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 .
Claims 1-15 are pending and under consideration.
Priority
Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged. Applicant has not complied with one or more conditions for receiving the benefit of an earlier filing date under 35 U.S.C. 119(e) as follows:
The later-filed application must be an application for a patent for an invention which is also disclosed in the prior application (the parent or original nonprovisional application or provisional application). The disclosure of the invention in the parent application and in the later-filed application must be sufficient to comply with the requirements of 35 U.S.C. 112(a) or the first paragraph of pre-AIA 35 U.S.C. 112, except for the best mode requirement. See Transco Products, Inc. v. Performance Contracting, Inc., 38 F.3d 551, 32 USPQ2d 1077 (Fed. Cir. 1994).
The disclosure of the prior-filed application, Application No. 63/112,924, fails to provide adequate support or enablement in the manner provided by 35 U.S.C. 112(a) or pre-AIA 35 U.S.C. 112, first paragraph for one or more claims of this application.
While the provisional application generically discloses steroid hormone receptor coactivator and lists: “the erythroblast transformation-specific transcription factor ERG; p160 coactivators inclusive of steroid receptor coactivators, SRC-1, SRC-2, SRC-3; Vav3 a Rho GTPase guanine nucleotide exchange factor; E2F1; ATAD2; CBP/p300; Leupaxin; FHL2; and the ARA family of proteins.,” (Page 40, lines 29-32; Page 40, lines 34-37; and Page 51-52, lines 37-2), it does not name the species of “steroid hormone receptor coactivator(s)” of BRAC1 or Zac1, and therefore lacks support.
Claim 1 has an effective filing date of 11/12/2020, which is the filing date of provisional application 63/112,924.
Claims 2-15 have an effective filing date of 11/12/2021, which is the filing date of PCT/NZ/2021/050201.
Information Disclosure Statement
Receipt of the information disclosure statement on 12/18/2024 is acknowledged. The signed and initialed PTO-1449 has been mailed with this action.
Drawings
The drawings are objected to because Figure 2, 3, and 4 recite the title as “Insitu androgen IVT assay”. It would be remedial to add a space between in and situ to recite “In situ androgen IVT assay” as the figure title(s).
Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Specification
The disclosure is objected to because of the following informalities: Applicant discloses BRAC1 as a coactivator of a steroid hormone receptor, however, no such protein exists in nature. It would be remedial to change BRAC1 to BRCA1, a known androgen receptor coactivator; see pages 32 and 46 of instant specification. It is noted that Applicant properly discloses BRCA1 in Example 10 at Line 17 on page 101.
Appropriate correction is required.
Claim Objections
Claim 1 is objected to because of the following informalities: Applicant claims, “…where the response element (b) is located between the promoter sequence (a) and the reporter construct (c)…”. It would be remedial to amend the phrase “is located between the promoter sequence (a) and…” to “is located between the polymerase promoter sequence (a) and …” such that consistent claim terminology is used.
Claim 2 is objected to because of the following informalities:
Applicant is claiming BRAC1 as a coactivator of a steroid hormone receptor, however, no such protein exists in nature. “BRAC1” is a simple typographical error that should be changed to “BRCA1”.
Applicant is claiming, “…erythroblast transformation-specific transcription factor ERG;…,” and ERG is the official symbol of ETS transcription factor (NCBI Gene ID: 2078). Please amend claim to recite … “erythroblast transformation-specific transcription factor (ERG);…”.
Applicant is claiming SRC-2 as well as GRIP1, which are both alternative names for nuclear receptor coactivator 2 (NCBI Gene ID: 10499). Please amend to recite only one of the alternative names.
Applicant uses a combination of spelling out full protein names and using official symbols. It would be remedial to spell out each protein name as Applicant has already done for instant claim 3.
Appropriate correction is required.
Claims 4-15 are objected to under 37 CFR 1.75(c) as being in improper form because a multiple dependent claim cannot depend from any other multiple dependent claim(s). See MPEP § 608.01(n). Accordingly, the claims have not been further treated on the merits.
