP 2112 for inherency).
More so, the amended claims reciting treatment or minimization of disease risk based on the determination are also anticipated. Koon teaches applying the disclosed assessment methodologies to therapeutic decision-making, including in vivo and ex vivo treatment of diseases involving splice defects, genome editing, and evaluation of disease progression or treatment efficacy (Paragraphs 835, 1145 and 1269). Thus, the additional treatment limitations do not distinguish over Koon.
Accordingly, Koon teaches each and every element of claims 9-28, arranged as claimed, including assessment of splice-site/branch-point spacing, determination of structural sufficiency for lariat formation, evaluation of splice operability, and application to disease-associated variants and treatment, since the amendments merely narrow or optimize parameters already taught by Koon. As a result, the rejection under 35 USC 102 (a)(1) and (a)(2) is therefore maintained.
New Rejections
Claim Rejections - 35 USC § 102
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 the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 29-33 are rejected under 35 U.S.C. 102 (a)(1) and (a)(2) as being anticipated by Koon et al. (WO 2016/205749 A1, published 12/22/2016).
Regarding claims 29-30, Koon teaches that a single promoter drives expression of a transcript encoding a nucleic acid-targeting effector protein and a guide RNA or related branch point site embedded within one or more intron sequences (i.e., each in a different intron, two or more in at least one intron, or all in a single intron) that are operably linked to and expressed to form a lariat or loop or specified configuration (Paragraph 816, lines 5-15).
Also, Koon teaches that a guide sequence is any polynucleotide sequence having sufficient complementarity with a target polynucleotide sequence to hybridize with the target sequence or 5’ splice site and direct sequence-specific binding or related branch point of a nucleic acid-targeting complex to the target sequence via degree of complementarity or number of nucleotides between a guide sequence and its corresponding target sequence, when optimally aligned using a suitable alignment algorithm, is about or more than about 50%, 60%, 75%, 80%, 85%, 90%, 95%, 97.5%, 99%, or more (Paragraph 817, lines 1-5). Koon teaches that a guide sequence or pre-mRNA splice site is about or more than about 5, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 35, 40, 45, 50, 75, or more nucleotides in length (Paragraph 817, lines 5-15).
Regarding claim 31, Koon teaches methodology including additional engineered receptors for immunoresponsive cells, for example to improve targeting of a T-cell attack and/or minimize side effects or development of cancer (Paragraph 1269, lines 10-15) involving the therapeutic method of treatment may comprise gene or genome editing, or gene therapy (Paragraph 56, lines 1-3).
Regarding claims 32-33, Koon teaches that these properties allow in vivo treatment to be applied to a wider range of diseases than ex vivo therapies (Paragraph 1145, lines 5-10). Koon also teaches that the nucleic acid components may comprise a putative CRISPR RNA (crRNA) sequence and that the pre-crRNA may comprise secondary structure that is sufficient for processing to yield the mature crRNA as well as crRNA loading onto the effector protein (Paragraph 38, lines 1-5), specifically, when targeting diseases within disease-causing splice-defects or splice-sites (Paragraph 692, line 1). Additionally, Koon teaches that the genetic variants or genome wide library includes an intron as a non-coding sequence, regulatory sequence or 5’ or 3’ splice-site or splice-defect (Paragraph 865, lines 1-5).
Koon also teaches that the polynucleotide is derived from genomic DNA and that the expression may include splicing of the mRNA in a eukaryotic cell and can further be linear or branched (i.e., modified amino acids, and it may be interrupted by non-amino acids) (Paragraph 786, lines 45-60). Further, Koon teaches that two or more of the elements expressed from the same or different regulatory elements, may be combined in a single vector, with one or more additional vectors or sequences providing any components of the nucleic acid-targeting system not included in the first vector (i.e., the coding sequence of one element may be located on the same or opposite strand of the coding sequence of a second element, and oriented in the same or opposite direction) (Paragraph 816, lines 5-15). Further, Koon teaches that a single promoter drives expression of a transcript encoding a nucleic acid-targeting effector protein and a guide RNA or related branch point site embedded within one or more intron sequences (i.e., each in a different intron, two or more in at least one intron, or all in a single intron) that are operably linked to and expressed to form a lariat or loop or specified configuration (Paragraph 816, lines 5-15).
Koon teaches each and every limitation of claims 29-33, and therefore Koon anticipates claims 29-33.
Conclusions
No claim is 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 extension fee 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 date of this final action.
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/ELIZABETH ROSE LAFAVE/ Examiner, Art Unit 1684
/HEATHER CALAMITA/ Supervisory Patent Examiner, Art Unit 1684