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 filed 01/02/2026 has been received and considered entered. This is a response to amendments and arguments filed 01/02/2026.
Claims Status
Claims 2, 18-19 is/are cancelled. Claim 21 is newly added. Claims 1, 3-17, and 20-21 is/are currently pending. Claims 1, 3-17, and 20-21 is/are under examination.
Information Disclosure Statement
The listing of references in the specification or in Applicant’s arguments is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, they have not been considered. Applicant has cited Lim (2020) and Lu-Nguyen (2021) on page 10 of arguments, but has not provided copies of either reference with an IDS. The Examiner has provided copies of these references with form PTO-892, such that these references are made part of the prosecution record.
Specification
The disclosure is objected to because it contains an embedded hyperlink and/or other form of browser-executable code. Applicant is required to delete the embedded hyperlink and/or other form of browser-executable code; references to websites should be limited to the top-level domain name without any prefix such as http:// or other browser-executable code. See MPEP § 608.01. Hyperlinks were found in paragraph [0032]. Applicant is advised to review the specification in order to ensure that all hyperlinks are identified and appropriately removed. Applicant has removed the http:// prefix from one hyperlink in paragraph [0032] but not the other.
Claim Interpretation
Claim 3 recites “at least two different base sequences encoding the guide RNA” but does not provide limitations regarding the second base sequence, wherein the first is interpreted to be one of SEQ ID NOs:1-4, 20, 51, 68, 138, 142, 146, 156, 158, and 161. The broadest reasonable interpretation is that “at least two different base sequences encoding the guide RNA” encompasses any additional sequence, including a tracrRNA (see specification paragraph [0019], “When Cas9 is used as the CRISPR effector protein, the ‘guide RNA’ refers to chimera RNA (to be referred to as ‘single guide RNA (sgRNA)’) comprising crRNA and trans-activating crRNA attached to its 3’-terminal (to be referred to as ‘tracrRNA’)”).
Claim Rejections - 35 USC § 112
112(a):
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.
Enablement:
Claims 20-21 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 enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention. This rejection is amended to address the addition of new claim 21, and is maintained.
The factors to be considered in determining whether a disclosure would require undue experimentation include:
A) The breadth of the claims;
(B) The nature of the invention;
(C) The state of the prior art;
(D) The level of one of ordinary skill;
(E) The level of predictability in the art;
(F) The amount of direction provided by the inventor;
(G) The existence of working examples; and
(H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure.
In re Wands, 8 USPQ2d, 1400 (CAFC 1988) and MPEP 2164.01.
The breadth of the claims:
With respect to claim breadth, the standard under 35 U.S.C. §112, first paragraph, entails the determination of what the claims recite and what the claims mean as a whole. As such, the broadest reasonable interpretation of the claimed methods is that they encompass methods of treating or preventing the disease fascioscapulohumeral muscular dystrophy (FSHD) by administering a gene editing complex comprising a guide RNA and a fusion protein comprising a nuclease-deficient CRISPR effector protein and a transcription repressor, and, more broadly encompassed by claim 21, reduction of DUX4 gene expression in vivo in “a subject in need thereof”, wherein “a subject in need thereof” is interpreted as being a subject with FSHD (see specification [0056]). A skilled artisan would not know how to use the methods with a reasonable expectation of success based solely on what is disclosed in the specification.
The amount of direction provided by the inventor and the level of predictability in the art:
The specification teaches that “[p]revention of the activation of DUX4 is expected to lead to the treatment of FSHD” (paragraph [0003]) and that “the present invention is expected to be able to treat FSHD” (paragraph [0012]) (emphasis added). The current state of the art teaches that, while dCas9-KRAB-gRNA systems have been used to reduce DUX4 expression in vitro, efficacy of clinical therapeutic applications of these systems has not yet been determined. Furthermore, the art teaches that that it is unclear whether dCas9-KRAB-gRNA systems could provide long-term gene silencing, or if reduction of DUX4 expression would provide a clinical benefit or slow disease progression, and teaches that representative animal models are lacking in the art, as large animal models would likely model human FSHD better than the existing small animal models (see Mariot, 2022: pages 3-6, 8-9). The specification as filed does not provide guidance that overcomes this unpredictability within the art.