Claim Interpretation
Claim 1 recites the limitation of “… (ii) a nucleic acid molecule comprising: (a) a polymerase promoter sequence comprising or consisting in SEQ ID NO: 85; ...”.
When determining the broadest reasonable interpretation of claim 1, when the phrase “consisting of” appears in the claim body, rather than the preamble, the MPEP (Chapter 2111.03(II)) states, “…the "consisting of" phrase limits only the element set forth in that clause; other elements are not excluded from the claim as a whole. Mannesmann Demag Corp. v. Engineered Metal Products Co., 793 F.2d 1279, 230 USPQ 45 (Fed. Cir. 1986).”
In a more technology-related case, “In determining the scope of applicant’s claims directed to "a purified oligonucleotide comprising at least a portion of the nucleotide sequence of SEQ ID NO:1 wherein said portion consists of the nucleotide sequence from … to 2473 of SEQ ID NO:1, and wherein said portion of the nucleotide sequence of SEQ ID NO:1 has promoter activity," the court stated that the use of "consists" in the body of the claims did not limit the open-ended "comprising" language in the claims (emphases added). Id. at 1257, 73 USPQ2d at 1367. The court affirmed the Board’s interpretation that the transition phrase "consists" did not limit the claims to only the recited numbered nucleotide sequences of SEQ ID NO:1 and that "the transition language ‘comprising’ allowed the claims to cover the entire involucrin gene plus other portions of the plasmid, as long as the gene contained the specific portions of SEQ ID NO:1 recited by the claim[s]." Id. at 1256, 73 USPQ2d at 1366.).” See also In re Crish, 393 F.3d 1253, 73 USPQ2d 1364 (Fed. Cir. 2004)
Thus, for the purpose of broadest reasonable interpretation the “… (ii) a nucleic acid molecule comprising: (a) a polymerase promoter sequence comprising or consisting in SEQ ID NO: 85;” of claim 1 will be interpreted as a nucleic acid molecule comprising: (a) a polymerase promoter sequence comprising SEQ ID NO: 85; or (b) a polymerase promoter sequence found in SEQ ID NO: 85 (i.e., a T7 promoter sequence that is less than all of SEQ ID NO: 85 but is “in SEQ ID NO: 85.”
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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claim(s) 1 and 3 is/are rejected under 35 U.S.C. 103 as being obvious over Heather et al (US 2022/0214363 A1, with the effective filing date of May 7th, 2019) in view of Stech et al (Cell-free synthesis of functional antibodies using a coupled in vitro transcription-translation system based on CHO cell lysates, Scientific Reports, Vol 7, pages 1-15, 2017).
The applied reference has a common joint inventor of Alison Kay Heather with the instant application. Based upon the earlier effectively filed date of the reference, it constitutes prior art under 35 U.S.C. 102(a)(2).
Regarding instant claim 1 which recites,
A test kit for screening a test sample for the presence of a ligand capable of eliciting a steroid hormone genomic response, the test kit comprising:
a cell lysate comprising a steroid hormone receptor that is capable of forming a ligand-receptor complex with a ligand from the test sample; and
a nucleic acid molecule comprising:
(a) a polymerase promoter sequence comprising or consisting in SEQ ID NO: 85;
(b) a response element that is capable of being bound by the ligand-receptor complex; and
(c) a reporter construct
where the response element (b) is located between the promoter sequence (a) and the reporter construct (c), and (a), (b) and (c) are operably linked; and
(iii) optionally, a T7 RNA polymerase.
Heather et al teaches a test kit for screening a test sample for the presence of a ligand capable of eliciting a steroid hormone genomic response. More specifically, Heather et al teaches at paragraph [0039], “In yet a further aspect of the present invention there is provided a test kit for screening a sample for the presence of a ligand capable of eliciting a steroid hormone genomic response, the test kit comprising: [0040] (i) a steroid hormone receptor that is capable of forming a receptor-ligand complex with a ligand from the sample; [0041] (ii) a nucleic acid molecule comprising: [0042] (a) a T7 RNA polymerase promoter sequence; [0043] (b) a response element that is capable of being bound by the receptor-ligand complex; and [0044] (c) a reporter construct where the response element (b) is located between the promoter sequence (a) and the reporter construct (c), and (a), (b) and (c) are operably linked; and [0045] (iii) a T7 RNA polymerase,…”.