The existence of working examples:
What is enabled by the working examples is narrow in comparison to the breadth of the claims: The specification discloses methods of administering the claimed dCas9-KRAB-gRNA system to cells in vitro (specification paragraphs [0084]-[0098]).
The quantity of experimentation needed to make or use the invention:
The standard of an enabling disclosure is not the ability to make and test if the invention works but one of the ability to make and use with a reasonable expectation of success. A patent is granted for a completed invention, not the general suggestion of an idea (MPEP 2164.03 and Chiron Corp. v. Genentech Inc., 363 F.3d 1247, 1254, 70 USPQ2d 1321, 1325-26 (Fed. Cir. 2004). The instant specification is not enabling because one cannot follow the guidance presented therein, or within the art at the time of filing, and practice the claimed method without first making a substantial inventive contribution. Given that the nature of the invention encompasses the treatment of FSHD, a person having ordinary skill in the art would have to perform multiple further experiments, in human clinical trials, or in animal models that are predictive of treatment of FSHD in humans, in order to demonstrate the invention could be used with a reasonable expectation of success. The amount of experimentation required for enabling guidance, commensurate in scope with what is claimed, goes beyond what is considered ‘routine' within the art, and constitutes undue further experimentation in order to use the method with a reasonable expectation of successfully treating any CNS disorder or neurodegenerative disease. Therefore, claim 20 is rejected under 35 U.S.C. 112, first paragraph, for failing to meet the enablement requirement.
Response to Arguments
Applicant's arguments filed 01/02/2026 have been fully considered but they are not persuasive.
Applicant has argued that Lim (2020) and Lu-Nguyen (2021), teaching antisense oligonucleotides targeting DUX4 and producing a therapeutic effect in mouse models, enable the method of instant claim 20. However, as addressed in the rejection above, mouse models cannot be assumed to be predictive of treatment of FSHD—a human disease which is more accurately modeled by large organisms. Moreover, evidence of treatment in a mouse model is not evidence of prevention in a mouse model, as prevention requires that the disease never develop to begin with; thus, even if Lim and Lu-Nguyen could have enabled a method of treatment, they could not have enabled a method of disease prevention. Furthermore, the antisense oligonucleotide systems taught by Lim and Lu-Nguyen are not analogous art; they do not provide evidence that a dCas9-transcriptional repressor system could provide or could be assumed to provide a similar therapeutic benefit, as the mechanisms of action of these two systems are disparate. Applicants would be enabled for a method of reducing DUX4 expression in vitro, based on the examined art and the present disclosure.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (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 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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claim(s) 1, 3-11, 13-17 is/are rejected under 35 U.S.C. 103 as being unpatentable over Jones (WO2018057863A1), as evidenced by NCBI Reference Sequence NC_000004.12 (2019). This rejection is amended to address the amendment of claim 1, and is maintained.
Regarding claim 1, Jones teaches a polynucleotide (claim 13) encoding a gene editing complex comprising:
(a) a sequence encoding a fusion protein comprising a nuclease-deficient CRISPR effector protein and a transcription repressor (claims 1, 6-8, 10, 13); and
(b) a sequence encoding a guide RNA that hybridizes to a target nucleic acid sequence in the expression regulatory region of human DUX4 gene (claim 1) (the instant specification describes “the expression regulatory region of DUX4 gene” as “any region in which the expression of human DUX4 gene can be suppressed by binding RNP to that region”; claim 1 of Johnson teaches that binding of the gene editing complex to the D4Z4 macrosatellite repeat region results in inhibition of DUX4 gene expression).
While Jones does not teach a guide RNA sequence 100% identical to SEQ ID NOs:2-4, 20, 51, 68, 138, 142, 146, 156, 158, or 161, Jones does teach multiple guide RNAs targeting different regions of the DUX4 gene (see Fig. 2B, Table 1, and page 27 lines 15-16: gRNAs targeting p13-E11, NDE, the DUX4 promoter, exon 1 of DUX4, and exon 3 of DUX4). It would have been obvious for an artisan at the time of filing that any guide RNA sequence targeting these elements of the DUX4 gene could be designed and used in place of or in conjunction with the guide RNA sequences taught by Jones. Such guide RNA sequences rendered obvious by the teachings of Jones would encompass instant SEQ ID NOs:2-4, 20, 138, and 142, as these claimed gRNA sequences target regions of the DUX4 expression regulatory region also targeted by the gRNA of Jones (see table below, wherein the instant claimed gRNA sequences and the gRNA sequences of Jones were aligned with BLAST to the reference sequence of human chromosome 4, NCBI Reference Sequence NC_000004.12, and sorted by targeted sequence start position (“1st target”, “2nd target”); Jones Fig. 2A and Table 1 teach that Jones SEQ ID NOs:1-2 target the 5’ end of the p13-E11 sequence, SEQ ID NOs:3-5 target the NDE and exon 1, SEQ ID NOs:6-8 target the DUX4 promoter, SEQ ID NOs:9-11 target exon 3).