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Moreover, SEQ ID NO:85 of instant claim 1 does contain within it a T7 RNA polymerase promoter/initiator sequence, as recited SEQ ID NO: 1 by the Heather et al publication (see below).
(Page 32 of Heather et al).
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(Instant application).
Regarding instant claim 3, which recites,
The test kit according to claim 1 or claim 2, further comprising a steroid hormone receptor corepressor comprising at least one of:(i) heat shock protein 90 (HSP90);(ii) a complex of HSP90 and heat shock protein 70 (HSP70);(iii) a complex of HSP90, HSP70 and heat shock protein 40 (HSP40);(iv) a complex of HSP90, HSP70, HSP40 and p23; (v) a complex of HSP90, HSP70, HSP40, p23 and heat shock protein organizing protein (Hop); (vi) a complex of HSP90, HSP70, HSP40, p23, Hop and 48kD Hip protein (Hip); (vii) a complex of HSP90, HSP70, HSP40, p23, Hop, Hip and p60 (viii) a complex of HSP90, HSP70, HSP40, p23, Hop, Hip, p60 and FKBP52;and (ix) any combination of (i) to (viii).
Heather et al further teaches the limitations of claim 3, in which the test kit further comprises at least one of the steroid hormone receptor corepressors. More specifically, Heather et al discloses at paragraph [0047], “In yet a further aspect of the present invention there is provided a test kit for screening a sample for the presence of a ligand capable of eliciting a steroid hormone genomic response, the test kit comprising: [0048] (i) a steroid hormone receptor that is capable of forming a receptor-ligand complex with a ligand from the sample; [0049] (ii) a steroid hormone receptor cofactor selected from heat shock protein 90 (HSP90), a complex of HSP90 and heat shock protein 70 (HSP70), a complex of HSP90, HSP70 and heat shock protein 40 (HSP40), a complex of HSP90, HSP70, HSP40 and p23, a complex of HSP90, HSP70, HSP40, p23 and heat shock protein organizing protein (Hop), a complex of HSP90, HSP70, HSP40, p23, Hop and 48 kD Hip protein (Hip), a complex of HSP90, HSP70, HSP40, p23, Hop, Hip and p60, and a complex of HSP90, HSP70, HSP40, p23, Hop, Hip, p60 and FKBP52; [0050] (iii) a nucleic acid molecule comprising: [0051] (a) a T7 RNA polymerase promoter sequence defined by SEQ ID NO: 1; [0052] (b) a response element that is capable of being bound by the receptor-ligand complex; and [0053] (c) a reporter construct where the response element (b) is located between the promoter sequence (a) and the reporter construct (c), and (a), (b) and (c) are operably linked; and [0054] (iv) a T7 RNA polymerase…”
Heather et al teaches a kit that is very similar to the kit of claim 1 except that Heather et al teaches that the kit comprises a steroid hormone receptor that is capable of forming a receptor-ligand complex with a ligand from a test sample, without indicating that the receptor hormone receptor is comprised in a cell lysate. More specifically, the only difference between instant claim 1 and [0031] of Heather et al, is that instant claim 1 requires “a cell lysate comprising a steroid hormone receptor.
Stech et al teaches combining cell lysates with template DNA to circumvent conventional issues with cell-based expression platforms. More specifically,
“In cell-free systems, protein synthesis is disconnected from cell viability and fate since the reactions are usually conducted using thoroughly prepared cell lysates which contain the molecular components necessary for translation, such as ribosomes, translation factors and enzymes. To initiate protein synthesis, the cell lysate is mixed with template DNA or mRNA and supplemented with amino acids and energy-regenerating components. This easy-to-handle working process circumvents many of the issues connected with conventional cell-based expression platforms. For example, cell-free reactions can be performed in a flexible scale, from microliter to milliliter over liter scale, depending on the amount of protein needed for further analysis. This easy adjustment of the manufacturing scale facilitates miniaturization, parallelization, and high-throughput analysis. Moreover, the system easily allows interventions to optimize protein synthesis or folding, since metabolic processes can be exclusively directed to the one target protein.”
(Page 2, paragraph 1, lines 10-20).
Given the success of Heather et al in teaching a test kit for screening a test sample for the presence of a ligand capable of eliciting a steroid hormone genomic response, teaching the limitations of adding in steroid hormone receptor cofactor(s), and the success of Stech et al with combining cellular lysates with template DNA to circumvent conventional issues related to cell-based expression systems, it would have been obvious to try to a person of ordinary skill in the art before the effective filling date of the claimed invention to utilize cell lysates as a form of an active steroid hormone receptor (teachings of Stech et al) with the test kit for screening a test sample for the presence of a ligand capable of eliciting a steroid hormone genomic response (teachings of Heather et al). One of ordinary skill in the art would have been motivated to take the suggestion of Heather et al paragraph [0500], “A person skilled in the art would also recognize that any steroid hormone receptor may be employed in the test kits, assays and methods of the present invention, provided that it retains the ability to bind to, and be activated by, a ligand of interest for detection. This includes, steroid hormone receptors, based on endogenous cellular forms, as well as recombinant or synthetic forms.”, and combine it with the teachings of Stech et al to yield the predictable results of a test kit comprising (a) a cell lysate comprising a steroid hormone receptor that is capable of forming a ligand-receptor complex with a ligand from the test sample.
Thus, claims 1 and 3 are obvious in view of the prior art.
This rejection under 35 U.S.C. 103 might be overcome by: (1) a showing under 37 CFR 1.130(a) that the subject matter disclosed in the reference was obtained directly or indirectly from the inventor or a joint inventor of this application and is thus not prior art in accordance with 35 U.S.C.102(b)(2)(A); (2) a showing under 37 CFR 1.130(b) of a prior public disclosure under 35 U.S.C. 102(b)(2)(B); or (3) a statement pursuant to 35 U.S.C. 102(b)(2)(C) establishing that, not later than the effective filing date of the claimed invention, the subject matter disclosed and the claimed invention were either owned by the same person or subject to an obligation of assignment to the same person or subject to a joint research agreement. See generally MPEP § 717.02.
Claim 1 is rejected under 35 U.S.C. 103 as being unpatentable over Tracey et al (Cited on IDS from 12/18/2024, NPL #7) in view of Byers et al (Cited on IDS from 12/18/2024, Foreign Patent Documents #2).
Regarding claim 1, which recites:
A test kit for screening a test sample for the presence of a ligand capable of eliciting a steroid hormone genomic response, the test kit comprising:
(i) a cell lysate comprising a steroid hormone receptor that is capable of forming a ligand-receptor complex with a ligand from the test sample; and
(ii) a nucleic acid molecule comprising:
(a) a polymerase promoter sequence comprising or consisting in SEQ ID NO: 85;
(b) a response element that is capable of being bound by the ligand-receptor complex; and
(c) a reporter construct
where the response element (b) is located between the promoter sequence (a) and the reporter construct (c), and (a), (b) and (c) are operably linked; and
(iii) optionally, a T7 RNA polymerase.
Tracey et al teaches the identification of a novel region in the rat oxytocin receptor promoter that contains an upstream palindromic estrogen response element capable of inducing transcription of the oxytocin receptor gene via E2 treatment of MCF7 cells. More specifically, Tracey et al teaches an MCF7 cell lysate comprising an oxytocin receptor that forms an estradiol-receptor complex with estradiol from a sample (Abstract, Fig. 6 and Fig. 8), and a reporter gene construct comprising a T7 promoter sequence (Fig. 3 and Page 1152-Section: Reporter constructs, Paragraph 2, Line 4), an estrogen response element (ERE) (Abstract, Fig. 1 and 3), and a reporter gene, the rat oxytocin receptor (Abstract, Fig. 7).