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Based on the table above and Jones Fig. 2A and Table 1, instant SEQ ID NOs:2-4 and 138 target the NDE, and instant SEQ ID NOs:142 and 20 target the DUX4 promoter. Furthermore, Jones teaches that gRNA targeting the NDE and the DUX4 promoter region exhibit the greatest reduction of DUX4 expression, compared to gRNAs targeting the p13-E11 sequence or DUX4 exon 3 (see Fig. 3A). Based on the gRNA sequences, DUX4 expression regulatory region map, and transcriptional repression results taught by Jones, it would have been obvious to a person of ordinary skill in the art at the time of filing to design gRNAs targeting alternate sequences in the DUX4 NDE and promoter regions for use with the dCas9-KRAB fusion protein of Jones in the gene editing complex of Jones. Based on the results taught by Jones in Fig. 3A, such an artisan would have a reasonable expectation of success in reducing expression of DUX4 using gRNAs targeting alternate sequences in the DUX4 NDE and promoter regions.
Regarding claim 3, Jones teaches that the gRNA-encoding sequence comprises the additional different base sequence of a tracrRNA sequence (page 10 lines 14-16).
Regarding claims 4-5, Jones teaches that the transcriptional repressor is KRAB (claim 11).
Regarding claims 6-7, Jones teaches that the CRISPR effector protein is S. aureus dCas9 (claims 6-8).
Regarding claim 8, Jones teaches that the polynucleotide further comprises a promoter sequence operably linked to the sequence encoding the guide RNA and a promoter sequence operably linked to the sequence encoding the fusion protein (pages 24 line 26-page 25 line 13).
Regarding claims 9-10, Jones teaches that the promoter sequence operably linked to the sequence encoding the guide RNA is the U6 promoter (pages 24 line 26-page 25 line 13).
Regarding claim 11, Jones teaches that the promoter sequence operably linked to the sequence encoding the fusion protein is a ubiquitous promoter (pages 24 line 26-page 25 line 13: promoter is EF1).
Regarding claim 13, Jones teaches a vector comprising the polynucleotide encoding the gene editing complex (claims 13-16).
Regarding claims 14-17, Jones teaches that the vector is an AAV vector (claim 16), and specifically an AAV1, AAV2, AAV6, AAV7, AAV8, or AAV9 (page 23 lines 10-25).
Claim(s) 1, 8-17 is/are rejected under 35 U.S.C. 103 as being unpatentable over Jones (WO2018057863A1), as evidenced by NCBI Reference Sequence NC_000004.12 (2019), as applied to claims 1, 8-11 and 13-17 above, and further in view of Lau (2017). This rejection is maintained.
The teachings of Jones render obvious the limitations of claims 1, 8, and 11, as described above.
However, Jones does not teach that the ubiquitous promoter is the EFS promoter, CMV promoter, or CAG promoter.
Lau teaches promoters operably linked to a sequence encoding a CRISPR protein.
Regarding claims 9-10, Lau teaches that the U6 promoter or H1 promoter can be used to express gRNA in multiple tissues (Table 2).
Regarding claim 12, Lau teaches that the EFS, CMV, and CAG promoters are used to express CRISPR nucleases in different tissues and cell types by placing the genes encoding the CRISPR nucleases under the control of the EFS, CMV, or CAG promoters (page 11; Fig. 1C; Table 2).
Regarding claims 13-17, Lau teaches that AAV serotypes AAV1, AAV2, AAV6, AAV9, and AAVrh74 are used to introduce CRISPR systems into different tissues (see Table 2).