Despite Tracey et al teaching a cell lysate capable of forming a ligand-receptor complex with a ligand from a sample, and a nucleic acid that contains a T7 promoter sequence, a receptor element, and a reporter construct. Tracey et al does not teach “consisting or comprising SEQ ID NO: 85.”
Byers et al cures this deficiency by disclosing a plasmid, pLEV1 13 (SEQ ID NO: 14), with human leptin (a protein hormone) gene comprising a promoter sequence that is 100% identity match to the instant application’s SEQ ID NO: 85.
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It would have been obvious to a person of ordinary skill in the art before the effective filing date of the claimed invention to substitute the T7 promoter sequence in the Byers et al plasmid with the T7 sequence taught by Tracey et al. One would have been motivated to make this modification to yield a gene reporter construct with increased reporter output.
Claim 2 is rejected under 35 U.S.C. 103 as being unpatentable over Tracey et al (Cited on IDS from 12/18/2024, NPL #7) in view of Byers et al (Cited on IDS from 12/18/2024, Foreign Patent Documents #2), as applied to claim 1 above and further in view of Lee et al (Dissecting the molecular mechanism of nuclear receptor action: transcript coactivators and corepressors, Experimental and Molecular Medicine, Vol 32, No. 2, pages 53-60, 2000).
The combined disclosures of Tracey et al and Byers et al are described above and applied as before. However, these disclosures do not teach steroid hormone receptor coactivator(s) of instant claim 2.
Regarding claim 2, which recites:
The test kit according to claim 1, further comprising at least one steroid hormone receptor coactivator selected from erythroblast transformation-specific transcription factor ERG; one or more p160 coactivators inclusive of steroid receptor coactivators, SRC-1, SRC-2, SRC-3; Vav3 a Rho GTPase guanine nucleotide exchange factor; E2F1; ATAD2; CBP/p300; Leupaxin; FHL2; the ARA family of proteins; GRIP1; BRAC1; and Zac1.
Lee et al teaches that, “Genetic studies implicated that transcription cofactors with no specific DNA-binding activity are essential components of transcriptional regulation, which ultimately led to identify a series of nuclear receptor-interacting coregulatory proteins…” (Page 53, Column 1, lines 12-16). More specifically, Lee et al teaches “A group of related proteins were found to enhance ligand-induced transactivation function of several nuclear receptors, named the p160 family. These proteins are grouped into three subclasses based on their sequence homology; i.e., SRC-1/NCoA-1 (Hong et al., 1997; Torchia et al., 1997; Voegel et al., 1998), TIF2/GRIP1/NCoA-2 (Hong et al., 1997; Voegel et al., 1998), and p/CIP/ ACTR/AIB1/xSRC-3…” (Page 53, Column 2, lines 9-16). Lee et al further teaches, “For nuclear receptors, the interaction with CBP/p300 is ligand- and AF2-dependent, although this direct interaction does not appear to be essential with many nuclear receptors.” (Page 54, Column 1, Lines 8-11).
Given the knowledge in the field that transcriptional cofactors with no specific DNA-binding activity are essential components of transcriptional regulation, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to add at least one steroid hormone receptor coactivator to the test kit according to claim 1. One would have been motivated to include coactivators such as SRC-1, GRIP1, SRC-3, and/or CBP/p300 to yield the predictable result of including essential components for transcriptional regulation.
Claim 3 is rejected under 35 U.S.C. 103 as being unpatentable over Tracey et al (Cited on IDS from 12/18/2024, NPL #7) in view of Byers et al (Cited on IDS from 12/18/2024, Foreign Patent Documents #2), in view of Lee et al (Dissecting the molecular mechanism of nuclear receptor action: transcript coactivators and corepressors, Experimental and Molecular Medicine, Vol 32, No. 2, pages 53-60, 2000) as applied to claim 1 and 2 above and further in view of Smith et al (The Intersection of Steroid Receptors with Molecular Chaperones: Observations and Questions, Molecular Endocrinology, Vol 22, Page 2229-2240, 2008).
The combined disclosures of Tracey et al, Byers et al, and Lee at al are described above and applied as before. However, these disclosures do not teach steroid hormone receptor corepressor(s) of instant claim 3.
Regarding claim 3, which recites:
The test kit according to claim 1 or claim 2, further comprising a steroid hormone receptor corepressor comprising at least one of:(i) heat shock protein 90 (HSP90);(ii) a complex of HSP90 and heat shock protein 70 (HSP70);(iii) a complex of HSP90, HSP70 and heat shock protein 40 (HSP40);(iv) a complex of HSP90, HSP70, HSP40 and p23; (v) a complex of HSP90, HSP70, HSP40, p23 and heat shock protein organizing protein (Hop); (vi) a complex of HSP90, HSP70, HSP40, p23, Hop and 48kD Hip protein (Hip); (vii) a complex of HSP90, HSP70, HSP40, p23, Hop, Hip and p60 (viii) a complex of HSP90, HSP70, HSP40, p23, Hop, Hip, p60 and FKBP52;and (ix) any combination of (i) to (viii).
Smith et al teaches that, “All steroid receptors associate with associate with heat shock protein 90…. Receptor association with chaperones occurs in an ordered step-wise fashion and is necessary for the maintenance of unliganded receptor in a state ready to bind and respond to hormone. Chaperones additionally modulate how receptors response to hormone and activate target genes.” (Abstract, page 2229). Smith et al further teaches that, “Hsp90 in isolation does not bind the receptor LBD; instead, other chaperones must have established prior interactions on the LBD to recruit Hsp90 for direct binding. In vitro assemblies with purified proteins were used to define Hsp40, Hsp70, Hop, Hsp90, and p23 as the minimal system for efficient assembly of GR or PR complexes that have robust hormone-binding ability.” (Page 2230; Section “Multistep pathway for assembly of Hsp90 with Receptor”, paragraph 1). Smith et al further teaches, “The Hsp90 cochaperone proteins FKBP52, FKBP51, CyP40, and PP5 compete for a common Hsp90-binding site, and each can probably be identified at some level in all steroid receptor complexes… When present in PR, GR, or AR complexes, FKBP52 elevates hormone-binding affinity 2- to 5-fold as compared with complexes containing FKBP51, CyP40, or PP5.” (Page 2232-2233; Section “Cochaperones and modulation of steroid receptor activity”, paragraph 1).
Given the knowledge in the field that all steroid receptors associate with Hsp90, and that receptor association with chaperones is necessary for the maintenance of unliganded receptor(s) in a state ready to bind and respond to a hormone, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to add at least one steroid hormone receptor corepressor to the test kit according to claim(s) 1 or 2. One would have been motivated to include such corepressors and combinations thereof to yield the predictable result of including essential components for hormone/ligand binding and transcriptional regulation.
Conclusion
Citation of Pertinent Prior Art
The prior art made of record and not relied upon is considered pertinent to applicant's disclosure.
Dominy et al (US 11878060 B2, effective filing date of 08/07/2016)
Paragraph [0427] “cDNA encoding a target protein (e.g., see Tables 1-7) was cloned into a vector designed to drive RNA polymerase-mediated transcription from a T7 RNA polymerase promoter.” As well as, SEQ ID NO: 36, SEQ ID NO: 45, SEQ ID NO: 48, SEQ ID NO: 51, and SEQ ID NO: 54, are sequences that encompass the identical sequence of instant claim 1 SEQ ID: 85.
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No claims are allowed.
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/L.M.T./Examiner, Art Unit 1637
/J. E. ANGELL, Ph.D./Primary Examiner, Art Unit 1637