Jones teaches that the Cas nuclease-encoding sequence has associated regulatory sequences, including a promoter (page 23 lines 10-14). While the only example of such a promoter taught by Jones is the EF1 promoter, it would have been obvious to a person of ordinary skill in the art at the time of filing that any known promoter sequence could be used, so long as the known promoter sequence was capable of driving expression of a transgene. Lau teaches a variety of promoters, including ubiquitous promoters EFS, CMV, and CAG, which have been used to drive expression of a Cas nuclease. It thus would have been obvious to an artisan that the EFS, CMV, and CAG promoters could be used in the invention of Jones to drive expression of the dCas9-KRAB fusion protein.
Claim(s) 1-17 is/are rejected under 35 U.S.C. 103 as being unpatentable over Himeda (WO2021211325A1; effective filing date 04/17/2020), in view of Lau (2017), as evidenced by NCBI Reference Sequence NC_000004.12 (2019). This rejection is amended to address the amendment of claim 1, and is maintained.
Regarding claim 1, Himeda teaches a polynucleotide encoding:
(a) a guide RNA of SEQ ID NO:43 (SEQ ID NO:43 is 95.5% identical to instant SEQ ID NO:2, wherein SEQ ID NO:43 comprises a deletion of nucleotide 1 of instant SEQ ID NO:2 and comprises the continuous sequence of nucleotides 2-22 of instant SEQ ID NO:2, see alignment below), targeting the DUX4 locus (claim 3); and
(b) a fusion protein comprising a nuclease-deficient CRISPR effector and a transcription repressor (epigenetic repressor) (claims 1, 7).
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Himeda teaches that an “sgRNA sequence can be determined, for example, by identifying [an] sgRNA binding site by locating a PAM sequence in the target DNA, and then choosing about 12 to 20 or more nucleotides immediately upstream of the PAM site” and that the sgRNA comprises at least 12-20 nucleotides complementary to a target DNA sequence (page 21 lines 20-27). Instant SEQ ID NO:2 and Himeda SEQ ID NO:43 are 100% complementary to the same region of the reference human chromosome 4 sequence of NC_000004.12 (see alignment below between instant SEQ ID NO:2 and the reference chromosome sequence). Himeda teaches that the targeting sequence of an sgRNA may be longer than 20 nucleotides, including longer than 21 nucleotides (SEQ ID NO:43 is 21 nucleotides long). The only difference between Himeda SEQ ID NO:43 and instant SEQ ID NO:2 is that instant SEQ ID NO:2 comprises one more nucleotide upstream compared to SEQ ID NO:43. Given that Himeda teaches that an sgRNA targeting sequence may be longer, and that Himeda teaches an sgRNA targeting the same sequence within the DUX4 gene, and Himeda teaches that sgRNA #6 (SEQ ID NO:43) used with MeCP2-dCas9 significantly reduces DUX4 expression (Fig. 2B; Table 2), it would have been obvious to an artisan that sgRNA molecules targeting the same DUX4 sequence but with shorter or longer targeting sequences, within the parameters set by Himeda, would be equivalent to the sgRNA of SEQ ID NO:43 of Himeda, and would be obvious alternatives.
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Regarding claim 3, Himeda teaches that the polynucleotide encoding the gRNA sequence further comprises a “common scaffold RNA sequence” or tracrRNA sequence (page 21 lines 20-23).
Regarding claim 4, Himeda teaches that the transcriptional repressor is KRAB (page 67 lines 1-5), MeCP2, or HP1A (claim 6).
Regarding claim 5, Himeda teaches that the transcriptional repressor is KRAB (page 67 lines 1-5).
Regarding claims 6-7, Himeda teaches that the nuclease-deficient CRISPR effector protein is dCas9 from S. aureus (claim 5: “dSaCas9” is dCas9 from S. aureus; see also page 23 lines 3-4).
Regarding claim 8, Himeda teaches that the polynucleotide further comprises a first promoter operably linked to the sequence encoding the guide RNA (claim 2) and a second promoter operably linked to the sequence encoding the fusion protein (page 21 line 28-page 22 line 11).
Regarding claims 9-10, Himeda teaches that the first promoter operably linked to the sequence encoding the gRNA is the U6 promoter (claim 2).
Regarding claims 13-15, Himeda teaches an AAV vector comprising the polynucleotide encoding the gRNA and fusion protein (claims 10, 19).
Regarding claims 16-17, Himeda teaches that the AAV vector is serotype AAV9 (page 66 lines 17-24; page 69 lines 5-7).
However, Himeda does not teach that the second promoter operably linked to the sequence encoding the fusion protein is a ubiquitous promoter. Himeda teaches that the second promoter is a skeletal muscle-specific CKM promoter (page 22 lines 8-11).
Lau teaches ubiquitous promoters which are active in skeletal muscle.
Regarding claims 9-10, Lau teaches that the U6 promoter or H1 promoter can be used to express gRNA in multiple tissues (Table 2).
Regarding claims 11-12, Himeda teaches that a sequence encoding Cas9 can be placed under the control of ubiquitous promoter CMV or EFS, which are active in skeletal muscle (Fig. 1C; page 11; Table 2).
Regarding claims 13-17, Lau teaches that AAV serotypes AAV1, AAV2, AAV6, AAV9, and AAVrh74 are used to introduce CRISPR systems into different tissues (see Table 2).
Himeda teaches that the gene editing complex is expressed in skeletal muscle cells by placing the fusion protein-encoding sequence under the control of skeletal muscle-specific promoter CKM. It would have been obvious to a person of ordinary skill in the art at the time of filing that the CKM promoter of Himeda could be replaced with CMV or EFS promoter sequences, taught by Lau to be active in multiple tissue types, in order to enable expression of the gene editing complex in skeletal muscle cells and other tissues.
Response to Arguments
Applicant's arguments filed 01/02/2026 have been fully considered but they are not persuasive.
Applicant has argued that because the claimed gRNA sequences were shown in the specification to “effectively suppress the expression level of DUX4”, the claimed gRNAs “exhibit a remarkable effect beyond what a person skilled in the art could have predicted” and that “[n]othing in the cited references suggested that such sequences existed or guided a person skill in the art to them”, regarding both the rejections over Jones and over Himeda (pages 11-12).
Jones teaches in Figure 3A that all of the gRNAs tested which targeted the promoter region of DUX4 gene suppressed DUX4-fl expression. An artisan would have reasonably assumed that any gRNA targeting a sequence within or between the sequences targeted by Jones SEQ ID NOs:3-8 (such as a gRNA of instant SEQ ID NO:2, as shown in the table in the rejection above) would also reduce DUX4-fl expression, and thus would be obvious to try in a composition or method for reducing DUX4 expression.
The gRNA of SEQ ID NO:43 taught by Himeda is one nucleotide shorter than the gRNA of instant SEQ ID NO:2, but targets the same sequence within the DUX4 gene. Himeda teaches that an “sgRNA sequence can be determined, for example, by identifying [an] sgRNA binding site by locating a PAM sequence in the target DNA, and then choosing about 12 to 20 or more nucleotides immediately upstream of the PAM site” and that the sgRNA comprises at least 12-20 nucleotides complementary to a target DNA sequence (page 21 lines 20-27). Instant SEQ ID NO:2 and Himeda SEQ ID NO:43 are 100% complementary to the reference human chromosome 4 sequence of NC_000004.12. Himeda teaches that the targeting sequence of an sgRNA may be longer than 20 nucleotides, including longer than 21 nucleotides (SEQ ID NO:43 is 21 nucleotides long). The only difference between Himeda SEQ ID NO:43 and instant SEQ ID NO:2 is that instant SEQ ID NO:2 comprises one more nucleotide upstream from the PAM site compared to SEQ ID NO:43. Given that Himeda teaches that an sgRNA targeting sequence may be longer, and that Himeda teaches an sgRNA targeting the same sequence within the DUX4 gene, and Himeda teaches that sgRNA #6 (SEQ ID NO:43) used with MeCP2-dCas9 significantly reduces DUX4 expression (Fig. 2B; Table 2), it would have been obvious to an artisan that sgRNA molecules targeting the same DUX4 sequence but with shorter or longer targeting sequences, within the parameters set by Himeda, would be equivalent to the sgRNA of SEQ ID NO:43 of Himeda, and would be obvious alternatives.
Conclusion
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.
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/AFRICA M MCLEOD/ Examiner, Art Unit 1635
/KIMBERLY CHONG/ Primary Examiner, Art Unit 1636